---
_id: '3932'
abstract:
- lang: eng
  text: 'OBJECTIVES: The EGFR is expressed in malignant ovarian tumor tissue, and
    tissue content of EGFR has been directly associated with poor prognosis in patients
    with ovarian cancer. The uPA system plays a role in pericellular proteolysis,
    cell migration, invasion, and is over-expressed in ovarian cancer. This study
    explored the effects of EGF on uPAR expression in the ovarian cancer cell line
    OVCAR-3. METHODS: We used OVCAR-3 cells and the following methods: cell migration
    assay, time-lapse video microscopy, real-time PCR, assays for cellular binding
    of 125I-uPA and cellular degradation of 125I-uPA:PAI-1 complex, biosynthetic labeling
    using 35S-methionin, Western blot, Northern blot, and ELISAs for uPA, PAI-1, and
    uPAR. RESULTS: EGF up-regulates both protein and mRNA not only for uPAR, but also
    for the ligand uPA and its inhibitor PAI-1. Cell surface uPAR, in control as well
    as EGF-stimulated cells, is present only in the intact, not the cleaved, form.
    Ligand binding experiments showed an increase of endogenously occupied uPAR, whereas
    non-occupied receptor sites were not increased. In addition, EGF treatment resulted
    in decreased degradation of radiolabeled uPA:PAI-1 complex. This suggests decreased
    internalization of uPAR, since the complex is internalized together with uPAR.
    Like EGF, colchicine, which inhibits endocytosis, increased cell surface expression
    of uPAR. In addition, we found an immediate increase of uPAR after exposing the
    cells to EGF and this was accompanied by a transient increase of cell migration.
    The increase of cell surface uPAR in response to EGF is accompanied by increased
    release of the soluble form of uPAR (suPAR) to the medium as well as by increased
    cell migration. Both uPAR and suPAR increased in cells treated with the endocytosis
    inhibitor colchicine even though cell migration was inhibited, suggesting that
    the mechanism of uPAR shedding is not related to cell migration. CONCLUSION: Increased
    cell surface uPAR in response to EGF stimulation results from mobilization of
    uPAR from detergent-resistant domains, increased expression of uPAR mRNA, and
    decreased internalization and degradation of uPAR. Both the anti-uPAR antibody
    R3, which inhibits binding of uPA, and the EGFR phosphorylation inhibitor Iressa
    inhibited cell migration in response to uPA as well as to EGF, suggesting that
    EGFR and uPAR are engaged in the same multiprotein assembly on the cell surface.'
author:
- first_name: Emir
  full_name: Henic, Emir
  last_name: Henic
- first_name: Michael K
  full_name: Michael Sixt
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
- first_name: Stefan
  full_name: Hansson, Stefan
  last_name: Hansson
- first_name: Gunilla
  full_name: Høyer-Hansen, Gunilla
  last_name: Høyer Hansen
- first_name: Bertil
  full_name: Casslén, Bertil
  last_name: Casslén
citation:
  ama: Henic E, Sixt MK, Hansson S, Høyer Hansen G, Casslén B. EGF-stimulated migration
    in ovarian cancer cells is associated with decreased internalization, increased
    surface expression, and increased shedding of the urokinase plasminogen activator
    receptor. <i>Gynecologic Oncology</i>. 2006;101(1):28-39. doi:<a href="https://doi.org/10.1016/j.ygyno.2005.09.038">10.1016/j.ygyno.2005.09.038</a>
  apa: Henic, E., Sixt, M. K., Hansson, S., Høyer Hansen, G., &#38; Casslén, B. (2006).
    EGF-stimulated migration in ovarian cancer cells is associated with decreased
    internalization, increased surface expression, and increased shedding of the urokinase
    plasminogen activator receptor. <i>Gynecologic Oncology</i>. Elsevier. <a href="https://doi.org/10.1016/j.ygyno.2005.09.038">https://doi.org/10.1016/j.ygyno.2005.09.038</a>
  chicago: Henic, Emir, Michael K Sixt, Stefan Hansson, Gunilla Høyer Hansen, and
    Bertil Casslén. “EGF-Stimulated Migration in Ovarian Cancer Cells Is Associated
    with Decreased Internalization, Increased Surface Expression, and Increased Shedding
    of the Urokinase Plasminogen Activator Receptor.” <i>Gynecologic Oncology</i>.
    Elsevier, 2006. <a href="https://doi.org/10.1016/j.ygyno.2005.09.038">https://doi.org/10.1016/j.ygyno.2005.09.038</a>.
  ieee: E. Henic, M. K. Sixt, S. Hansson, G. Høyer Hansen, and B. Casslén, “EGF-stimulated
    migration in ovarian cancer cells is associated with decreased internalization,
    increased surface expression, and increased shedding of the urokinase plasminogen
    activator receptor,” <i>Gynecologic Oncology</i>, vol. 101, no. 1. Elsevier, pp.
    28–39, 2006.
  ista: Henic E, Sixt MK, Hansson S, Høyer Hansen G, Casslén B. 2006. EGF-stimulated
    migration in ovarian cancer cells is associated with decreased internalization,
    increased surface expression, and increased shedding of the urokinase plasminogen
    activator receptor. Gynecologic Oncology. 101(1), 28–39.
  mla: Henic, Emir, et al. “EGF-Stimulated Migration in Ovarian Cancer Cells Is Associated
    with Decreased Internalization, Increased Surface Expression, and Increased Shedding
    of the Urokinase Plasminogen Activator Receptor.” <i>Gynecologic Oncology</i>,
    vol. 101, no. 1, Elsevier, 2006, pp. 28–39, doi:<a href="https://doi.org/10.1016/j.ygyno.2005.09.038">10.1016/j.ygyno.2005.09.038</a>.
  short: E. Henic, M.K. Sixt, S. Hansson, G. Høyer Hansen, B. Casslén, Gynecologic
    Oncology 101 (2006) 28–39.
date_created: 2018-12-11T12:05:57Z
date_published: 2006-04-01T00:00:00Z
date_updated: 2021-01-12T07:53:17Z
day: '01'
doi: 10.1016/j.ygyno.2005.09.038
extern: 1
intvolume: '       101'
issue: '1'
month: '04'
page: 28 - 39
publication: Gynecologic Oncology
publication_status: published
publisher: Elsevier
publist_id: '2194'
quality_controlled: 0
status: public
title: EGF-stimulated migration in ovarian cancer cells is associated with decreased
  internalization, increased surface expression, and increased shedding of the urokinase
  plasminogen activator receptor
type: journal_article
volume: 101
year: '2006'
...
---
_id: '3934'
abstract:
- lang: eng
  text: T cells develop in the thymus in a highly specialized cellular and extracellular
    microenvironment. The basement membrane molecule, laminin-5 (LN-5), is predominantly
    found in the medulla of the human thymic lobules. Using high-resolution light
    microscopy, we show here that LN-5 is localized in a bi-membranous conduit-like
    structure, together with other typical basement membrane components including
    collagen type IV, nidogen and perlecan. Other interstitial matrix components,
    such as fibrillin-1 or -2, tenascin-C or fibrillar collagen types, were also associated
    with these structures. Three-dimensional (3D) confocal microscopy suggested a
    tubular structure, whereas immunoelectron and transmission electron microscopy
    showed that the core of these tubes contained fibrillar collagens enwrapped by
    the LN-5-containing membrane. These medullary conduits are surrounded by thymic
    epithelial cells, which in vitro were found to bind LN-5, but also fibrillin and
    tenascin-C. Dendritic cells were also detected in close vicinity to the conduits.
    Both of these stromal cell types express major histocompatibility complex (MHC)
    class II molecules capable of antigen presentation. The conduits are connected
    to blood vessels but, with an average diameter of 2 mum, they are too small to
    transport cells. However, evidence is provided that smaller molecules such as
    a 10 kDa dextran, but not large molecules (&gt;500 kDa), can be transported in
    the conduits. These results clearly demonstrate that a conduit system, which is
    also known from secondary lymphatic organs such as lymph nodes and spleen, is
    present in the medulla of the human thymus, and that it might serve to transport
    small blood-borne molecules or chemokines to defined locations within the medulla.
author:
- first_name: Mihaela
  full_name: Drumea-Mirancea, Mihaela
  last_name: Drumea Mirancea
- first_name: Johannes
  full_name: Wessels, Johannes T
  last_name: Wessels
- first_name: Claudia
  full_name: Müller, Claudia A
  last_name: Müller
- first_name: Mike
  full_name: Essl, Mike
  last_name: Essl
- first_name: Johannes
  full_name: Eble, Johannes A
  last_name: Eble
- first_name: Eva
  full_name: Tolosa, Eva
  last_name: Tolosa
- first_name: Manuel
  full_name: Koch, Manuel
  last_name: Koch
- first_name: Dieter
  full_name: Reinhardt, Dieter P
  last_name: Reinhardt
- first_name: Michael K
  full_name: Michael Sixt
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
- first_name: Lydia
  full_name: Sorokin, Lydia
  last_name: Sorokin
- first_name: York
  full_name: Stierhof, York-Dieter
  last_name: Stierhof
- first_name: Heinz
  full_name: Schwarz, Heinz
  last_name: Schwarz
- first_name: Gerd
  full_name: Klein, Gerd
  last_name: Klein
citation:
  ama: 'Drumea Mirancea M, Wessels J, Müller C, et al. Characterization of a conduit
    system containing laminin-5 in the human thymus: a potential transport system
    for small molecules. <i>Journal of Cell Science</i>. 2006;119(Pt 7):1396-1405.
    doi:<a href="https://doi.org/10.1242/​jcs.02840">10.1242/​jcs.02840</a>'
  apa: 'Drumea Mirancea, M., Wessels, J., Müller, C., Essl, M., Eble, J., Tolosa,
    E., … Klein, G. (2006). Characterization of a conduit system containing laminin-5
    in the human thymus: a potential transport system for small molecules. <i>Journal
    of Cell Science</i>. Company of Biologists. <a href="https://doi.org/10.1242/​jcs.02840">https://doi.org/10.1242/​jcs.02840</a>'
  chicago: 'Drumea Mirancea, Mihaela, Johannes Wessels, Claudia Müller, Mike Essl,
    Johannes Eble, Eva Tolosa, Manuel Koch, et al. “Characterization of a Conduit
    System Containing Laminin-5 in the Human Thymus: A Potential Transport System
    for Small Molecules.” <i>Journal of Cell Science</i>. Company of Biologists, 2006.
