Focal adhesion kinase-dependent activation of the early endocytic protein Rab5 is associated with cell migration.
PTK2 protein tyrosine kinase 2 (PTK2)
Rab5
cell migration
early endosome
endocytic trafficking
focal adhesion
focal adhesion kinase (FAK)
integrin complex
metastasis
small GTPase
tumor
Journal
The Journal of biological chemistry
ISSN: 1083-351X
Titre abrégé: J Biol Chem
Pays: United States
ID NLM: 2985121R
Informations de publication
Date de publication:
23 08 2019
23 08 2019
Historique:
received:
01
04
2019
revised:
17
06
2019
pubmed:
12
7
2019
medline:
31
3
2020
entrez:
12
7
2019
Statut:
ppublish
Résumé
Focal adhesion kinase (FAK) is a central regulator of integrin-dependent cell adhesion and migration and has recently been shown to co-localize with endosomal proteins. The early endocytic protein Rab5 controls integrin trafficking, focal adhesion disassembly, and cell migration and has been shown to be activated upon integrin engagement by mechanisms that remain unclear. Because FAK is a critical regulator of integrin-dependent signaling and Rab5 recapitulates FAK-mediated effects, we evaluated the possibility that FAK activates Rab5 and contributes to cell migration. Pulldown assays revealed that Rab5-GTP levels are decreased upon treatment with a pharmacological inhibitor of FAK, PF562,271, in resting A549 cells. These events were associated with decreased peripheral Rab5 puncta and a reduced number of early endosome antigen 1 (EEA1)-positive early endosomes. Accordingly, as indicated by FAK inhibition experiments and in FAK-null fibroblasts, adhesion-induced FAK activity increased Rab5-GTP levels. In fact, expression of WT FAK and FAK/Y180A/M183A (open conformation), but not FAK/Arg
Identifiants
pubmed: 31292193
pii: S0021-9258(20)30315-X
doi: 10.1074/jbc.RA119.008667
pmc: PMC6709621
doi:
Substances chimiques
Focal Adhesion Kinase 1
EC 2.7.10.2
PTK2 protein, human
EC 2.7.10.2
RAB5C protein, human
EC 3.6.1.-
rab5 GTP-Binding Proteins
EC 3.6.5.2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
12836-12845Informations de copyright
© 2019 Arriagada et al.
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