The cleaved FAS ligand activates the Na+/H+ exchanger NHE1 through Akt/ROCK1 to stimulate cell motility View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-06-15

AUTHORS

Michael Monet, Mallorie Poët, Sébastien Tauzin, Amélie Fouqué, Auréa Cophignon, Dominique Lagadic-Gossmann, Pierre Vacher, Patrick Legembre, Laurent Counillon

ABSTRACT

Transmembrane CD95L (Fas ligand) can be cleaved to release a promigratory soluble ligand, cl-CD95L, which can contribute to chronic inflammation and cancer cell dissemination. The motility signaling pathway elicited by cl-CD95L remains poorly defined. Here, we show that in the presence of cl-CD95L, CD95 activates the Akt and RhoA signaling pathways, which together orchestrate an allosteric activation of the Na(+)/H(+) exchanger NHE1. Pharmacologic inhibition of Akt or ROCK1 independently blocks the cl-CD95L-induced migration. Confirming these pharmacologic data, disruption of the Akt and ROCK1 phosphorylation sites on NHE1 decreases cell migration in cells exposed to cl-CD95L. Together, these findings demonstrate that NHE1 is a novel molecular actor in the CD95 signaling pathway that drives the cl-CD95L-induced cell migration through both the Akt and RhoA signaling pathways. More... »

PAGES

28008

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep28008

DOI

http://dx.doi.org/10.1038/srep28008

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1030131515

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27302366


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