    <a href="https://doi.org/10.1242/​jcs.02840">https://doi.org/10.1242/​jcs.02840</a>.'
  ieee: 'M. Drumea Mirancea <i>et al.</i>, “Characterization of a conduit system containing
    laminin-5 in the human thymus: a potential transport system for small molecules,”
    <i>Journal of Cell Science</i>, vol. 119, no. Pt 7. Company of Biologists, pp.
    1396–1405, 2006.'
  ista: 'Drumea Mirancea M, Wessels J, Müller C, Essl M, Eble J, Tolosa E, Koch M,
    Reinhardt D, Sixt MK, Sorokin L, Stierhof Y, Schwarz H, Klein G. 2006. Characterization
    of a conduit system containing laminin-5 in the human thymus: a potential transport
    system for small molecules. Journal of Cell Science. 119(Pt 7), 1396–1405.'
  mla: 'Drumea Mirancea, Mihaela, et al. “Characterization of a Conduit System Containing
    Laminin-5 in the Human Thymus: A Potential Transport System for Small Molecules.”
    <i>Journal of Cell Science</i>, vol. 119, no. Pt 7, Company of Biologists, 2006,
    pp. 1396–405, doi:<a href="https://doi.org/10.1242/​jcs.02840">10.1242/​jcs.02840</a>.'
  short: M. Drumea Mirancea, J. Wessels, C. Müller, M. Essl, J. Eble, E. Tolosa, M.
    Koch, D. Reinhardt, M.K. Sixt, L. Sorokin, Y. Stierhof, H. Schwarz, G. Klein,
    Journal of Cell Science 119 (2006) 1396–1405.
date_created: 2018-12-11T12:05:58Z
date_published: 2006-04-01T00:00:00Z
date_updated: 2021-01-12T07:53:18Z
day: '01'
doi: 10.1242/​jcs.02840
extern: 1
intvolume: '       119'
issue: Pt 7
month: '04'
page: 1396 - 1405
publication: Journal of Cell Science
publication_status: published
publisher: Company of Biologists
publist_id: '2192'
quality_controlled: 0
status: public
title: 'Characterization of a conduit system containing laminin-5 in the human thymus:
  a potential transport system for small molecules'
type: journal_article
volume: 119
year: '2006'
...
---
_id: '3935'
abstract:
- lang: eng
  text: Integrins regulate cell behavior through the assembly of multiprotein complexes
    at the site of cell adhesion. Parvins are components of such a multiprotein complex.
    They consist of three members (alpha-, beta-, and gamma-parvin), form a functional
    complex with integrin-linked kinase (ILK) and PINCH, and link integrins to the
    actin cytoskeleton. Whereas alpha- and beta-parvins are widely expressed, gamma-parvin
    has been reported to be expressed in hematopoietic organs. In the present study,
    we report the expression pattern of the parvins in hematopoietic cells and the
    phenotypic analysis of gamma-parvin-deficient mice. Whereas alpha-parvin is not
    expressed in hematopoietic cells, beta-parvin is only found in myeloid cells and
    gamma-parvin is present in both cells of the myeloid and lymphoid lineages, where
    it binds ILK. Surprisingly, loss of gamma-parvin expression had no effect on blood
    cell differentiation, proliferation, and survival and no consequence for the T-cell-dependent
    antibody response and lymphocyte and dendritic cell migration. These data indicate
    that despite the high expression of gamma-parvin in hematopoietic cells it must
    play a more subtle role for blood cell homeostasis.
author:
- first_name: Haiyan
  full_name: Chu, Haiyan
  last_name: Chu
- first_name: Ingo
  full_name: Thievessen, Ingo
  last_name: Thievessen
- first_name: Michael K
  full_name: Michael Sixt
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
- first_name: Tim
  full_name: Lämmermann, Tim
  last_name: Lämmermann
- first_name: Ari
  full_name: Waisman, Ari
  last_name: Waisman
- first_name: Attila
  full_name: Braun, Attila
  last_name: Braun
- first_name: Angelika
  full_name: Noegel, Angelika A
  last_name: Noegel
- first_name: Reinhard
  full_name: Fässler, Reinhard
  last_name: Fässler
citation:
  ama: Chu H, Thievessen I, Sixt MK, et al. γ-Parvin is dispensable for hematopoiesis,
    leukocyte trafficking, and T-cell-dependent antibody response. <i>Molecular and
    Cellular Biology</i>. 2006;26(5):1817-1825. doi:<a href="https://doi.org/10.1128/MCB.26.5.1817-1825.2006">10.1128/MCB.26.5.1817-1825.2006</a>
  apa: Chu, H., Thievessen, I., Sixt, M. K., Lämmermann, T., Waisman, A., Braun, A.,
    … Fässler, R. (2006). γ-Parvin is dispensable for hematopoiesis, leukocyte trafficking,
    and T-cell-dependent antibody response. <i>Molecular and Cellular Biology</i>.
    American Society for Microbiology. <a href="https://doi.org/10.1128/MCB.26.5.1817-1825.2006">https://doi.org/10.1128/MCB.26.5.1817-1825.2006</a>
  chicago: Chu, Haiyan, Ingo Thievessen, Michael K Sixt, Tim Lämmermann, Ari Waisman,
    Attila Braun, Angelika Noegel, and Reinhard Fässler. “γ-Parvin Is Dispensable
    for Hematopoiesis, Leukocyte Trafficking, and T-Cell-Dependent Antibody Response.”
    <i>Molecular and Cellular Biology</i>. American Society for Microbiology, 2006.
    <a href="https://doi.org/10.1128/MCB.26.5.1817-1825.2006">https://doi.org/10.1128/MCB.26.5.1817-1825.2006</a>.
  ieee: H. Chu <i>et al.</i>, “γ-Parvin is dispensable for hematopoiesis, leukocyte
    trafficking, and T-cell-dependent antibody response,” <i>Molecular and Cellular
    Biology</i>, vol. 26, no. 5. American Society for Microbiology, pp. 1817–1825,
    2006.
  ista: Chu H, Thievessen I, Sixt MK, Lämmermann T, Waisman A, Braun A, Noegel A,
    Fässler R. 2006. γ-Parvin is dispensable for hematopoiesis, leukocyte trafficking,
    and T-cell-dependent antibody response. Molecular and Cellular Biology. 26(5),
    1817–1825.
  mla: Chu, Haiyan, et al. “γ-Parvin Is Dispensable for Hematopoiesis, Leukocyte Trafficking,
    and T-Cell-Dependent Antibody Response.” <i>Molecular and Cellular Biology</i>,
    vol. 26, no. 5, American Society for Microbiology, 2006, pp. 1817–25, doi:<a href="https://doi.org/10.1128/MCB.26.5.1817-1825.2006">10.1128/MCB.26.5.1817-1825.2006</a>.
  short: H. Chu, I. Thievessen, M.K. Sixt, T. Lämmermann, A. Waisman, A. Braun, A.
    Noegel, R. Fässler, Molecular and Cellular Biology 26 (2006) 1817–1825.
date_created: 2018-12-11T12:05:58Z
date_published: 2006-03-01T00:00:00Z
date_updated: 2021-01-12T07:53:18Z
day: '01'
doi: 10.1128/MCB.26.5.1817-1825.2006
extern: 1
intvolume: '        26'
issue: '5'
month: '03'
page: 1817 - 1825
publication: Molecular and Cellular Biology
publication_status: published
publisher: American Society for Microbiology
publist_id: '2193'
quality_controlled: 0
status: public
title: γ-Parvin is dispensable for hematopoiesis, leukocyte trafficking, and T-cell-dependent
  antibody response
type: journal_article
volume: 26
year: '2006'
...
---
_id: '3936'
abstract:
- lang: eng
  text: At least eight of the twelve known members of the beta1 integrin family are
    expressed on hematopoietic cells. Among these, the VCAM-1 receptor alpha4beta1
    has received most attention as a main factor mediating firm adhesion to the endothelium
    during blood cell extravasation. Therapeutic trials are ongoing into the use of
    antibodies and small molecule inhibitors to target this interaction and hence
    obtain anti-inflammatory effects. However, extravasation is only one possible
    process that is mediated by beta1 integrins and there is evidence that they also
    mediate leukocyte retention and positioning in the tissue, lymphocyte activation
    and possibly migration within the interstitium. Genetic mouse models where integrins
    are selectively deleted on blood cells have been used to investigate these functions
    and further studies will be invaluable to critically evaluate therapeutic trials.
author:
- first_name: Michael K
  full_name: Michael Sixt
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
- first_name: Martina
  full_name: Bauer, Martina
  last_name: Bauer
- first_name: Tim
  full_name: Lämmermann, Tim
  last_name: Lämmermann
- first_name: Reinhard
  full_name: Fässler, Reinhard
  last_name: Fässler
citation:
  ama: 'Sixt MK, Bauer M, Lämmermann T, Fässler R. β1 integrins: zip codes and signaling
    relay for blood cells. <i>Current Opinion in Cell Biology</i>. 2006;18(5):482-490.
    doi:<a href="https://doi.org/10.1016/j.ceb.2006.08.007">10.1016/j.ceb.2006.08.007</a>'
  apa: 'Sixt, M. K., Bauer, M., Lämmermann, T., &#38; Fässler, R. (2006). β1 integrins:
    zip codes and signaling relay for blood cells. <i>Current Opinion in Cell Biology</i>.
    Elsevier. <a href="https://doi.org/10.1016/j.ceb.2006.08.007">https://doi.org/10.1016/j.ceb.2006.08.007</a>'
  chicago: 'Sixt, Michael K, Martina Bauer, Tim Lämmermann, and Reinhard Fässler.
