---
_id: '1321'
abstract:
- lang: eng
text: Most migrating cells extrude their front by the force of actin polymerization.
Polymerization requires an initial nucleation step, which is mediated by factors
establishing either parallel filaments in the case of filopodia or branched filaments
that form the branched lamellipodial network. Branches are considered essential
for regular cell motility and are initiated by the Arp2/3 complex, which in turn
is activated by nucleation-promoting factors of the WASP and WAVE families. Here
we employed rapid amoeboid crawling leukocytes and found that deletion of the
WAVE complex eliminated actin branching and thus lamellipodia formation. The cells
were left with parallel filaments at the leading edge, which translated, depending
on the differentiation status of the cell, into a unipolar pointed cell shape
or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased
speed and enormous directional persistence, while they were unable to turn towards
chemotactic gradients. Cells with multiple filopodia retained chemotactic activity
but their migration was progressively impaired with increasing geometrical complexity
of the extracellular environment. These findings establish that diversified leading
edge protrusions serve as explorative structures while they slow down actual locomotion.
acknowledged_ssus:
- _id: SSU
acknowledgement: "This work was supported by the German Research Foundation (DFG)
Priority Program SP 1464 to T.E.B.S. and M.S., and European Research Council (ERC
GA 281556) and Human Frontiers Program grants to M.S.\r\nService Units of IST Austria
for excellent technical support."
article_processing_charge: No
article_type: original
author:
- first_name: Alexander F
full_name: Leithner, Alexander F
id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87
last_name: Leithner
orcid: 0000-0002-1073-744X
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Jan
full_name: Müller, Jan
id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D
last_name: Müller
- first_name: Anne
full_name: Reversat, Anne
id: 35B76592-F248-11E8-B48F-1D18A9856A87
last_name: Reversat
orcid: 0000-0003-0666-8928
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Jan
full_name: Schwarz, Jan
id: 346C1EC6-F248-11E8-B48F-1D18A9856A87
last_name: Schwarz
- first_name: Jack
full_name: Merrin, Jack
id: 4515C308-F248-11E8-B48F-1D18A9856A87
last_name: Merrin
orcid: 0000-0001-5145-4609
- first_name: David
full_name: De Gorter, David
last_name: De Gorter
- first_name: Florian
full_name: Schur, Florian
id: 48AD8942-F248-11E8-B48F-1D18A9856A87
last_name: Schur
orcid: 0000-0003-4790-8078
- first_name: Jonathan
full_name: Bayerl, Jonathan
last_name: Bayerl
- first_name: Ingrid
full_name: De Vries, Ingrid
id: 4C7D837E-F248-11E8-B48F-1D18A9856A87
last_name: De Vries
- first_name: Stefan
full_name: Wieser, Stefan
id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
last_name: Wieser
orcid: 0000-0002-2670-2217
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Frank
full_name: Lai, Frank
last_name: Lai
- first_name: Markus
full_name: Moser, Markus
last_name: Moser
- first_name: Dontscho
full_name: Kerjaschki, Dontscho
last_name: Kerjaschki
- first_name: Klemens
full_name: Rottner, Klemens
last_name: Rottner
- first_name: Victor
full_name: Small, Victor
last_name: Small
- first_name: Theresia
full_name: Stradal, Theresia
last_name: Stradal
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote
environmental exploration but are dispensable for locomotion of leukocytes. Nature
Cell Biology. 2016;18:1253-1259. doi:10.1038/ncb3426
apa: Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz,
J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental
exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology.
Nature Publishing Group. https://doi.org/10.1038/ncb3426
chicago: Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus
Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote
Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature
Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/ncb3426.
ieee: A. F. Leithner et al., “Diversified actin protrusions promote environmental
exploration but are dispensable for locomotion of leukocytes,” Nature Cell
Biology, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016.
ista: Leithner AF, Eichner A, Müller J, Reversat A, Brown M, Schwarz J, Merrin J,
De Gorter D, Schur FK, Bayerl J, de Vries I, Wieser S, Hauschild R, Lai F, Moser
M, Kerjaschki D, Rottner K, Small V, Stradal T, Sixt MK. 2016. Diversified actin
protrusions promote environmental exploration but are dispensable for locomotion
of leukocytes. Nature Cell Biology. 18, 1253–1259.
mla: Leithner, Alexander F., et al. “Diversified Actin Protrusions Promote Environmental
Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell
Biology, vol. 18, Nature Publishing Group, 2016, pp. 1253–59, doi:10.1038/ncb3426.
