---
_id: '8988'
abstract:
- lang: eng
text: The differentiation of cells depends on a precise control of their internal
organization, which is the result of a complex dynamic interplay between the cytoskeleton,
molecular motors, signaling molecules, and membranes. For example, in the developing
neuron, the protein ADAP1 (ADP-ribosylation factor GTPase-activating protein [ArfGAP]
with dual pleckstrin homology [PH] domains 1) has been suggested to control dendrite
branching by regulating the small GTPase ARF6. Together with the motor protein
KIF13B, ADAP1 is also thought to mediate delivery of the second messenger phosphatidylinositol
(3,4,5)-trisphosphate (PIP3) to the axon tip, thus contributing to PIP3 polarity.
However, what defines the function of ADAP1 and how its different roles are coordinated
are still not clear. Here, we studied ADAP1’s functions using in vitro reconstitutions.
We found that KIF13B transports ADAP1 along microtubules, but that PIP3 as well
as PI(3,4)P2 act as stop signals for this transport instead of being transported.
We also demonstrate that these phosphoinositides activate ADAP1’s enzymatic activity
to catalyze GTP hydrolysis by ARF6. Together, our results support a model for
the cellular function of ADAP1, where KIF13B transports ADAP1 until it encounters
high PIP3/PI(3,4)P2 concentrations in the plasma membrane. Here, ADAP1 disassociates
from the motor to inactivate ARF6, promoting dendrite branching.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: EM-Fac
acknowledgement: "We thank Urban Bezeljak, Natalia Baranova, Mar Lopez-Pelegrin, Catarina
Alcarva, and Victoria Faas for sharing reagents and helpful discussions. We thank
Veronika Szentirmai for help with protein purifications. We thank Carrie Bernecky,
Sascha Martens, and the M.L. lab for comments on the manuscript. We thank the bioimaging
facility, the life science facility, and Armel Nicolas from the mass spec facility
at the Institute of Science and Technology (IST) Austria for technical support.
C.D. acknowledges funding from the IST fellowship program; this work was supported
by Human Frontier Science Program Young Investigator Grant\r\nRGY0083/2016. "
article_number: e2010054118
article_processing_charge: No
article_type: original
author:
- first_name: Christian F
full_name: Düllberg, Christian F
id: 459064DC-F248-11E8-B48F-1D18A9856A87
last_name: Düllberg
orcid: 0000-0001-6335-9748
- first_name: Albert
full_name: Auer, Albert
id: 3018E8C2-F248-11E8-B48F-1D18A9856A87
last_name: Auer
orcid: 0000-0002-3580-2906
- first_name: Nikola
full_name: Canigova, Nikola
id: 3795523E-F248-11E8-B48F-1D18A9856A87
last_name: Canigova
orcid: 0000-0002-8518-5926
- first_name: Katrin
full_name: Loibl, Katrin
id: 3760F32C-F248-11E8-B48F-1D18A9856A87
last_name: Loibl
orcid: 0000-0002-2429-7668
- first_name: Martin
full_name: Loose, Martin
id: 462D4284-F248-11E8-B48F-1D18A9856A87
last_name: Loose
orcid: 0000-0001-7309-9724
citation:
ama: Düllberg CF, Auer A, Canigova N, Loibl K, Loose M. In vitro reconstitution
reveals phosphoinositides as cargo-release factors and activators of the ARF6
GAP ADAP1. PNAS. 2021;118(1). doi:10.1073/pnas.2010054118
apa: Düllberg, C. F., Auer, A., Canigova, N., Loibl, K., & Loose, M. (2021).