    “Β1 Integrins: Zip Codes and Signaling Relay for Blood Cells.” <i>Current Opinion
    in Cell Biology</i>. Elsevier, 2006. <a href="https://doi.org/10.1016/j.ceb.2006.08.007">https://doi.org/10.1016/j.ceb.2006.08.007</a>.'
  ieee: 'M. K. Sixt, M. Bauer, T. Lämmermann, and R. Fässler, “β1 integrins: zip codes
    and signaling relay for blood cells,” <i>Current Opinion in Cell Biology</i>,
    vol. 18, no. 5. Elsevier, pp. 482–490, 2006.'
  ista: 'Sixt MK, Bauer M, Lämmermann T, Fässler R. 2006. β1 integrins: zip codes
    and signaling relay for blood cells. Current Opinion in Cell Biology. 18(5), 482–490.'
  mla: 'Sixt, Michael K., et al. “Β1 Integrins: Zip Codes and Signaling Relay for
    Blood Cells.” <i>Current Opinion in Cell Biology</i>, vol. 18, no. 5, Elsevier,
    2006, pp. 482–90, doi:<a href="https://doi.org/10.1016/j.ceb.2006.08.007">10.1016/j.ceb.2006.08.007</a>.'
  short: M.K. Sixt, M. Bauer, T. Lämmermann, R. Fässler, Current Opinion in Cell Biology
    18 (2006) 482–490.
date_created: 2018-12-11T12:05:59Z
date_published: 2006-10-01T00:00:00Z
date_updated: 2021-01-12T07:53:19Z
day: '01'
doi: 10.1016/j.ceb.2006.08.007
extern: 1
intvolume: '        18'
issue: '5'
month: '10'
page: 482 - 490
publication: Current Opinion in Cell Biology
publication_status: published
publisher: Elsevier
publist_id: '2191'
quality_controlled: 0
status: public
title: 'β1 integrins: zip codes and signaling relay for blood cells'
type: journal_article
volume: 18
year: '2006'
...
---
_id: '3978'
abstract:
- lang: eng
  text: Evaluating the quality of experimentally determined protein structural models
    is an essential step toward identifying potential errors and guiding further structural
    refinement. Herein, we report the use of proton local density as a sensitive measure
    to assess the quality of nuclear magnetic resonance (NMR) structures. Using 256
    high-resolution crystal structures with protons added and optimized, we show that
    the local density of different proton types display distinct distributions. These
    distributions can be characterized by statistical moments and are used to establish
    local density Z-scores for evaluating both global and local packing for individual
    protons. Analysis of 546 crystal structures at various resolutions shows that
    the local density Z-scores increase as the structural resolution decreases and
    correlate well with the ClashScore (Word et al. J Mol Biol 1999;285(4):1711-1733)
    generated by all atom contact analysis. Local density Z-scores for NMR structures
    exhibit a significantly wider range of values than for X-ray structures and demonstrate
    a combination of potentially problematic inflation and compression. Water-refined
    NMR structures show improved packing quality. Our analysis of a high-quality structural
    ensemble of ubiquitin refined against order parameters shows proton density distributions
    that correlate nearly perfectly with our standards derived from crystal structures,
    further validating our approach. We present an automated analysis and visualization
    tool for proton packing to evaluate the quality of NMR structures.
author:
- first_name: Yih
  full_name: Ban, Yih-En Andrew
  last_name: Ban
- first_name: Johannes
  full_name: Rudolph, Johannes
  last_name: Rudolph
- first_name: Pei
  full_name: Zhou, Pei
  last_name: Zhou
- first_name: Herbert
  full_name: Herbert Edelsbrunner
  id: 3FB178DA-F248-11E8-B48F-1D18A9856A87
  last_name: Edelsbrunner
  orcid: 0000-0002-9823-6833
citation:
  ama: 'Ban Y, Rudolph J, Zhou P, Edelsbrunner H. Evaluating the quality of NMR structures
    by local density of protons. <i>Proteins: Structure, Function and Bioinformatics</i>.
    2006;62(4):852-864. doi:<a href="https://doi.org/10.1002/prot.20811">10.1002/prot.20811</a>'
  apa: 'Ban, Y., Rudolph, J., Zhou, P., &#38; Edelsbrunner, H. (2006). Evaluating
    the quality of NMR structures by local density of protons. <i>Proteins: Structure,
    Function and Bioinformatics</i>. Wiley-Blackwell. <a href="https://doi.org/10.1002/prot.20811">https://doi.org/10.1002/prot.20811</a>'
  chicago: 'Ban, Yih, Johannes Rudolph, Pei Zhou, and Herbert Edelsbrunner. “Evaluating
    the Quality of NMR Structures by Local Density of Protons.” <i>Proteins: Structure,
    Function and Bioinformatics</i>. Wiley-Blackwell, 2006. <a href="https://doi.org/10.1002/prot.20811">https://doi.org/10.1002/prot.20811</a>.'
  ieee: 'Y. Ban, J. Rudolph, P. Zhou, and H. Edelsbrunner, “Evaluating the quality
    of NMR structures by local density of protons,” <i>Proteins: Structure, Function
    and Bioinformatics</i>, vol. 62, no. 4. Wiley-Blackwell, pp. 852–864, 2006.'
  ista: 'Ban Y, Rudolph J, Zhou P, Edelsbrunner H. 2006. Evaluating the quality of
    NMR structures by local density of protons. Proteins: Structure, Function and
    Bioinformatics. 62(4), 852–864.'
  mla: 'Ban, Yih, et al. “Evaluating the Quality of NMR Structures by Local Density
    of Protons.” <i>Proteins: Structure, Function and Bioinformatics</i>, vol. 62,
    no. 4, Wiley-Blackwell, 2006, pp. 852–64, doi:<a href="https://doi.org/10.1002/prot.20811">10.1002/prot.20811</a>.'
  short: 'Y. Ban, J. Rudolph, P. Zhou, H. Edelsbrunner, Proteins: Structure, Function
    and Bioinformatics 62 (2006) 852–864.'
date_created: 2018-12-11T12:06:14Z
date_published: 2006-03-01T00:00:00Z
date_updated: 2021-01-12T07:53:36Z
day: '01'
doi: 10.1002/prot.20811
extern: 1
intvolume: '        62'
issue: '4'
month: '03'
page: 852 - 864
publication: 'Proteins: Structure, Function and Bioinformatics'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '2146'
quality_controlled: 0
status: public
title: Evaluating the quality of NMR structures by local density of protons
type: journal_article
volume: 62
year: '2006'
...
---
_id: '3979'
abstract:
- lang: eng
  text: Protein-protein interactions, which form the basis for most cellular processes,
    result in the formation of protein interfaces. Believing that the local shape
    of proteins is crucial, we take a geometric approach and present a definition
    of an interface surface formed by two or more proteins as a subset of their Voronoi
    diagram. The definition deals with the difficult and important problem of specifying
    interface boundaries by invoking methods used in the alpha shape representation
    of molecules, the discrete flow on Delaunay simplices to define pockets and reconstruct
    surfaces, and the assessment of the importance of topological features. We present
    an algorithm to construct the surface and define a hierarchy that distinguishes
    core and peripheral regions. This hierarchy is shown to have correlation with
    hot-spots in protein-protein interactions. Finally, we study the geometric and
    topological properties of interface surfaces and show their high degree of contortion.
author:
- first_name: Yih
  full_name: Ban, Yih-En Andrew
  last_name: Ban
- first_name: Herbert
  full_name: Herbert Edelsbrunner
  id: 3FB178DA-F248-11E8-B48F-1D18A9856A87
  last_name: Edelsbrunner
  orcid: 0000-0002-9823-6833
- first_name: Johannes
  full_name: Rudolph, Johannes
  last_name: Rudolph
citation:
  ama: Ban Y, Edelsbrunner H, Rudolph J. Interface surfaces for protein-protein complexes.
    <i>Journal of the ACM</i>. 2006;53(3):361-378. doi:<a href="https://doi.org/10.1145/1147954.1147957">10.1145/1147954.1147957</a>
  apa: Ban, Y., Edelsbrunner, H., &#38; Rudolph, J. (2006). Interface surfaces for
    protein-protein complexes. <i>Journal of the ACM</i>. ACM. <a href="https://doi.org/10.1145/1147954.1147957">https://doi.org/10.1145/1147954.1147957</a>
  chicago: Ban, Yih, Herbert Edelsbrunner, and Johannes Rudolph. “Interface Surfaces
    for Protein-Protein Complexes.” <i>Journal of the ACM</i>. ACM, 2006. <a href="https://doi.org/10.1145/1147954.1147957">https://doi.org/10.1145/1147954.1147957</a>.
  ieee: Y. Ban, H. Edelsbrunner, and J. Rudolph, “Interface surfaces for protein-protein
    complexes,” <i>Journal of the ACM</i>, vol. 53, no. 3. ACM, pp. 361–378, 2006.
  ista: Ban Y, Edelsbrunner H, Rudolph J. 2006. Interface surfaces for protein-protein
    complexes. Journal of the ACM. 53(3), 361–378.
  mla: Ban, Yih, et al. “Interface Surfaces for Protein-Protein Complexes.” <i>Journal
    of the ACM</i>, vol. 53, no. 3, ACM, 2006, pp. 361–78, doi:<a href="https://doi.org/10.1145/1147954.1147957">10.1145/1147954.1147957</a>.
  short: Y. Ban, H. Edelsbrunner, J. Rudolph, Journal of the ACM 53 (2006) 361–378.
date_created: 2018-12-11T12:06:14Z
date_published: 2006-05-01T00:00:00Z
date_updated: 2021-01-12T07:53:37Z
day: '01'
doi: 10.1145/1147954.1147957
extern: 1
intvolume: '        53'
issue: '3'
month: '05'
page: 361 - 378
publication: Journal of the ACM
publication_status: published
publisher: ACM
publist_id: '2147'
quality_controlled: 0
status: public
title: Interface surfaces for protein-protein complexes
type: journal_article
volume: 53
year: '2006'
...
---
_id: '3980'
abstract:
- lang: eng
  text: Given a smoothly embedded 2-manifold in R-3, we define the elevation of a
    point as the height difference to a canonically defined second point on the same
    manifold. Our definition is invariant under rigid motions and can be used to define
    features such as lines of discontinuous or continuous but non-smooth elevation.
    We give an algorithm for finding points of locally maximum elevation, which we
    suggest mark cavities and protrusions and are useful in matching shapes as for
    example in protein docking.
author:
- first_name: Pankaj
  full_name: Agarwal, Pankaj K
  last_name: Agarwal
- first_name: Herbert
  full_name: Herbert Edelsbrunner
  id: 3FB178DA-F248-11E8-B48F-1D18A9856A87
  last_name: Edelsbrunner
  orcid: 0000-0002-9823-6833
- first_name: John
  full_name: Harer, John
  last_name: Harer
- first_name: Yusu
  full_name: Wang, Yusu
  last_name: Wang
citation:
  ama: Agarwal P, Edelsbrunner H, Harer J, Wang Y. Extreme elevation on a 2-manifold.