short: A.F. Leithner, A. Eichner, J. Müller, A. Reversat, M. Brown, J. Schwarz,
J. Merrin, D. De Gorter, F.K. Schur, J. Bayerl, I. de Vries, S. Wieser, R. Hauschild,
F. Lai, M. Moser, D. Kerjaschki, K. Rottner, V. Small, T. Stradal, M.K. Sixt,
Nature Cell Biology 18 (2016) 1253–1259.
date_created: 2018-12-11T11:51:21Z
date_published: 2016-10-24T00:00:00Z
date_updated: 2024-03-25T23:30:09Z
day: '24'
ddc:
- '570'
department:
- _id: MiSi
- _id: NanoFab
- _id: Bio
doi: 10.1038/ncb3426
ec_funded: 1
file:
- access_level: open_access
checksum: e1411cb7c99a2d9089c178a6abef25e7
content_type: application/pdf
creator: dernst
date_created: 2020-05-14T16:33:46Z
date_updated: 2020-07-14T12:44:43Z
file_id: '7844'
file_name: 2018_NatureCell_Leithner.pdf
file_size: 4433280
relation: main_file
file_date_updated: 2020-07-14T12:44:43Z
has_accepted_license: '1'
intvolume: ' 18'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Submitted Version
page: 1253 - 1259
project:
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '281556'
name: Cytoskeletal force generation and force transduction of migrating leukocytes
(EU)
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5949'
quality_controlled: '1'
related_material:
record:
- id: '323'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Diversified actin protrusions promote environmental exploration but are dispensable
for locomotion of leukocytes
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 18
year: '2016'
...
---
_id: '2242'
abstract:
- lang: eng
text: MicroRNAs (miRNAs) are small RNAs that play important regulatory roles in
many cellular pathways. MiRNAs associate with members of the Argonaute protein
family and bind to partially complementary sequences on mRNAs and induce translational
repression or mRNA decay. Using deep sequencing and Northern blotting, we characterized
miRNA expression in wild type and miR-155-deficient dendritic cells (DCs) and
macrophages. Analysis of different stimuli (LPS, LDL, eLDL, oxLDL) reveals a direct
influence of miR-155 on the expression levels of other miRNAs. For example, miR-455
is negatively regulated in miR-155-deficient cells possibly due to inhibition
of the transcription factor C/EBPbeta by miR-155. Based on our comprehensive data
sets, we propose a model of hierarchical miRNA expression dominated by miR-155
in DCs and macrophages.
author:
- first_name: Anne
full_name: Dueck, Anne
last_name: Dueck
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Gunter
full_name: Meister, Gunter
last_name: Meister
citation:
ama: Dueck A, Eichner A, Sixt MK, Meister G. A miR-155-dependent microRNA hierarchy
in dendritic cell maturation and macrophage activation. FEBS Letters. 2014;588(4):632-640.
doi:10.1016/j.febslet.2014.01.009
apa: Dueck, A., Eichner, A., Sixt, M. K., & Meister, G. (2014). A miR-155-dependent
microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS
Letters. Elsevier. https://doi.org/10.1016/j.febslet.2014.01.009
chicago: Dueck, Anne, Alexander Eichner, Michael K Sixt, and Gunter Meister. “A
MiR-155-Dependent MicroRNA Hierarchy in Dendritic Cell Maturation and Macrophage
Activation.” FEBS Letters. Elsevier, 2014. https://doi.org/10.1016/j.febslet.2014.01.009.
ieee: A. Dueck, A. Eichner, M. K. Sixt, and G. Meister, “A miR-155-dependent microRNA
hierarchy in dendritic cell maturation and macrophage activation,” FEBS Letters,
vol. 588, no. 4. Elsevier, pp. 632–640, 2014.
ista: Dueck A, Eichner A, Sixt MK, Meister G. 2014. A miR-155-dependent microRNA
hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters.
588(4), 632–640.
mla: Dueck, Anne, et al. “A MiR-155-Dependent MicroRNA Hierarchy in Dendritic Cell
Maturation and Macrophage Activation.” FEBS Letters, vol. 588, no. 4, Elsevier,
2014, pp. 632–40, doi:10.1016/j.febslet.2014.01.009.
short: A. Dueck, A. Eichner, M.K. Sixt, G. Meister, FEBS Letters 588 (2014) 632–640.
date_created: 2018-12-11T11:56:31Z
date_published: 2014-02-14T00:00:00Z
date_updated: 2021-01-12T06:56:14Z
day: '14'
department:
- _id: MiSi
doi: 10.1016/j.febslet.2014.01.009
intvolume: ' 588'
issue: '4'
language:
- iso: eng
month: '02'
oa_version: None
page: 632 - 640
publication: FEBS Letters
publication_identifier:
issn:
- '00145793'
publication_status: published
publisher: Elsevier
publist_id: '4714'
quality_controlled: '1'
scopus_import: 1
status: public
title: A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage
activation
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 588
year: '2014'
...