In vitro reconstitution reveals phosphoinositides as cargo-release factors and
activators of the ARF6 GAP ADAP1. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.2010054118
chicago: Düllberg, Christian F, Albert Auer, Nikola Canigova, Katrin Loibl, and
Martin Loose. “In Vitro Reconstitution Reveals Phosphoinositides as Cargo-Release
Factors and Activators of the ARF6 GAP ADAP1.” PNAS. National Academy of
Sciences, 2021. https://doi.org/10.1073/pnas.2010054118.
ieee: C. F. Düllberg, A. Auer, N. Canigova, K. Loibl, and M. Loose, “In vitro reconstitution
reveals phosphoinositides as cargo-release factors and activators of the ARF6
GAP ADAP1,” PNAS, vol. 118, no. 1. National Academy of Sciences, 2021.
ista: Düllberg CF, Auer A, Canigova N, Loibl K, Loose M. 2021. In vitro reconstitution
reveals phosphoinositides as cargo-release factors and activators of the ARF6
GAP ADAP1. PNAS. 118(1), e2010054118.
mla: Düllberg, Christian F., et al. “In Vitro Reconstitution Reveals Phosphoinositides
as Cargo-Release Factors and Activators of the ARF6 GAP ADAP1.” PNAS, vol.
118, no. 1, e2010054118, National Academy of Sciences, 2021, doi:10.1073/pnas.2010054118.
short: C.F. Düllberg, A. Auer, N. Canigova, K. Loibl, M. Loose, PNAS 118 (2021).
date_created: 2021-01-03T23:01:23Z
date_published: 2021-01-05T00:00:00Z
date_updated: 2023-08-04T11:20:46Z
day: '05'
department:
- _id: MaLo
- _id: MiSi
doi: 10.1073/pnas.2010054118
external_id:
isi:
- '000607270100018'
pmid:
- '33443153'
intvolume: ' 118'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1073/pnas.2010054118
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2599F062-B435-11E9-9278-68D0E5697425
grant_number: RGY0083/2016
name: Reconstitution of cell polarity and axis determination in a cell-free system
publication: PNAS
publication_identifier:
eissn:
- '10916490'
issn:
- '00278424'
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
scopus_import: '1'
status: public
title: In vitro reconstitution reveals phosphoinositides as cargo-release factors
and activators of the ARF6 GAP ADAP1
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 118
year: '2021'
...
---
_id: '660'
abstract:
- lang: eng
text: Growing microtubules are protected from depolymerization by the presence of
a GTP or GDP/Pi cap. End-binding proteins of the EB1 family bind to the stabilizing
cap, allowing monitoring of its size in real time. The cap size has been shown
to correlate with instantaneous microtubule stability. Here we have quantitatively
characterized the properties of cap size fluctuations during steadystate growth
and have developed a theory predicting their timescale and amplitude from the
kinetics of microtubule growth and cap maturation. In contrast to growth speed
fluctuations, cap size fluctuations show a characteristic timescale, which is
defined by the lifetime of the cap sites. Growth fluctuations affect the amplitude
of cap size fluctuations; however, cap size does not affect growth speed, indicating
that microtubules are far from instability during most of their time of growth.
Our theory provides the basis for a quantitative understanding of microtubule
stability fluctuations during steady-state growth.
acknowledgement: We thank Philippe Cluzel for helpful discussions and Gunnar Pruessner
for data analysis advice. This work was supported by the Francis Crick Institute,
which receives its core funding from Cancer Research UK Grant FC001163, Medical
Research Council Grant FC001163, and Wellcome Trust Grant FC001163. This work was
also supported by European Research Council Advanced Grant Project 323042 (to C.D.
and T.S.).
author:
- first_name: Jamie
full_name: Rickman, Jamie
last_name: Rickman
- first_name: Christian F
full_name: Düllberg, Christian F
id: 459064DC-F248-11E8-B48F-1D18A9856A87
last_name: Düllberg
orcid: 0000-0001-6335-9748
- first_name: Nicholas
full_name: Cade, Nicholas
last_name: Cade
- first_name: Lewis
full_name: Griffin, Lewis
last_name: Griffin
- first_name: Thomas
full_name: Surrey, Thomas
last_name: Surrey
citation:
ama: Rickman J, Düllberg CF, Cade N, Griffin L, Surrey T. Steady state EB cap size
fluctuations are determined by stochastic microtubule growth and maturation. PNAS.
2017;114(13):3427-3432. doi:10.1073/pnas.1620274114
apa: Rickman, J., Düllberg, C. F., Cade, N., Griffin, L., & Surrey, T. (2017).
