Imperial College London
Alternate

ProfessorVaniaBraga

Faculty of Medicine, National Heart & Lung Institute

Professor of Cellular Signalling
 
 
 
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Contact

 

+44 (0)20 7594 3233v.braga

 
 
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Location

 

Office no. 105Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Erasmus:2015:10.1016/j.cellsig.2015.04.014,
author = {Erasmus, JC and Welsh, NJ and Braga, VMM},
doi = {10.1016/j.cellsig.2015.04.014},
journal = {Cellular Signalling},
pages = {1905--1913},
title = {Cooperation of distinct Rac-dependent pathways to stabilise E-cadherin adhesion},
url = {http://dx.doi.org/10.1016/j.cellsig.2015.04.014},
volume = {27},
year = {2015}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - The precise mechanisms via which Rac1 is activated by cadherin junctions are not fully known. In keratinocytesRac1 activation by cadherin junctions requires EGFR signalling, but how EGFR does so is unclear. To addresswhich activator could mediate E-cadherin signalling to Rac1, we investigated EGFR and two Rac1 GEFs, SOS1and DOCK180. EGFR RNAi prevented junction-induced Rac1 activation and led to fragmented localization ofE-cadherin at cadherin contacts. In contrast, depletion of another EGFR family member, ErbB3, did not interferewith either process. DOCK180 RNAi, but not SOS1, prevented E-cadherin-induced Rac1 activation. However, in astrong divergence from EGFR RNAi phenotype, DOCK180 depletion did not perturb actin recruitment orcadherin localisation at junctions. Rather, reduced DOCK180 levels impaired the resistance to mechanicalstress of pre-formed cell aggregates. Thus, within the same cell type, EGFR and DOCK180 regulate Rac1activation by newly-formed contacts, but control separate cellular events that cooperate to stabilisejunctions
AU  - Erasmus,JC
AU  - Welsh,NJ
AU  - Braga,VMM
DO  - 10.1016/j.cellsig.2015.04.014
EP  - 1913
PY  - 2015///
SN  - 1873-3913
SP  - 1905
TI  - Cooperation of distinct Rac-dependent pathways to stabilise E-cadherin adhesion
T2  - Cellular Signalling
UR  - http://dx.doi.org/10.1016/j.cellsig.2015.04.014
UR  - http://hdl.handle.net/10044/1/26250
VL  - 27
ER  -
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