---
_id: '2946'
abstract:
- lang: eng
text: MicroRNAs (miRNAs) are small noncoding RNAs that function in literally all
cellular processes. miRNAs interact with Argonaute (Ago) proteins and guide them
to specific target sites located in the 3′-untranslated region (3′-UTR) of target
mRNAs leading to translational repression and deadenylation-induced mRNA degradation.
Most miRNAs are processed from hairpin-structured precursors by the consecutive
action of the RNase III enzymes Drosha and Dicer. However, processing of miR-451
is Dicer independent and cleavage is mediated by the endonuclease Ago2. Here we
have characterized miR-451 sequence and structure requirements for processing
as well as sorting of miRNAs into different Ago proteins. Pre-miR-451 appears
to be optimized for Ago2 cleavage and changes result in reduced processing. In
addition, we show that the mature miR-451 only associates with Ago2 suggesting
that mature miRNAs are not exchanged between different members of the Ago protein
family. Based on cloning and deep sequencing of endogenous miRNAs associated with
Ago1-3, we do not find evidence for miRNA sorting in human cells. However, Ago
identity appears to influence the length of some miRNAs, while others remain unaffected.
acknowledgement: "Deutsche Forschungsgemeinschaft (DFG) (SFB 960 and FOR855); European
Research Council (ERC grant ‘sRNAs’); European Union (FP7 project ‘ONCOMIRs’); German
Bundesministerium für Bildung und Forschung (BMBF, NGFN+, FKZ PIM-01GS0804-5); Bavarian
Genome Research Network (BayGene to G.M.); The Netherlands Organization for Scientific
Research (NWO, VIDI grant to E.B.). Funding for open access charge: DFG via the
open access publishing program. \r\n\r\nWe thank Sigrun Ammon and Corinna Friederich
for technical assistance and Sebastian Petri and Daniel Schraivogel for helpful
discussions."
author:
- first_name: Anne
full_name: Dueck, Anne
last_name: Dueck
- first_name: Christian
full_name: Ziegler, Christian
last_name: Ziegler
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Eugène
full_name: Berezikov, Eugène
last_name: Berezikov
- first_name: Gunter
full_name: Meister, Gunter
last_name: Meister
citation:
ama: Dueck A, Ziegler C, Eichner A, Berezikov E, Meister G. MicroRNAs associated
with the different human Argonaute proteins. Nucleic Acids Research. 2012;40(19):9850-9862.
doi:10.1093/nar/gks705
apa: Dueck, A., Ziegler, C., Eichner, A., Berezikov, E., & Meister, G. (2012).
MicroRNAs associated with the different human Argonaute proteins. Nucleic Acids
Research. Oxford University Press. https://doi.org/10.1093/nar/gks705
chicago: Dueck, Anne, Christian Ziegler, Alexander Eichner, Eugène Berezikov, and
Gunter Meister. “MicroRNAs Associated with the Different Human Argonaute Proteins.”
Nucleic Acids Research. Oxford University Press, 2012. https://doi.org/10.1093/nar/gks705.
ieee: A. Dueck, C. Ziegler, A. Eichner, E. Berezikov, and G. Meister, “MicroRNAs
associated with the different human Argonaute proteins,” Nucleic Acids Research,
vol. 40, no. 19. Oxford University Press, pp. 9850–9862, 2012.
ista: Dueck A, Ziegler C, Eichner A, Berezikov E, Meister G. 2012. MicroRNAs associated
with the different human Argonaute proteins. Nucleic Acids Research. 40(19), 9850–9862.
mla: Dueck, Anne, et al. “MicroRNAs Associated with the Different Human Argonaute
Proteins.” Nucleic Acids Research, vol. 40, no. 19, Oxford University Press,
2012, pp. 9850–62, doi:10.1093/nar/gks705.
short: A. Dueck, C. Ziegler, A. Eichner, E. Berezikov, G. Meister, Nucleic Acids
Research 40 (2012) 9850–9862.