Steady state EB cap size fluctuations are determined by stochastic microtubule
growth and maturation. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1620274114
chicago: Rickman, Jamie, Christian F Düllberg, Nicholas Cade, Lewis Griffin, and
Thomas Surrey. “Steady State EB Cap Size Fluctuations Are Determined by Stochastic
Microtubule Growth and Maturation.” PNAS. National Academy of Sciences,
2017. https://doi.org/10.1073/pnas.1620274114.
ieee: J. Rickman, C. F. Düllberg, N. Cade, L. Griffin, and T. Surrey, “Steady state
EB cap size fluctuations are determined by stochastic microtubule growth and maturation,”
PNAS, vol. 114, no. 13. National Academy of Sciences, pp. 3427–3432, 2017.
ista: Rickman J, Düllberg CF, Cade N, Griffin L, Surrey T. 2017. Steady state EB
cap size fluctuations are determined by stochastic microtubule growth and maturation.
PNAS. 114(13), 3427–3432.
mla: Rickman, Jamie, et al. “Steady State EB Cap Size Fluctuations Are Determined
by Stochastic Microtubule Growth and Maturation.” PNAS, vol. 114, no. 13,
National Academy of Sciences, 2017, pp. 3427–32, doi:10.1073/pnas.1620274114.
short: J. Rickman, C.F. Düllberg, N. Cade, L. Griffin, T. Surrey, PNAS 114 (2017)
3427–3432.
date_created: 2018-12-11T11:47:46Z
date_published: 2017-03-28T00:00:00Z
date_updated: 2021-01-12T08:08:09Z
day: '28'
department:
- _id: MaLo
doi: 10.1073/pnas.1620274114
external_id:
pmid:
- '28280102'
intvolume: ' 114'
issue: '13'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380103/
month: '03'
oa: 1
oa_version: Submitted Version
page: 3427 - 3432
pmid: 1
publication: PNAS
publication_identifier:
issn:
- '00278424'
publication_status: published
publisher: National Academy of Sciences
publist_id: '7073'
quality_controlled: '1'
scopus_import: 1
status: public
title: Steady state EB cap size fluctuations are determined by stochastic microtubule
growth and maturation
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 114
year: '2017'
...
---
_id: '960'
abstract:
- lang: eng
text: The human cerebral cortex is the seat of our cognitive abilities and composed
of an extraordinary number of neurons, organized in six distinct layers. The establishment
of specific morphological and physiological features in individual neurons needs
to be regulated with high precision. Impairments in the sequential developmental
programs instructing corticogenesis lead to alterations in the cortical cytoarchitecture
which is thought to represent the major underlying cause for several neurological
disorders including neurodevelopmental and psychiatric diseases. In this review
we discuss the role of cell polarity at sequential stages during cortex development.
We first provide an overview of morphological cell polarity features in cortical
neural stem cells and newly-born postmitotic neurons. We then synthesize a conceptual
molecular and biochemical framework how cell polarity is established at the cellular
level through a break in symmetry in nascent cortical projection neurons. Lastly
we provide a perspective how the molecular mechanisms applying to single cells
could be probed and integrated in an in vivo and tissue-wide context.
article_number: '176'
article_processing_charge: Yes
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Christian F
full_name: Düllberg, Christian F
id: 459064DC-F248-11E8-B48F-1D18A9856A87
last_name: Düllberg
orcid: 0000-0001-6335-9748
- first_name: Christine
full_name: Mieck, Christine
id: 34CAE85C-F248-11E8-B48F-1D18A9856A87
last_name: Mieck
orcid: 0000-0003-1919-7416
- first_name: Martin
full_name: Loose, Martin
id: 462D4284-F248-11E8-B48F-1D18A9856A87
last_name: Loose
orcid: 0000-0001-7309-9724
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. Cell polarity in cerebral
cortex development - cellular architecture shaped by biochemical networks. Frontiers
in Cellular Neuroscience. 2017;11. doi:10.3389/fncel.2017.00176
apa: Hansen, A. H., Düllberg, C. F., Mieck, C., Loose, M., & Hippenmeyer, S.