    <i>Discrete &#38; Computational Geometry</i>. 2006;36(4):553-572. doi:<a href="https://doi.org/10.1007/s00454-006-1265-8">10.1007/s00454-006-1265-8</a>
  apa: Agarwal, P., Edelsbrunner, H., Harer, J., &#38; Wang, Y. (2006). Extreme elevation
    on a 2-manifold. <i>Discrete &#38; Computational Geometry</i>. Springer. <a href="https://doi.org/10.1007/s00454-006-1265-8">https://doi.org/10.1007/s00454-006-1265-8</a>
  chicago: Agarwal, Pankaj, Herbert Edelsbrunner, John Harer, and Yusu Wang. “Extreme
    Elevation on a 2-Manifold.” <i>Discrete &#38; Computational Geometry</i>. Springer,
    2006. <a href="https://doi.org/10.1007/s00454-006-1265-8">https://doi.org/10.1007/s00454-006-1265-8</a>.
  ieee: P. Agarwal, H. Edelsbrunner, J. Harer, and Y. Wang, “Extreme elevation on
    a 2-manifold,” <i>Discrete &#38; Computational Geometry</i>, vol. 36, no. 4. Springer,
    pp. 553–572, 2006.
  ista: Agarwal P, Edelsbrunner H, Harer J, Wang Y. 2006. Extreme elevation on a 2-manifold.
    Discrete &#38; Computational Geometry. 36(4), 553–572.
  mla: Agarwal, Pankaj, et al. “Extreme Elevation on a 2-Manifold.” <i>Discrete &#38;
    Computational Geometry</i>, vol. 36, no. 4, Springer, 2006, pp. 553–72, doi:<a
    href="https://doi.org/10.1007/s00454-006-1265-8">10.1007/s00454-006-1265-8</a>.
  short: P. Agarwal, H. Edelsbrunner, J. Harer, Y. Wang, Discrete &#38; Computational
    Geometry 36 (2006) 553–572.
date_created: 2018-12-11T12:06:15Z
date_published: 2006-12-01T00:00:00Z
date_updated: 2021-01-12T07:53:38Z
day: '01'
doi: 10.1007/s00454-006-1265-8
extern: 1
intvolume: '        36'
issue: '4'
month: '12'
page: 553 - 572
publication: Discrete & Computational Geometry
publication_status: published
publisher: Springer
publist_id: '2148'
quality_controlled: 0
status: public
title: Extreme elevation on a 2-manifold
type: journal_article
volume: 36
year: '2006'
...
---
_id: '4140'
abstract:
- lang: eng
  text: Wnt11 is a key signal, determining cell polarization and migration during
    vertebrate gastrulation. It is known that Wnt11 functionally interacts with several
    signaling components, the homologues of which control planar cell polarity in
    Drosophila melanogaster. Although in D. melanogaster these components are thought
    to polarize cells by asymmetrically localizing at the plasma membrane, it is not
    yet clear whether their subcellular localization plays a similarly important role
    in vertebrates. We show that in zebrafish embryonic cells, Wnt11 locally functions
    at the plasma membrane by accumulating its receptor, Frizzled 7, on adjacent sites
    of cell contacts. Wnt11-induced Frizzled 7 accumulations recruit the intracellular
    Wnt signaling mediator Dishevelled, as well as Wnt11 itself, and locally increase
    cell contact persistence. This increase in cell contact persistence is mediated
    by the local interaction of Wnt11, Frizzled 7, and the atypical cadherin Flamingo
    at the plasma membrane, and it does not require the activity of further downstream
    effectors of Wnt11 signaling, such as RhoA and Rok2. We propose that Wnt11, by
    interacting with Frizzled 7 and Flamingo, modulates local cell contact persistence
    to coordinate cell movements during gastrulation.
article_processing_charge: No
author:
- first_name: Sabine
  full_name: Witzel, Sabine
  last_name: Witzel
- first_name: Vitaly
  full_name: Zimyanin, Vitaly
  last_name: Zimyanin
- first_name: Filipa
  full_name: Carreira Barbosa, Filipa
  last_name: Carreira Barbosa
- first_name: Masazumi
  full_name: Tada, Masazumi
  last_name: Tada
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Witzel S, Zimyanin V, Carreira Barbosa F, Tada M, Heisenberg C-PJ. Wnt11 controls
    cell contact persistence by local accumulation of Frizzled 7 at the plasma membrane.
    <i>Journal of Cell Biology</i>. 2006;175(5):791-802. doi:<a href="https://doi.org/10.1083/jcb.200606017">10.1083/jcb.200606017</a>
  apa: Witzel, S., Zimyanin, V., Carreira Barbosa, F., Tada, M., &#38; Heisenberg,
    C.-P. J. (2006). Wnt11 controls cell contact persistence by local accumulation
    of Frizzled 7 at the plasma membrane. <i>Journal of Cell Biology</i>. Rockefeller
    University Press. <a href="https://doi.org/10.1083/jcb.200606017">https://doi.org/10.1083/jcb.200606017</a>
  chicago: Witzel, Sabine, Vitaly Zimyanin, Filipa Carreira Barbosa, Masazumi Tada,
    and Carl-Philipp J Heisenberg. “Wnt11 Controls Cell Contact Persistence by Local
    Accumulation of Frizzled 7 at the Plasma Membrane.” <i>Journal of Cell Biology</i>.
    Rockefeller University Press, 2006. <a href="https://doi.org/10.1083/jcb.200606017">https://doi.org/10.1083/jcb.200606017</a>.
  ieee: S. Witzel, V. Zimyanin, F. Carreira Barbosa, M. Tada, and C.-P. J. Heisenberg,
    “Wnt11 controls cell contact persistence by local accumulation of Frizzled 7 at
    the plasma membrane,” <i>Journal of Cell Biology</i>, vol. 175, no. 5. Rockefeller
    University Press, pp. 791–802, 2006.
  ista: Witzel S, Zimyanin V, Carreira Barbosa F, Tada M, Heisenberg C-PJ. 2006. Wnt11
    controls cell contact persistence by local accumulation of Frizzled 7 at the plasma
    membrane. Journal of Cell Biology. 175(5), 791–802.
  mla: Witzel, Sabine, et al. “Wnt11 Controls Cell Contact Persistence by Local Accumulation
    of Frizzled 7 at the Plasma Membrane.” <i>Journal of Cell Biology</i>, vol. 175,
    no. 5, Rockefeller University Press, 2006, pp. 791–802, doi:<a href="https://doi.org/10.1083/jcb.200606017">10.1083/jcb.200606017</a>.
  short: S. Witzel, V. Zimyanin, F. Carreira Barbosa, M. Tada, C.-P.J. Heisenberg,
    Journal of Cell Biology 175 (2006) 791–802.
date_created: 2018-12-11T12:07:11Z
date_published: 2006-12-04T00:00:00Z
date_updated: 2021-01-12T07:54:48Z
day: '04'
doi: 10.1083/jcb.200606017
extern: '1'
intvolume: '       175'
issue: '5'
language:
- iso: eng
month: '12'
oa_version: None
page: 791 - 802
publication: Journal of Cell Biology
publication_status: published
publisher: Rockefeller University Press
publist_id: '1980'
status: public
title: Wnt11 controls cell contact persistence by local accumulation of Frizzled 7
  at the plasma membrane
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 175
year: '2006'
...
---
_id: '4145'
abstract:
- lang: eng
  text: The detection of microRNAs (miRNAs) at single-cell resolution is important
    for studying the role of these posttranscriptional regulators. Here, we use a
    dual-fluorescent green fluorescent protein (GFP)-reporter/monomeric red fluorescent
    protein (mRFP)-sensor (DFRS) plasmid, injected into zebrafish blastomeres or electroporated
    into defined tissues of mouse embryos in utero or ex utero, to monitor the dynamics
    of specific miRNAs in individual live cells. This approach reveals, for example,
    that in the developing mouse central nervous system,, miR-124a is expressed not
    only in postmitotic neurons but also in neuronal progenitor cells. Collectively,
    our results demonstrate that acute administration of DFRS plasmids.offers an alternative
    to previous in situ hybridization and transgenic approaches and allows the monitoring
    of miRNA appearance and disappearance in defined cell lineages during vertebrate
    development.
article_processing_charge: No
author:
- first_name: Davide
  full_name: Tonelli, Davide
  last_name: Tonelli
- first_name: Frederico
  full_name: Calegari, Frederico
  last_name: Calegari
- first_name: Ji
  full_name: Fei, Ji
  last_name: Fei
- first_name: Tadashi
  full_name: Nomura, Tadashi
  last_name: Nomura
- first_name: Noriko
  full_name: Osumi, Noriko
  last_name: Osumi
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
- first_name: Wieland
  full_name: Huttner, Wieland
  last_name: Huttner
citation:
  ama: Tonelli D, Calegari F, Fei J, et al. Single-cell detection of microRNAs in
    developing vertebrate embryos after acute administration of a dual-fluorescence
    reporter/sensor plasmid. <i>Biotechniques</i>. 2006;41(6):727-732. doi:<a href="https://doi.org/10.2144/000112296">10.2144/000112296</a>
  apa: Tonelli, D., Calegari, F., Fei, J., Nomura, T., Osumi, N., Heisenberg, C.-P.
    J., &#38; Huttner, W. (2006). Single-cell detection of microRNAs in developing
    vertebrate embryos after acute administration of a dual-fluorescence reporter/sensor
    plasmid. <i>Biotechniques</i>. Informa Healthcare. <a href="https://doi.org/10.2144/000112296">https://doi.org/10.2144/000112296</a>
  chicago: Tonelli, Davide, Frederico Calegari, Ji Fei, Tadashi Nomura, Noriko Osumi,
    Carl-Philipp J Heisenberg, and Wieland Huttner. “Single-Cell Detection of MicroRNAs
    in Developing Vertebrate Embryos after Acute Administration of a Dual-Fluorescence
    Reporter/Sensor Plasmid.” <i>Biotechniques</i>. Informa Healthcare, 2006. <a href="https://doi.org/10.2144/000112296">https://doi.org/10.2144/000112296</a>.
  ieee: D. Tonelli <i>et al.</i>, “Single-cell detection of microRNAs in developing
    vertebrate embryos after acute administration of a dual-fluorescence reporter/sensor
    plasmid,” <i>Biotechniques</i>, vol. 41, no. 6. Informa Healthcare, pp. 727–732,
    2006.
  ista: Tonelli D, Calegari F, Fei J, Nomura T, Osumi N, Heisenberg C-PJ, Huttner
    W. 2006. Single-cell detection of microRNAs in developing vertebrate embryos after
    acute administration of a dual-fluorescence reporter/sensor plasmid. Biotechniques.