date_created: 2018-12-11T12:00:29Z
date_published: 2012-10-01T00:00:00Z
date_updated: 2021-01-12T07:39:57Z
day: '01'
ddc:
- '570'
department:
- _id: MiSi
doi: 10.1093/nar/gks705
file:
- access_level: open_access
checksum: 1bb8d1ff894014b481657a21083c941c
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:12Z
date_updated: 2020-07-14T12:45:55Z
file_id: '4993'
file_name: IST-2015-383-v1+1_Nucl._Acids_Res.-2012-Dueck-9850-62.pdf
file_size: 8126936
relation: main_file
file_date_updated: 2020-07-14T12:45:55Z
has_accepted_license: '1'
intvolume: ' 40'
issue: '19'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 9850 - 9862
publication: Nucleic Acids Research
publication_status: published
publisher: Oxford University Press
publist_id: '3786'
pubrep_id: '383'
quality_controlled: '1'
scopus_import: 1
status: public
title: MicroRNAs associated with the different human Argonaute proteins
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 40
year: '2012'
...
---
_id: '491'
abstract:
- lang: eng
text: In their search for antigens, lymphocytes continuously shuttle among blood
vessels, lymph vessels, and lymphatic tissues. Chemokines mediate entry of lymphocytes
into lymphatic tissues, and sphingosine 1-phosphate (S1P) promotes localization
of lymphocytes to the vasculature. Both signals are sensed through G protein-coupled
receptors (GPCRs). Most GPCRs undergo ligand-dependent homologous receptor desensitization,
a process that decreases their signaling output after previous exposure to high
ligand concentration. Such desensitization can explain why lymphocytes do not
take an intermediate position between two signals but rather oscillate between
them. The desensitization of S1P receptor 1 (S1PR1) is mediated by GPCR kinase
2 (GRK2). Deletion of GRK2 in lymphocytes compromises desensitization by high
vascular S1P concentrations, thereby reducing responsiveness to the chemokine
signal and trapping the cells in the vascular compartment. The desensitization
kinetics of S1PR1 allows lymphocytes to dynamically shuttle between vasculature
and lymphatic tissue, although the positional information in both compartments
is static.
article_number: pe43
author:
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
citation:
ama: Eichner A, Sixt MK. Setting the clock for recirculating lymphocytes. Science
Signaling. 2011;4(198). doi:10.1126/scisignal.2002617
apa: Eichner, A., & Sixt, M. K. (2011). Setting the clock for recirculating
lymphocytes. Science Signaling. American Association for the Advancement
of Science. https://doi.org/10.1126/scisignal.2002617
chicago: Eichner, Alexander, and Michael K Sixt. “Setting the Clock for Recirculating
Lymphocytes.” Science Signaling. American Association for the Advancement
of Science, 2011. https://doi.org/10.1126/scisignal.2002617.
ieee: A. Eichner and M. K. Sixt, “Setting the clock for recirculating lymphocytes,”
Science Signaling, vol. 4, no. 198. American Association for the Advancement
of Science, 2011.
ista: Eichner A, Sixt MK. 2011. Setting the clock for recirculating lymphocytes.
Science Signaling. 4(198), pe43.
mla: Eichner, Alexander, and Michael K. Sixt. “Setting the Clock for Recirculating
Lymphocytes.” Science Signaling, vol. 4, no. 198, pe43, American Association
for the Advancement of Science, 2011, doi:10.1126/scisignal.2002617.
short: A. Eichner, M.K. Sixt, Science Signaling 4 (2011).
date_created: 2018-12-11T11:46:46Z
date_published: 2011-11-08T00:00:00Z
date_updated: 2021-01-12T08:01:02Z
day: '08'
department:
- _id: MiSi
doi: 10.1126/scisignal.2002617
intvolume: ' 4'
issue: '198'
language:
- iso: eng
month: '11'
oa_version: None
publication: Science Signaling
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '7329'
quality_controlled: '1'
scopus_import: 1
status: public
title: Setting the clock for recirculating lymphocytes
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 4
year: '2011'
...
