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@ARTICLE{Janotiak:137714,
author = {Janoštiak, Radoslav and Brábek, Jan and Auernheimer, Vera
and Tatárová, Zuzana and Lautscham, Lena A. and Dey, Tuli
and Gemperle, Jakub and Merkel, Rudolf and Goldmann,
Wolfgang H. and Fabry, Ben and Rösel, Daniel},
title = {{CAS} directly interacts with vinculin to control
mechanosensing and focal adhesion dynamics},
journal = {Cellular and molecular life sciences},
volume = {71},
number = {4},
issn = {1420-9071},
address = {Basel},
publisher = {Birkhäuser},
reportid = {FZJ-2013-04042},
pages = {727-744},
year = {2014},
abstract = {Focal adhesions are cellular structures through which both
mechanical forces and regulatory signals are transmitted.
Two focal adhesion-associated proteins, Crk-associated
substrate (CAS) and vinculin, were both independently shown
to be crucial for the ability of cells to transmit
mechanical forces and to regulate cytoskeletal tension.
Here, we identify a novel, direct binding interaction
between CAS and vinculin. This interaction is mediated by
the CAS SRC homology 3 domain and a proline-rich sequence in
the hinge region of vinculin. We show that CAS localization
in focal adhesions is partially dependent on vinculin, and
that CAS–vinculin coupling is required for stretch-induced
activation of CAS at the Y410 phosphorylation site.
Moreover, CAS–vinculin binding significantly affects the
dynamics of CAS and vinculin within focal adhesions as well
as the size of focal adhesions. Finally, disruption of CAS
binding to vinculin reduces cell stiffness and traction
force generation. Taken together, these findings strongly
implicate a crucial role of CAS–vinculin interaction in
mechanosensing and focal adhesion dynamics},
cin = {ICS-7},
ddc = {570},
cid = {I:(DE-Juel1)ICS-7-20110106},
pnm = {453 - Physics of the Cell (POF2-453)},
pid = {G:(DE-HGF)POF2-453},
typ = {PUB:(DE-HGF)16},
UT = {WOS:000330586500013},
doi = {10.1007/s00018-013-1450-x},
url = {https://juser.fz-juelich.de/record/137714},
}