(2017). Cell polarity in cerebral cortex development - cellular architecture shaped
by biochemical networks. Frontiers in Cellular Neuroscience. Frontiers
Research Foundation. https://doi.org/10.3389/fncel.2017.00176
chicago: Hansen, Andi H, Christian F Düllberg, Christine Mieck, Martin Loose, and
Simon Hippenmeyer. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture
Shaped by Biochemical Networks.” Frontiers in Cellular Neuroscience. Frontiers
Research Foundation, 2017. https://doi.org/10.3389/fncel.2017.00176.
ieee: A. H. Hansen, C. F. Düllberg, C. Mieck, M. Loose, and S. Hippenmeyer, “Cell
polarity in cerebral cortex development - cellular architecture shaped by biochemical
networks,” Frontiers in Cellular Neuroscience, vol. 11. Frontiers Research
Foundation, 2017.
ista: Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. 2017. Cell polarity
in cerebral cortex development - cellular architecture shaped by biochemical networks.
Frontiers in Cellular Neuroscience. 11, 176.
mla: Hansen, Andi H., et al. “Cell Polarity in Cerebral Cortex Development - Cellular
Architecture Shaped by Biochemical Networks.” Frontiers in Cellular Neuroscience,
vol. 11, 176, Frontiers Research Foundation, 2017, doi:10.3389/fncel.2017.00176.
short: A.H. Hansen, C.F. Düllberg, C. Mieck, M. Loose, S. Hippenmeyer, Frontiers
in Cellular Neuroscience 11 (2017).
date_created: 2018-12-11T11:49:25Z
date_published: 2017-06-28T00:00:00Z
date_updated: 2024-03-25T23:30:23Z
day: '28'
ddc:
- '570'
department:
- _id: SiHi
- _id: MaLo
doi: 10.3389/fncel.2017.00176
ec_funded: 1
external_id:
isi:
- '000404486700001'
file:
- access_level: open_access
checksum: dc1f5a475b918d09a0f9f587400b1626
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:40Z
date_updated: 2020-07-14T12:48:16Z
file_id: '4764'
file_name: IST-2017-830-v1+1_2017_Hansen_CellPolarity.pdf
file_size: 2153858
relation: main_file
file_date_updated: 2020-07-14T12:48:16Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25985A36-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T00817-B21
name: The biochemical basis of PAR polarization
publication: Frontiers in Cellular Neuroscience
publication_identifier:
issn:
- '16625102'
publication_status: published
publisher: Frontiers Research Foundation
publist_id: '6445'
pubrep_id: '830'
quality_controlled: '1'
related_material:
record:
- id: '9962'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Cell polarity in cerebral cortex development - cellular architecture shaped
by biochemical networks
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 11
year: '2017'
...
---
_id: '453'
abstract:
- lang: eng
text: Most kinesin motors move in only one direction along microtubules. Members
of the kinesin-5 subfamily were initially described as unidirectional plus-end-directed
motors and shown to produce piconewton forces. However, some fungal kinesin-5
motors are bidirectional. The force production of a bidirectional kinesin-5 has
not yet been measured. Therefore, it remains unknown whether the mechanism of
the unconventional minus-end-directed motility differs fundamentally from that
of plus-end-directed stepping. Using force spectroscopy, we have measured here
the forces that ensembles of purified budding yeast kinesin-5 Cin8 produce in
microtubule gliding assays in both plus- and minus-end direction. Correlation
analysis of pause forces demonstrated that individual Cin8 molecules produce additive
forces in both directions of movement. In ensembles, Cin8 motors were able to
produce single-motor forces up to a magnitude of ∼1.5 pN. Hence, these properties
appear to be conserved within the kinesin-5 subfamily. Force production was largely
independent of the directionality of movement, indicating similarities between
the motility mechanisms for both directions. These results provide constraints
for the development of models for the bidirectional motility mechanism of fission
yeast kinesin-5 and provide insight into the function of this mitotic motor.