---
_id: '518'
abstract:
- lang: eng
text: Cancer stem cells or cancer initiating cells are believed to contribute to
cancer recurrence after therapy. MicroRNAs (miRNAs) are short RNA molecules with
fundamental roles in gene regulation. The role of miRNAs in cancer stem cells
is only poorly understood. Here, we report miRNA expression profiles of glioblastoma
stem cell-containing CD133 + cell populations. We find that miR-9, miR-9 * (referred
to as miR-9/9 *), miR-17 and miR-106b are highly abundant in CD133 + cells. Furthermore,
inhibition of miR-9/9 * or miR-17 leads to reduced neurosphere formation and stimulates
cell differentiation. Calmodulin-binding transcription activator 1 (CAMTA1) is
a putative transcription factor, which induces the expression of the anti-proliferative
cardiac hormone natriuretic peptide A (NPPA). We identify CAMTA1 as an miR-9/9
* and miR-17 target. CAMTA1 expression leads to reduced neurosphere formation
and tumour growth in nude mice, suggesting that CAMTA1 can function as tumour
suppressor. Consistently, CAMTA1 and NPPA expression correlate with patient survival.
Our findings could provide a basis for novel strategies of glioblastoma therapy.
article_processing_charge: No
article_type: original
author:
- first_name: Daniel
full_name: Schraivogel, Daniel
last_name: Schraivogel
- first_name: Lasse
full_name: Weinmann, Lasse
last_name: Weinmann
- first_name: Dagmar
full_name: Beier, Dagmar
last_name: Beier
- first_name: Ghazaleh
full_name: Tabatabai, Ghazaleh
last_name: Tabatabai
- first_name: Alexander
full_name: Eichner, Alexander
id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87
last_name: Eichner
- first_name: Jia
full_name: Zhu, Jia
last_name: Zhu
- first_name: Martina
full_name: Anton, Martina
last_name: Anton
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-6620-9179
- first_name: Michael
full_name: Weller, Michael
last_name: Weller
- first_name: Christoph
full_name: Beier, Christoph
last_name: Beier
- first_name: Gunter
full_name: Meister, Gunter
last_name: Meister
citation:
ama: Schraivogel D, Weinmann L, Beier D, et al. CAMTA1 is a novel tumour suppressor
regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. 2011;30(20):4309-4322.
doi:10.1038/emboj.2011.301
apa: Schraivogel, D., Weinmann, L., Beier, D., Tabatabai, G., Eichner, A., Zhu,
J., … Meister, G. (2011). CAMTA1 is a novel tumour suppressor regulated by miR-9/9
* in glioblastoma stem cells. EMBO Journal. Wiley-Blackwell. https://doi.org/10.1038/emboj.2011.301
chicago: Schraivogel, Daniel, Lasse Weinmann, Dagmar Beier, Ghazaleh Tabatabai,
Alexander Eichner, Jia Zhu, Martina Anton, et al. “CAMTA1 Is a Novel Tumour Suppressor
Regulated by MiR-9/9 * in Glioblastoma Stem Cells.” EMBO Journal. Wiley-Blackwell,
2011. https://doi.org/10.1038/emboj.2011.301.
ieee: D. Schraivogel et al., “CAMTA1 is a novel tumour suppressor regulated
by miR-9/9 * in glioblastoma stem cells,” EMBO Journal, vol. 30, no. 20.
Wiley-Blackwell, pp. 4309–4322, 2011.
ista: Schraivogel D, Weinmann L, Beier D, Tabatabai G, Eichner A, Zhu J, Anton M,
Sixt MK, Weller M, Beier C, Meister G. 2011. CAMTA1 is a novel tumour suppressor
regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. 30(20), 4309–4322.
mla: Schraivogel, Daniel, et al. “CAMTA1 Is a Novel Tumour Suppressor Regulated
by MiR-9/9 * in Glioblastoma Stem Cells.” EMBO Journal, vol. 30, no. 20,
Wiley-Blackwell, 2011, pp. 4309–22, doi:10.1038/emboj.2011.301.
short: D. Schraivogel, L. Weinmann, D. Beier, G. Tabatabai, A. Eichner, J. Zhu,
M. Anton, M.K. Sixt, M. Weller, C. Beier, G. Meister, EMBO Journal 30 (2011) 4309–4322.
date_created: 2018-12-11T11:46:55Z
date_published: 2011-10-19T00:00:00Z
date_updated: 2021-01-12T08:01:19Z
day: '19'
department:
- _id: MiSi
doi: 10.1038/emboj.2011.301
external_id:
pmid:
- '21857646'
intvolume: ' 30'
issue: '20'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199389/
month: '10'
oa: 1
oa_version: Submitted Version
page: 4309 - 4322
pmid: 1
publication: EMBO Journal
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7301'
quality_controlled: '1'
scopus_import: 1
status: public
title: CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma
stem cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 30
year: '2011'
...