    41(6), 727–732.
  mla: Tonelli, Davide, et al. “Single-Cell Detection of MicroRNAs in Developing Vertebrate
    Embryos after Acute Administration of a Dual-Fluorescence Reporter/Sensor Plasmid.”
    <i>Biotechniques</i>, vol. 41, no. 6, Informa Healthcare, 2006, pp. 727–32, doi:<a
    href="https://doi.org/10.2144/000112296">10.2144/000112296</a>.
  short: D. Tonelli, F. Calegari, J. Fei, T. Nomura, N. Osumi, C.-P.J. Heisenberg,
    W. Huttner, Biotechniques 41 (2006) 727–732.
date_created: 2018-12-11T12:07:12Z
date_published: 2006-12-01T00:00:00Z
date_updated: 2021-01-12T07:54:50Z
day: '01'
doi: 10.2144/000112296
extern: '1'
intvolume: '        41'
issue: '6'
language:
- iso: eng
month: '12'
oa_version: None
page: 727 - 732
publication: Biotechniques
publication_status: published
publisher: Informa Healthcare
publist_id: '1974'
status: public
title: Single-cell detection of microRNAs in developing vertebrate embryos after acute
  administration of a dual-fluorescence reporter/sensor plasmid
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 41
year: '2006'
...
---
_id: '4173'
abstract:
- lang: eng
  text: 'Background: Zebrafish (D. rerio) has become a powerful and widely used model
    system for the analysis of vertebrate embryogenesis and organ development. While
    genetic methods are readily available in zebrafish, protocols for two dimensional
    (2D) gel electrophoresis and proteomics have yet to be developed. Results: As
    a prerequisite to carry out proteomic experiments with early zebrafish embryos,
    we developed a method to efficiently remove the yolk from large batches of embryos.
    This method enabled high resolution 2D gel electrophoresis and improved Western
    blotting considerably. Here, we provide detailed protocols for proteomics in zebrafish
    from sample preparation to mass spectrometry (MS), including a comparison of databases
    for MS identification of zebrafish proteins. Conclusion: The provided protocols
    for proteomic analysis of early embryos enable research to be taken in novel directions
    in embryogenesis.'
article_processing_charge: No
author:
- first_name: Vinzenz
  full_name: Link, Vinzenz
  last_name: Link
- first_name: Andrej
  full_name: Shevchenko, Andrej
  last_name: Shevchenko
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Link V, Shevchenko A, Heisenberg C-PJ. Proteomics of early zebrafish embryos.
    <i>BMC Developmental Biology</i>. 2006;6:1-9. doi:<a href="https://doi.org/10.1186/1471-213X-6-1">10.1186/1471-213X-6-1</a>
  apa: Link, V., Shevchenko, A., &#38; Heisenberg, C.-P. J. (2006). Proteomics of
    early zebrafish embryos. <i>BMC Developmental Biology</i>. BioMed Central. <a
    href="https://doi.org/10.1186/1471-213X-6-1">https://doi.org/10.1186/1471-213X-6-1</a>
  chicago: Link, Vinzenz, Andrej Shevchenko, and Carl-Philipp J Heisenberg. “Proteomics
    of Early Zebrafish Embryos.” <i>BMC Developmental Biology</i>. BioMed Central,
    2006. <a href="https://doi.org/10.1186/1471-213X-6-1">https://doi.org/10.1186/1471-213X-6-1</a>.
  ieee: V. Link, A. Shevchenko, and C.-P. J. Heisenberg, “Proteomics of early zebrafish
    embryos,” <i>BMC Developmental Biology</i>, vol. 6. BioMed Central, pp. 1–9, 2006.
  ista: Link V, Shevchenko A, Heisenberg C-PJ. 2006. Proteomics of early zebrafish
    embryos. BMC Developmental Biology. 6, 1–9.
  mla: Link, Vinzenz, et al. “Proteomics of Early Zebrafish Embryos.” <i>BMC Developmental
    Biology</i>, vol. 6, BioMed Central, 2006, pp. 1–9, doi:<a href="https://doi.org/10.1186/1471-213X-6-1">10.1186/1471-213X-6-1</a>.
  short: V. Link, A. Shevchenko, C.-P.J. Heisenberg, BMC Developmental Biology 6 (2006)
    1–9.
date_created: 2018-12-11T12:07:23Z
date_published: 2006-01-13T00:00:00Z
date_updated: 2021-01-12T07:55:02Z
day: '13'
doi: 10.1186/1471-213X-6-1
extern: '1'
intvolume: '         6'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
main_file_link:
- open_access: '1'
  url: http://www.biomedcentral.com/1471-213X/6/1
month: '01'
oa: 1
oa_version: None
page: 1 - 9
publication: BMC Developmental Biology
publication_status: published
publisher: BioMed Central
publist_id: '1945'
status: public
title: Proteomics of early zebrafish embryos
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 6
year: '2006'
...
---
_id: '4176'
abstract:
- lang: eng
  text: 'During vertebrate gastrulation, a well-orchestrated series of morphogenetic
    changes leads to the formation of the three germ layers: the ectoderm, mesoderm
    and endoderm. The analysis of gene expression patterns during gastrulation has
    been central to the identification of genes involved in germ layer formation.
    However, many proteins are regulated on a translational or post-translational
    level and are thus undetectable by gene expression analysis. Therefore, we developed
    a 2D-gel-based comparative proteomic approach to target proteins involved in germ
    layer morphogenesis during zebrafish gastrulation. Proteomes of ectodermal and
    mesendodermal progenitor cells were compared and 35 significantly regulated proteins
    were identified by mass spectrometry, including several proteins with predicted
    functions in cytoskeletal organization. A comparison of our proteomic results
    with data obtained in an accompanying microarray-based gene expression analysis
    revealed no significant overlap, confirming the complementary nature of proteomics
    and transcriptomics. The regulation of ezrin2, which was identified based on a
    reduction in spot intensity in mesendodermal cells, was independently validated.
    Furthermore, we show that ezrin2 is activated by phosphorylation in mesendodermal
    cells and is required for proper germ layer morphogenesis. We demonstrate the
    feasibility of proteomics in zebrafish, concluding that proteomics is a valuable
    tool for analysis of early development.'
article_processing_charge: No
author:
- first_name: Vinzenz
  full_name: Link, Vinzenz
  last_name: Link
- first_name: Lara
  full_name: Carvalho, Lara
  last_name: Carvalho
- first_name: Irinka
  full_name: Castanon, Irinka
  last_name: Castanon
- first_name: Petra
  full_name: Stockinger, Petra
  last_name: Stockinger
- first_name: Andrej
  full_name: Shevchenko, Andrej
  last_name: Shevchenko
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Link V, Carvalho L, Castanon I, Stockinger P, Shevchenko A, Heisenberg C-PJ.
    Identification of regulators of germ layer morphogenesis using proteomics in zebrafish.
    <i>Journal of Cell Science</i>. 2006;119(10):2073-2083. doi:<a href="https://doi.org/10.1242/jcs.02928">10.1242/jcs.02928</a>
  apa: Link, V., Carvalho, L., Castanon, I., Stockinger, P., Shevchenko, A., &#38;
    Heisenberg, C.-P. J. (2006). Identification of regulators of germ layer morphogenesis
    using proteomics in zebrafish. <i>Journal of Cell Science</i>. Company of Biologists.
    <a href="https://doi.org/10.1242/jcs.02928">https://doi.org/10.1242/jcs.02928</a>
  chicago: Link, Vinzenz, Lara Carvalho, Irinka Castanon, Petra Stockinger, Andrej
    Shevchenko, and Carl-Philipp J Heisenberg. “Identification of Regulators of Germ
    Layer Morphogenesis Using Proteomics in Zebrafish.” <i>Journal of Cell Science</i>.
    Company of Biologists, 2006. <a href="https://doi.org/10.1242/jcs.02928">https://doi.org/10.1242/jcs.02928</a>.
  ieee: V. Link, L. Carvalho, I. Castanon, P. Stockinger, A. Shevchenko, and C.-P.
    J. Heisenberg, “Identification of regulators of germ layer morphogenesis using
    proteomics in zebrafish,” <i>Journal of Cell Science</i>, vol. 119, no. 10. Company
    of Biologists, pp. 2073–2083, 2006.
  ista: Link V, Carvalho L, Castanon I, Stockinger P, Shevchenko A, Heisenberg C-PJ.
    2006. Identification of regulators of germ layer morphogenesis using proteomics
    in zebrafish. Journal of Cell Science. 119(10), 2073–2083.
  mla: Link, Vinzenz, et al. “Identification of Regulators of Germ Layer Morphogenesis
    Using Proteomics in Zebrafish.” <i>Journal of Cell Science</i>, vol. 119, no.
    10, Company of Biologists, 2006, pp. 2073–83, doi:<a href="https://doi.org/10.1242/jcs.02928">10.1242/jcs.02928</a>.
  short: V. Link, L. Carvalho, I. Castanon, P. Stockinger, A. Shevchenko, C.-P.J.
    Heisenberg, Journal of Cell Science 119 (2006) 2073–2083.
date_created: 2018-12-11T12:07:24Z
date_published: 2006-05-15T00:00:00Z
date_updated: 2021-01-12T07:55:04Z
day: '15'
doi: 10.1242/jcs.02928
extern: '1'
intvolume: '       119'
issue: '10'
language:
- iso: eng
month: '05'
oa_version: None
page: 2073 - 2083
publication: Journal of Cell Science
publication_status: published
publisher: Company of Biologists
publist_id: '1944'
status: public
title: Identification of regulators of germ layer morphogenesis using proteomics in
  zebrafish
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 119
year: '2006'
...
---
_id: '4178'
abstract:
- lang: eng
  text: Detailed reconstruction of the spatiotemporal history of embryonic cells is
    key to understanding tissue formation processes but is often complicated by the
    large number of cells involved, particularly so in vertebrates. Through a combination
    of high-resolution time-lapse lineage tracing and antibody staining, we have analyzed
    the movement of mesencephalic and metencephalic cell populations in the early
    zebrafish embryo. To facilitate the analysis of our cell tracking data, we have
    created TracePilot, a software tool that allows interactive manipulation and visualization
    of tracking data. We demonstrate its utility by showing novel visualizations of
    cell movement in the developing zebrafish brain. TracePilot (http://www.mpi-cbg.de/tracepilot)
    is Java-based, available free of charge, and has a program structure that allows
    the incorporation of additional analysis tools.
article_processing_charge: No
author:
- first_name: Tobias
  full_name: Langenberg, Tobias
  last_name: Langenberg
- first_name: Tadeusz
  full_name: Dracz, Tadeusz
  last_name: Dracz
- first_name: Andrew
  full_name: Oates, Andrew
  last_name: Oates
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
- first_name: Michael
  full_name: Brand, Michael
  last_name: Brand
citation:
  ama: Langenberg T, Dracz T, Oates A, Heisenberg C-PJ, Brand M. Analysis and visualization
    of cell movement in the developing zebrafish brain. <i>Developmental Dynamics</i>.