acknowledgement: 'The plasmid for full-length kinesin-1 was a gift from G. Holzwarth
and J. Macosko with permission from J. Howard. We thank I. Lueke and N. I. Cade
for technical assistance. G.P. thanks the Francis Crick Institute, and in particular
the Surrey and Salbreux groups, for their hospitality during his sabbatical stay,
as well as Imperial College London for making it possible. This work was supported
by the Francis Crick Institute, which receives its core funding from Cancer Research
UK (FC001163), the United Kingdom Medical Research Council (FC001163), and the Wellcome
Trust (FC001163), and by Imperial College London. J.R. was also supported by a Sir
Henry Wellcome Postdoctoral Fellowship (100145/Z/12/Z) and T.S. by the European
Research Council (Advanced Grant, project 323042). '
article_processing_charge: No
article_type: original
author:
- first_name: Todd
full_name: Fallesen, Todd
last_name: Fallesen
- first_name: Johanna
full_name: Roostalu, Johanna
last_name: Roostalu
- first_name: Christian F
full_name: Düllberg, Christian F
id: 459064DC-F248-11E8-B48F-1D18A9856A87
last_name: Düllberg
orcid: 0000-0001-6335-9748
- first_name: Gunnar
full_name: Pruessner, Gunnar
last_name: Pruessner
- first_name: Thomas
full_name: Surrey, Thomas
last_name: Surrey
citation:
ama: Fallesen T, Roostalu J, Düllberg CF, Pruessner G, Surrey T. Ensembles of bidirectional
kinesin Cin8 produce additive forces in both directions of movement. Biophysical
Journal. 2017;113(9):2055-2067. doi:10.1016/j.bpj.2017.09.006
apa: Fallesen, T., Roostalu, J., Düllberg, C. F., Pruessner, G., & Surrey, T.
(2017). Ensembles of bidirectional kinesin Cin8 produce additive forces in both
directions of movement. Biophysical Journal. Biophysical Society. https://doi.org/10.1016/j.bpj.2017.09.006
chicago: Fallesen, Todd, Johanna Roostalu, Christian F Düllberg, Gunnar Pruessner,
and Thomas Surrey. “Ensembles of Bidirectional Kinesin Cin8 Produce Additive Forces
in Both Directions of Movement.” Biophysical Journal. Biophysical Society,
2017. https://doi.org/10.1016/j.bpj.2017.09.006.
ieee: T. Fallesen, J. Roostalu, C. F. Düllberg, G. Pruessner, and T. Surrey, “Ensembles
of bidirectional kinesin Cin8 produce additive forces in both directions of movement,”
Biophysical Journal, vol. 113, no. 9. Biophysical Society, pp. 2055–2067,
2017.
ista: Fallesen T, Roostalu J, Düllberg CF, Pruessner G, Surrey T. 2017. Ensembles
of bidirectional kinesin Cin8 produce additive forces in both directions of movement.
Biophysical Journal. 113(9), 2055–2067.
mla: Fallesen, Todd, et al. “Ensembles of Bidirectional Kinesin Cin8 Produce Additive
Forces in Both Directions of Movement.” Biophysical Journal, vol. 113,
no. 9, Biophysical Society, 2017, pp. 2055–67, doi:10.1016/j.bpj.2017.09.006.
short: T. Fallesen, J. Roostalu, C.F. Düllberg, G. Pruessner, T. Surrey, Biophysical
Journal 113 (2017) 2055–2067.
date_created: 2018-12-11T11:46:33Z
date_published: 2017-11-07T00:00:00Z
date_updated: 2021-01-12T07:59:28Z
day: '07'
ddc:
- '570'
department:
- _id: MaLo
doi: 10.1016/j.bpj.2017.09.006
file:
- access_level: open_access
checksum: 99a2474088e20ac74b1882c4fbbb45b1
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:14:03Z
date_updated: 2020-07-14T12:46:31Z
file_id: '5052'
file_name: IST-2018-965-v1+1_2017_Duellberg_Ensembles_of.pdf
file_size: 977192
relation: main_file
file_date_updated: 2020-07-14T12:46:31Z
has_accepted_license: '1'
intvolume: ' 113'
issue: '9'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 2055 - 2067
publication: Biophysical Journal
publication_status: published
publisher: Biophysical Society
publist_id: '7369'
pubrep_id: '965'
quality_controlled: '1'
status: public
title: Ensembles of bidirectional kinesin Cin8 produce additive forces in both directions
of movement
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: 113
year: '2017'
...
