Imperial College London

DrJoseCortes Lopez

Faculty of EngineeringDepartment of Bioengineering

 
 
 
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Contact

 

+44 (0)7944 338 144j.e.corteslopez Website

 
 
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Location

 

B-122Bessemer BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Lachowski:2020:10.3389/fcell.2020.592628,
author = {Lachowski, D and Cortes, Lopez J and Matellan, C and Rice, A and Lee, DA and Thorpe, S and Del, Rio Hernandez A},
doi = {10.3389/fcell.2020.592628},
journal = {Frontiers in Cell and Developmental Biology},
title = {G protein-coupled estrogen receptor regulates actin cytoskeleton dynamics to impair cell polarization},
url = {http://dx.doi.org/10.3389/fcell.2020.592628},
volume = {8},
year = {2020}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Mechanical forces regulate cell functions through multiple pathways. G protein-coupled estrogen receptor (GPER) is a seven-transmembrane receptor that is ubiquitously expressed across tissues and mediates the acute cellular response to estrogens. Here, we demonstrate an unidentified role of GPER as a cellular mechanoregulator. G protein-coupled estrogen receptor signaling controls the assembly of stress fibers, the dynamics of the associated focal adhesions, and cell polarization via RhoA GTPase (RhoA). G protein-coupled estrogen receptor activation inhibits F-actin polymerization and subsequently triggers a negative feedback that transcriptionally suppresses the expression of monomeric G-actin. Given the broad expression of GPER and the range of cytoskeletal changes modulated by this receptor, our findings position GPER as a key player in mechanotransduction.
AU - Lachowski,D
AU - Cortes,Lopez J
AU - Matellan,C
AU - Rice,A
AU - Lee,DA
AU - Thorpe,S
AU - Del,Rio Hernandez A
DO - 10.3389/fcell.2020.592628
PY - 2020///
SN - 2296-634X
TI - G protein-coupled estrogen receptor regulates actin cytoskeleton dynamics to impair cell polarization
T2 - Frontiers in Cell and Developmental Biology
UR - http://dx.doi.org/10.3389/fcell.2020.592628
UR - http://hdl.handle.net/10044/1/83907
VL - 8
ER -