    2006;235(4):928-933. doi:<a href="https://doi.org/10.1002/dvdy.20692">10.1002/dvdy.20692</a>
  apa: Langenberg, T., Dracz, T., Oates, A., Heisenberg, C.-P. J., &#38; Brand, M.
    (2006). Analysis and visualization of cell movement in the developing zebrafish
    brain. <i>Developmental Dynamics</i>. Wiley-Blackwell. <a href="https://doi.org/10.1002/dvdy.20692">https://doi.org/10.1002/dvdy.20692</a>
  chicago: Langenberg, Tobias, Tadeusz Dracz, Andrew Oates, Carl-Philipp J Heisenberg,
    and Michael Brand. “Analysis and Visualization of Cell Movement in the Developing
    Zebrafish Brain.” <i>Developmental Dynamics</i>. Wiley-Blackwell, 2006. <a href="https://doi.org/10.1002/dvdy.20692">https://doi.org/10.1002/dvdy.20692</a>.
  ieee: T. Langenberg, T. Dracz, A. Oates, C.-P. J. Heisenberg, and M. Brand, “Analysis
    and visualization of cell movement in the developing zebrafish brain,” <i>Developmental
    Dynamics</i>, vol. 235, no. 4. Wiley-Blackwell, pp. 928–933, 2006.
  ista: Langenberg T, Dracz T, Oates A, Heisenberg C-PJ, Brand M. 2006. Analysis and
    visualization of cell movement in the developing zebrafish brain. Developmental
    Dynamics. 235(4), 928–933.
  mla: Langenberg, Tobias, et al. “Analysis and Visualization of Cell Movement in
    the Developing Zebrafish Brain.” <i>Developmental Dynamics</i>, vol. 235, no.
    4, Wiley-Blackwell, 2006, pp. 928–33, doi:<a href="https://doi.org/10.1002/dvdy.20692">10.1002/dvdy.20692</a>.
  short: T. Langenberg, T. Dracz, A. Oates, C.-P.J. Heisenberg, M. Brand, Developmental
    Dynamics 235 (2006) 928–933.
date_created: 2018-12-11T12:07:25Z
date_published: 2006-04-01T00:00:00Z
date_updated: 2021-01-12T07:55:04Z
day: '01'
doi: 10.1002/dvdy.20692
extern: '1'
intvolume: '       235'
issue: '4'
language:
- iso: eng
month: '04'
oa_version: None
page: 928 - 933
publication: Developmental Dynamics
publication_status: published
publisher: Wiley-Blackwell
publist_id: '1940'
status: public
title: Analysis and visualization of cell movement in the developing zebrafish brain
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 235
year: '2006'
...
---
_id: '4184'
abstract:
- lang: eng
  text: Epithelial morphogenesis depends on coordinated changes in cell shape, a process
    that is still poorly understood. During zebrafish epiboly and Drosophila dorsal
    closure, cell-shape changes at the epithelial margin are of critical importance.
    Here evidence is provided for a conserved mechanism of local actin and myosin
    2 recruitment during theses events. It was found that during epiboly of the zebrafish
    embryo, the movement of the outer epithelium (enveloping layer) over the yolk
    cell surface involves the constriction of marginal cells. This process depends
    on the recruitment of actin and myosin 2 within the yolk cytoplasm along the margin
    of the enveloping layer. Actin and myosin 2 recruitment within the yolk cytoplasm
    requires the Ste20-like kinase Msn1, an orthologue of Drosophila Misshapen. Similarly,
    in Drosophila, actin and myosin 2 localization and cell constriction at the margin
    of the epidermis mediate dorsal closure and are controlled by Misshapen. Thus,
    this study has characterized a conserved mechanism underlying coordinated cell-shape
    changes during epithelial morphogenesis.
article_processing_charge: No
author:
- first_name: Mathias
  full_name: Köppen, Mathias
  last_name: Köppen
- first_name: Beatriz
  full_name: Fernández, Beatriz
  last_name: Fernández
- first_name: Lara
  full_name: Carvalho, Lara
  last_name: Carvalho
- first_name: António
  full_name: Jacinto, António
  last_name: Jacinto
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: 'Köppen M, Fernández B, Carvalho L, Jacinto A, Heisenberg C-PJ. Coordinated
    cell-shape changes control epithelial movement in zebrafish and Drosophila. <i>Development</i>.
    2006;133(14):2671-2681. doi:<a href="https://doi.org/doi: 10.1242/dev.02439">doi:
    10.1242/dev.02439</a>'
  apa: 'Köppen, M., Fernández, B., Carvalho, L., Jacinto, A., &#38; Heisenberg, C.-P.
    J. (2006). Coordinated cell-shape changes control epithelial movement in zebrafish
    and Drosophila. <i>Development</i>. Company of Biologists. <a href="https://doi.org/doi:
    10.1242/dev.02439">https://doi.org/doi: 10.1242/dev.02439</a>'
  chicago: 'Köppen, Mathias, Beatriz Fernández, Lara Carvalho, António Jacinto, and
    Carl-Philipp J Heisenberg. “Coordinated Cell-Shape Changes Control Epithelial
    Movement in Zebrafish and Drosophila.” <i>Development</i>. Company of Biologists,
    2006. <a href="https://doi.org/doi: 10.1242/dev.02439">https://doi.org/doi: 10.1242/dev.02439</a>.'
  ieee: M. Köppen, B. Fernández, L. Carvalho, A. Jacinto, and C.-P. J. Heisenberg,
    “Coordinated cell-shape changes control epithelial movement in zebrafish and Drosophila,”
    <i>Development</i>, vol. 133, no. 14. Company of Biologists, pp. 2671–2681, 2006.
  ista: Köppen M, Fernández B, Carvalho L, Jacinto A, Heisenberg C-PJ. 2006. Coordinated
    cell-shape changes control epithelial movement in zebrafish and Drosophila. Development.
    133(14), 2671–2681.
  mla: 'Köppen, Mathias, et al. “Coordinated Cell-Shape Changes Control Epithelial
    Movement in Zebrafish and Drosophila.” <i>Development</i>, vol. 133, no. 14, Company
    of Biologists, 2006, pp. 2671–81, doi:<a href="https://doi.org/doi: 10.1242/dev.02439">doi:
    10.1242/dev.02439</a>.'
  short: M. Köppen, B. Fernández, L. Carvalho, A. Jacinto, C.-P.J. Heisenberg, Development
    133 (2006) 2671–2681.
date_created: 2018-12-11T12:07:27Z
date_published: 2006-07-15T00:00:00Z
date_updated: 2021-01-12T07:55:08Z
day: '15'
doi: 'doi: 10.1242/dev.02439'
extern: '1'
intvolume: '       133'
issue: '14'
language:
- iso: eng
month: '07'
oa_version: None
page: 2671 - 2681
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '1935'
status: public
title: Coordinated cell-shape changes control epithelial movement in zebrafish and
  Drosophila
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 133
year: '2006'
...
---
_id: '4218'
abstract:
- lang: eng
  text: The molecular and cellular mechanisms governing cell motility and directed
    migration in response to the chemokine SDF-1 are largely unknown. Here, we demonstrate
    that zebrafish primordial germ cells whose migration is guided by SDF-1 generate
    bleb-like protrusions that are powered by cytoplasmic flow. Protrusions are formed
    at sites of higher levels of free calcium where activation of myosin contraction
    occurs. Separation of the acto-myosin cortex from the plasma membrane at these
    sites is followed by a flow of cytoplasm into the forming bleb. We propose that
    polarized activation of the receptor CXCR4 leads to a rise in free calcium that
    in turn activates myosin contraction in the part of the cell responding to higher
    levels of the ligand SDF-1. The biased formation of new protrusions in a particular
    region of the cell in response to SDF-1 defines the leading edge and the direction
    of cell migration.
article_processing_charge: No
author:
- first_name: Heiko
  full_name: Blaser, Heiko
  last_name: Blaser
- first_name: Michal
  full_name: Reichman Fried, Michal
  last_name: Reichman Fried
- first_name: Irinka
  full_name: Castanon, Irinka
  last_name: Castanon
- first_name: Karin
  full_name: Dumstrei, Karin
  last_name: Dumstrei
- first_name: Florence
  full_name: Marlow, Florence
  last_name: Marlow
- first_name: Koichi
  full_name: Kawakami, Koichi
  last_name: Kawakami
- first_name: Lilianna
  full_name: Solnica Krezel, Lilianna
  last_name: Solnica Krezel
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
- first_name: Erez
  full_name: Raz, Erez
  last_name: Raz
citation:
  ama: 'Blaser H, Reichman Fried M, Castanon I, et al. Migration of zebrafish primordial
    germ cells: A role for myosin contraction and cytoplasmic flow. <i>Developmental
    Cell</i>. 2006;11(5):613-627. doi:<a href="https://doi.org/10.1016/j.devcel.2006.09.023">10.1016/j.devcel.2006.09.023</a>'
  apa: 'Blaser, H., Reichman Fried, M., Castanon, I., Dumstrei, K., Marlow, F., Kawakami,
    K., … Raz, E. (2006). Migration of zebrafish primordial germ cells: A role for
    myosin contraction and cytoplasmic flow. <i>Developmental Cell</i>. Cell Press.
    <a href="https://doi.org/10.1016/j.devcel.2006.09.023">https://doi.org/10.1016/j.devcel.2006.09.023</a>'
  chicago: 'Blaser, Heiko, Michal Reichman Fried, Irinka Castanon, Karin Dumstrei,
    Florence Marlow, Koichi Kawakami, Lilianna Solnica Krezel, Carl-Philipp J Heisenberg,
    and Erez Raz. “Migration of Zebrafish Primordial Germ Cells: A Role for Myosin
    Contraction and Cytoplasmic Flow.” <i>Developmental Cell</i>. Cell Press, 2006.