---
_id: '1139'
abstract:
- lang: eng
text: Microtubules switch stochastically between phases of growth and shrinkage.
The molecular mechanism responsible for the end of a growth phase, an event called
catastrophe, is still not understood. The probability for a catastrophe to occur
increases with microtubule age, putting constraints on the possible molecular
mechanism of catastrophe induction. Here we used microfluidics-Assisted fast tubulin
washout experiments to induce microtubule depolymerization in a controlled manner
at different times after the start of growth. We found that aging can also be
observed in this assay, providing valuable new constraints against which theoretical
models of catastrophe induction can be tested. We found that the data can be quantitatively
well explained by a simple kinetic threshold model that assumes an age-dependent
broadening of the protective cap at the microtubule end as a result of an evolving
tapered end structure; this leads to a decrease of the cap density and its stability.
This analysis suggests an intuitive picture of the role of morphological changes
of the protective cap for the age dependence of microtubule stability.
article_processing_charge: No
author:
- first_name: Christian F
full_name: Düllberg, Christian F
id: 459064DC-F248-11E8-B48F-1D18A9856A87
last_name: Düllberg
orcid: 0000-0001-6335-9748
- first_name: Nicholas
full_name: Cade, Nicholas
last_name: Cade
- first_name: Thomas
full_name: Surrey, Thomas
last_name: Surrey
citation:
ama: Düllberg CF, Cade N, Surrey T. Microtubule aging probed by microfluidics assisted
tubulin washout. Molecular Biology and Evolution. 2016;27(22):3563-3573.
doi:10.1091/mbc.E16-07-0548
apa: Düllberg, C. F., Cade, N., & Surrey, T. (2016). Microtubule aging probed
by microfluidics assisted tubulin washout. Molecular Biology and Evolution.
Oxford University Press. https://doi.org/10.1091/mbc.E16-07-0548
chicago: Düllberg, Christian F, Nicholas Cade, and Thomas Surrey. “Microtubule Aging
Probed by Microfluidics Assisted Tubulin Washout.” Molecular Biology and Evolution.
Oxford University Press, 2016. https://doi.org/10.1091/mbc.E16-07-0548.
ieee: C. F. Düllberg, N. Cade, and T. Surrey, “Microtubule aging probed by microfluidics
assisted tubulin washout,” Molecular Biology and Evolution, vol. 27, no.
22. Oxford University Press, pp. 3563–3573, 2016.
ista: Düllberg CF, Cade N, Surrey T. 2016. Microtubule aging probed by microfluidics
assisted tubulin washout. Molecular Biology and Evolution. 27(22), 3563–3573.
mla: Düllberg, Christian F., et al. “Microtubule Aging Probed by Microfluidics Assisted
Tubulin Washout.” Molecular Biology and Evolution, vol. 27, no. 22, Oxford
University Press, 2016, pp. 3563–73, doi:10.1091/mbc.E16-07-0548.
short: C.F. Düllberg, N. Cade, T. Surrey, Molecular Biology and Evolution 27 (2016)
3563–3573.
date_created: 2018-12-11T11:50:21Z
date_published: 2016-11-07T00:00:00Z
date_updated: 2021-01-12T06:48:34Z
day: '07'
doi: 10.1091/mbc.E16-07-0548
extern: '1'
intvolume: ' 27'
issue: '22'
language:
- iso: eng
month: '11'
oa_version: None
page: 3563 - 3573
publication: Molecular Biology and Evolution
publication_status: published
publisher: Oxford University Press
publist_id: '6218'
status: public
title: Microtubule aging probed by microfluidics assisted tubulin washout
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 27
year: '2016'
...