    <a href="https://doi.org/10.1016/j.devcel.2006.09.023">https://doi.org/10.1016/j.devcel.2006.09.023</a>.'
  ieee: 'H. Blaser <i>et al.</i>, “Migration of zebrafish primordial germ cells: A
    role for myosin contraction and cytoplasmic flow,” <i>Developmental Cell</i>,
    vol. 11, no. 5. Cell Press, pp. 613–627, 2006.'
  ista: 'Blaser H, Reichman Fried M, Castanon I, Dumstrei K, Marlow F, Kawakami K,
    Solnica Krezel L, Heisenberg C-PJ, Raz E. 2006. Migration of zebrafish primordial
    germ cells: A role for myosin contraction and cytoplasmic flow. Developmental
    Cell. 11(5), 613–627.'
  mla: 'Blaser, Heiko, et al. “Migration of Zebrafish Primordial Germ Cells: A Role
    for Myosin Contraction and Cytoplasmic Flow.” <i>Developmental Cell</i>, vol.
    11, no. 5, Cell Press, 2006, pp. 613–27, doi:<a href="https://doi.org/10.1016/j.devcel.2006.09.023">10.1016/j.devcel.2006.09.023</a>.'
  short: H. Blaser, M. Reichman Fried, I. Castanon, K. Dumstrei, F. Marlow, K. Kawakami,
    L. Solnica Krezel, C.-P.J. Heisenberg, E. Raz, Developmental Cell 11 (2006) 613–627.
date_created: 2018-12-11T12:07:39Z
date_published: 2006-11-06T00:00:00Z
date_updated: 2021-01-12T07:55:23Z
day: '06'
doi: 10.1016/j.devcel.2006.09.023
extern: '1'
intvolume: '        11'
issue: '5'
language:
- iso: eng
month: '11'
oa_version: None
page: 613 - 627
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '1898'
status: public
title: 'Migration of zebrafish primordial germ cells: A role for myosin contraction
  and cytoplasmic flow'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 11
year: '2006'
...
---
_id: '4235'
author:
- first_name: Harold
  full_name: Harold Vladar
  id: 2A181218-F248-11E8-B48F-1D18A9856A87
  last_name: Vladar
  orcid: 0000-0002-5985-7653
- first_name: J.
  full_name: González,J. A
  last_name: González
citation:
  ama: de Vladar H, González J. Dynamic response of cancer under the influence of
    immunological activity and therapy. <i>Journal of Theoretical Biology</i>. 2006:91-109.
  apa: de Vladar, H., &#38; González, J. (2006). Dynamic response of cancer under
    the influence of immunological activity and therapy. <i>Journal of Theoretical
    Biology</i>. Elsevier.
  chicago: Vladar, Harold de, and J. González. “Dynamic Response of Cancer under the
    Influence of Immunological Activity and Therapy.” <i>Journal of Theoretical Biology</i>.
    Elsevier, 2006.
  ieee: H. de Vladar and J. González, “Dynamic response of cancer under the influence
    of immunological activity and therapy,” <i>Journal of Theoretical Biology</i>.
    Elsevier, pp. 91–109, 2006.
  ista: de Vladar H, González J. 2006. Dynamic response of cancer under the influence
    of immunological activity and therapy. Journal of Theoretical Biology., 91–109.
  mla: de Vladar, Harold, and J. González. “Dynamic Response of Cancer under the Influence
    of Immunological Activity and Therapy.” <i>Journal of Theoretical Biology</i>,
    Elsevier, 2006, pp. 91–109.
  short: H. de Vladar, J. González, Journal of Theoretical Biology (2006) 91–109.
date_created: 2018-12-11T12:07:45Z
date_published: 2006-01-01T00:00:00Z
date_updated: 2021-01-12T07:55:30Z
day: '01'
extern: 1
month: '01'
page: 91 - 109
publication: Journal of Theoretical Biology
publication_status: published
publisher: Elsevier
publist_id: '1879'
quality_controlled: 0
status: public
title: Dynamic response of cancer under the influence of immunological activity and
  therapy
type: journal_article
year: '2006'
...
---
_id: '4237'
abstract:
- lang: eng
  text: The growth function of populations is central in biomathematics. The main
    dogma is the existence of density-dependence mechanisms, which can be modelled
    with distinct functional forms that depend on the size of the Population. One
    important class of regulatory functions is the theta-logistic, which generalizes
    the logistic equation. Using this model as a motivation, this paper introduces
    a simple dynamical reformulation that generalizes many growth functions. The reformulation
    consists of two equations, one for population size, and one for the growth rate.
    Furthermore, the model shows that although population is density-dependent, the
    dynamics of the growth rate does not depend either on population size, nor on
    the carrying capacity. Actually, the growth equation is uncoupled from the population
    size equation, and the model has only two parameters, a Malthusian parameter rho
    and a competition coefficient theta. Distinct sign combinations of these parameters
    reproduce not only the family of theta-logistics, but also the van Bertalanffy,
    Gompertz and Potential Growth equations, among other possibilities. It is also
    shown that, except for two critical points, there is a general size-scaling relation
    that includes those appearing in the most important allometric theories, including
    the recently proposed Metabolic Theory of Ecology. With this model, several issues
    of general interest are discussed such as the growth of animal population, extinctions,
    cell growth and allometry, and the effect of environment over a population. (c)
    2005 Elsevier Ltd. All rights reserved.
article_processing_charge: No
author:
- first_name: Harold
  full_name: de Vladar, Harold
  id: 2A181218-F248-11E8-B48F-1D18A9856A87
  last_name: de Vladar
  orcid: 0000-0002-5985-7653
citation:
  ama: de Vladar H. Density-dependence as a size-independent regulatory mechanism.
    <i>Journal of Theoretical Biology</i>. 2006;238(2):245-256. doi:<a href="https://doi.org/3802">3802</a>
  apa: de Vladar, H. (2006). Density-dependence as a size-independent regulatory mechanism.
    <i>Journal of Theoretical Biology</i>. Elsevier. <a href="https://doi.org/3802">https://doi.org/3802</a>
  chicago: Vladar, Harold de. “Density-Dependence as a Size-Independent Regulatory
    Mechanism.” <i>Journal of Theoretical Biology</i>. Elsevier, 2006. <a href="https://doi.org/3802">https://doi.org/3802</a>.
  ieee: H. de Vladar, “Density-dependence as a size-independent regulatory mechanism,”
    <i>Journal of Theoretical Biology</i>, vol. 238, no. 2. Elsevier, pp. 245–256,
    2006.
  ista: de Vladar H. 2006. Density-dependence as a size-independent regulatory mechanism.
    Journal of Theoretical Biology. 238(2), 245–256.
  mla: de Vladar, Harold. “Density-Dependence as a Size-Independent Regulatory Mechanism.”
    <i>Journal of Theoretical Biology</i>, vol. 238, no. 2, Elsevier, 2006, pp. 245–56,
    doi:<a href="https://doi.org/3802">3802</a>.
  short: H. de Vladar, Journal of Theoretical Biology 238 (2006) 245–256.
date_created: 2018-12-11T12:07:46Z
date_published: 2006-01-01T00:00:00Z
date_updated: 2021-01-12T07:55:31Z
day: '01'
doi: '3802'
extern: '1'
intvolume: '       238'
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 245 - 256
publication: Journal of Theoretical Biology
publication_status: published
publisher: Elsevier
publist_id: '1878'
status: public
title: Density-dependence as a size-independent regulatory mechanism
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 238
year: '2006'
...
---
_id: '4248'
abstract:
- lang: eng
  text: 'In finite populations, genetic drift generates interference between selected
    loci, causing advantageous alleles to be found more often on different chromosomes
    than on the same chromosome, which reduces the rate of adaptation. This “Hill–Robertson
    effect” generates indirect selection to increase recombination rates. We present
    a new method to quantify the strength of this selection. Our model represents
    a new beneficial allele (A) entering a population as a single copy, while another
    beneficial allele (B) is sweeping at another locus. A third locus affects the
    recombination rate between selected loci. Using a branching process model, we
    calculate the probability distribution of the number of copies of A on the different
    genetic backgrounds, after it is established but while it is still rare. Then,
    we use a deterministic model to express the change in frequency of the recombination
    modifier, due to hitchhiking, as A goes to fixation. We show that this method
    can give good estimates of selection for recombination. Moreover, it shows that
    recombination is selected through two different effects: it increases the fixation
    probability of new alleles, and it accelerates selective sweeps. The relative
    importance of these two effects depends on the relative times of occurrence of
    the beneficial alleles.'
author:
- first_name: Denis
  full_name: Roze, Denis
  last_name: Roze
- first_name: Nicholas H
  full_name: Nicholas Barton
  id: 4880FE40-F248-11E8-B48F-1D18A9856A87
  last_name: Barton
  orcid: 0000-0002-8548-5240
citation:
  ama: Roze D, Barton NH. The Hill-Robertson effect and the evolution of recombination.
    <i>Genetics</i>. 2006;173(3):1793-1811. doi:<a href="https://doi.org/10.1534/genetics.106.058586
    ">10.1534/genetics.106.058586 </a>
  apa: Roze, D., &#38; Barton, N. H. (2006). The Hill-Robertson effect and the evolution
    of recombination. <i>Genetics</i>. Genetics Society of America. <a href="https://doi.org/10.1534/genetics.106.058586
    ">https://doi.org/10.1534/genetics.106.058586 </a>
  chicago: Roze, Denis, and Nicholas H Barton. “The Hill-Robertson Effect and the
    Evolution of Recombination.” <i>Genetics</i>. Genetics Society of America, 2006.
    <a href="https://doi.org/10.1534/genetics.106.058586 ">https://doi.org/10.1534/genetics.106.058586
    </a>.
  ieee: D. Roze and N. H. Barton, “The Hill-Robertson effect and the evolution of
    recombination,” <i>Genetics</i>, vol. 173, no. 3. Genetics Society of America,
    pp. 1793–1811, 2006.
  ista: Roze D, Barton NH. 2006. The Hill-Robertson effect and the evolution of recombination.
    Genetics. 173(3), 1793–1811.
  mla: Roze, Denis, and Nicholas H. Barton. “The Hill-Robertson Effect and the Evolution
    of Recombination.” <i>Genetics</i>, vol. 173, no. 3, Genetics Society of America,
    2006, pp. 1793–811, doi:<a href="https://doi.org/10.1534/genetics.106.058586 ">10.1534/genetics.106.058586
    </a>.
  short: D. Roze, N.H. Barton, Genetics 173 (2006) 1793–1811.
date_created: 2018-12-11T12:07:50Z
date_published: 2006-07-01T00:00:00Z
date_updated: 2021-01-12T07:55:36Z
day: '01'
doi: '10.1534/genetics.106.058586 '
extern: 1
intvolume: '       173'
issue: '3'
month: '07'
page: 1793 - 1811
publication: Genetics
publication_status: published
publisher: Genetics Society of America
publist_id: '1854'
quality_controlled: 0
status: public
title: The Hill-Robertson effect and the evolution of recombination
type: journal_article
volume: 173
year: '2006'
...
---
_id: '4250'
abstract:
- lang: eng
  text: A recent analysis has shown that divergence between human and chimpanzee varies
    greatly across the genome. Although this is consistent with ‘hybridisation’ between
    the diverging human and chimp lineages, such observations can be explained more
    simply by the null model of allopatric speciation.
author:
- first_name: Nicholas H
  full_name: Nicholas Barton
  id: 4880FE40-F248-11E8-B48F-1D18A9856A87
  last_name: Barton
  orcid: 0000-0002-8548-5240
citation:
  ama: 'Barton NH. Evolutionary Biology: How did the human species form? <i>Current
    Biology</i>. 2006;16(16):647-650. doi:<a href="https://doi.org/10.1016/j.cub.2006.07.032">10.1016/j.cub.2006.07.032</a>'
  apa: 'Barton, N. H. (2006). Evolutionary Biology: How did the human species form?
    <i>Current Biology</i>. Cell Press. <a href="https://doi.org/10.1016/j.cub.2006.07.032">https://doi.org/10.1016/j.cub.2006.07.032</a>'
  chicago: 'Barton, Nicholas H. “Evolutionary Biology: How Did the Human Species Form?”
    <i>Current Biology</i>. Cell Press, 2006. <a href="https://doi.org/10.1016/j.cub.2006.07.032">https://doi.org/10.1016/j.cub.2006.07.032</a>.'
  ieee: 'N. H. Barton, “Evolutionary Biology: How did the human species form?,” <i>Current
    Biology</i>, vol. 16, no. 16. Cell Press, pp. 647–650, 2006.'
  ista: 'Barton NH. 2006. Evolutionary Biology: How did the human species form? Current
    Biology. 16(16), 647–650.'
  mla: 'Barton, Nicholas H. “Evolutionary Biology: How Did the Human Species Form?”
    <i>Current Biology</i>, vol. 16, no. 16, Cell Press, 2006, pp. 647–50, doi:<a
    href="https://doi.org/10.1016/j.cub.2006.07.032">10.1016/j.cub.2006.07.032</a>.'
  short: N.H. Barton, Current Biology 16 (2006) 647–650.
date_created: 2018-12-11T12:07:51Z
date_published: 2006-08-22T00:00:00Z
date_updated: 2019-04-26T07:22:41Z
day: '22'
doi: 10.1016/j.cub.2006.07.032
extern: 1
intvolume: '        16'
issue: '16'
month: '08'
page: 647 - 650
publication: Current Biology
publication_status: published
publisher: Cell Press
publist_id: '1850'
quality_controlled: 0
status: public
title: 'Evolutionary Biology: How did the human species form?'
type: review
volume: 16
year: '2006'
...
---
_id: '4345'
abstract:
- lang: eng
  text: Der Artikel beschäftigt sich mit dem Konzept der Bibliothek 2.0 (bzw. Library
    2.0). Er skizziert anhand einiger Beispiele die Entwicklung zum Web 2.0 und beschreibt,
    wie Web 2.0-Technologien und -Anwendungen in Bibliotheken eingesetzt werden. Im
    Mittelpunkt stehen Social-Tagging-Systeme, benutzerorientierte Erweiterungen von
    Bibliothekskatalogen und Dokumentenservern sowie der Einsatz von Weblogs an Bibliotheken.
    Ferner werden neue Anforderungen an Bibliothekare diskutiert.
author:
- first_name: Patrick
  full_name: Patrick Danowski
  id: 2EBD1598-F248-11E8-B48F-1D18A9856A87
  last_name: Danowski
  orcid: 0000-0002-6026-4409
- first_name: Lambert
  full_name: Heller,Lambert
  last_name: Heller
citation:
  ama: Danowski P, Heller L. Bibliothek 2.0 - Die Bibliothek der Zukunft? <i>Bibliotheksdienst</i>.
    2006;40(11):1250-1271. doi:<a href="https://doi.org/424">424</a>
  apa: Danowski, P., &#38; Heller, L. (2006). Bibliothek 2.0 - Die Bibliothek der
    Zukunft? <i>Bibliotheksdienst</i>. Zentral- und Landesbibliothek Berlin. <a href="https://doi.org/424">https://doi.org/424</a>
  chicago: Danowski, Patrick, and Lambert Heller. “Bibliothek 2.0 - Die Bibliothek
    Der Zukunft?” <i>Bibliotheksdienst</i>. Zentral- und Landesbibliothek Berlin,
    2006. <a href="https://doi.org/424">https://doi.org/424</a>.
  ieee: P. Danowski and L. Heller, “Bibliothek 2.0 - Die Bibliothek der Zukunft?,”
    <i>Bibliotheksdienst</i>, vol. 40, no. 11. Zentral- und Landesbibliothek Berlin,
    pp. 1250–1271, 2006.
  ista: Danowski P, Heller L. 2006. Bibliothek 2.0 - Die Bibliothek der Zukunft? Bibliotheksdienst.
    40(11), 1250–1271.
  mla: Danowski, Patrick, and Lambert Heller. “Bibliothek 2.0 - Die Bibliothek Der
    Zukunft?” <i>Bibliotheksdienst</i>, vol. 40, no. 11, Zentral- und Landesbibliothek
    Berlin, 2006, pp. 1250–71, doi:<a href="https://doi.org/424">424</a>.
  short: P. Danowski, L. Heller, Bibliotheksdienst 40 (2006) 1250–1271.
date_created: 2018-12-11T12:08:23Z
date_published: 2006-01-01T00:00:00Z
date_updated: 2021-01-12T07:56:17Z
day: '01'
doi: '424'
extern: 1
intvolume: '        40'
issue: '11'
main_file_link:
- open_access: '0'
  url: http://www.zlb.de/aktivitaeten/bd_neu/heftinhalte2006/DigitaleBib011106.pdf
month: '01'
page: 1250 - 1271
publication: Bibliotheksdienst
publication_status: published
publisher: Zentral- und Landesbibliothek Berlin
publist_id: '1229'
quality_controlled: 0
status: public
title: Bibliothek 2.0 - Die Bibliothek der Zukunft?
type: journal_article
volume: 40
year: '2006'
...
---
_id: '4351'
abstract:
- lang: eng
  text: 'BACKGROUND: Character mapping on phylogenies has played an important, if
    not critical role, in our understanding of molecular, morphological, and behavioral
    evolution. Until very recently we have relied on parsimony to infer character
    changes. Parsimony has a number of serious limitations that are drawbacks to our
    understanding. Recent statistical methods have been developed that free us from
    these limitations enabling us to overcome the problems of parsimony by accommodating
    uncertainty in evolutionary time, ancestral states, and the phylogeny. RESULTS:
    SIMMAP has been developed to implement stochastic character mapping that is useful
    to both molecular evolutionists, systematists, and bioinformaticians. Researchers
    can address questions about positive selection, patterns of amino acid substitution,
    character association, and patterns of morphological evolution. CONCLUSION: Stochastic
    character mapping, as implemented in the SIMMAP software, enables users to address
    questions that require mapping characters onto phylogenies using a probabilistic
    approach that does not rely on parsimony. Analyses can be performed using a fully
    Bayesian approach that is not reliant on considering a single topology, set of
    substitution model parameters, or reconstruction of ancestral states. Uncertainty
    in these quantities is accommodated by using MCMC samples from their respective
    posterior distributions.'
author:
- first_name: Jonathan P
  full_name: Jonathan Bollback
  id: 2C6FA9CC-F248-11E8-B48F-1D18A9856A87
  last_name: Bollback
  orcid: 0000-0002-4624-4612
citation:
  ama: 'Bollback JP. SIMMAP: stochastic character mapping of discrete traits on phylogenies.
    <i>BMC Bioinformatics</i>. 2006;7. doi:<a href="https://doi.org/10.1186/1471-2105-7-88">10.1186/1471-2105-7-88</a>'
  apa: 'Bollback, J. P. (2006). SIMMAP: stochastic character mapping of discrete traits
    on phylogenies. <i>BMC Bioinformatics</i>. BioMed Central. <a href="https://doi.org/10.1186/1471-2105-7-88">https://doi.org/10.1186/1471-2105-7-88</a>'
  chicago: 'Bollback, Jonathan P. “SIMMAP: Stochastic Character Mapping of Discrete
    Traits on Phylogenies.” <i>BMC Bioinformatics</i>. BioMed Central, 2006. <a href="https://doi.org/10.1186/1471-2105-7-88">https://doi.org/10.1186/1471-2105-7-88</a>.'
  ieee: 'J. P. Bollback, “SIMMAP: stochastic character mapping of discrete traits
    on phylogenies,” <i>BMC Bioinformatics</i>, vol. 7. BioMed Central, 2006.'
  ista: 'Bollback JP. 2006. SIMMAP: stochastic character mapping of discrete traits
    on phylogenies. BMC Bioinformatics. 7.'
  mla: 'Bollback, Jonathan P. “SIMMAP: Stochastic Character Mapping of Discrete Traits
    on Phylogenies.” <i>BMC Bioinformatics</i>, vol. 7, BioMed Central, 2006, doi:<a
    href="https://doi.org/10.1186/1471-2105-7-88">10.1186/1471-2105-7-88</a>.'
  short: J.P. Bollback, BMC Bioinformatics 7 (2006).
date_created: 2018-12-11T12:08:25Z
date_published: 2006-01-01T00:00:00Z
date_updated: 2021-01-12T07:56:20Z
day: '01'
doi: 10.1186/1471-2105-7-88
extern: 1
intvolume: '         7'
month: '01'
publication: BMC Bioinformatics
publication_status: published
publisher: BioMed Central
publist_id: '1109'
quality_controlled: 0
status: public
title: 'SIMMAP: stochastic character mapping of discrete traits on phylogenies'
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
volume: 7
year: '2006'
...
