◀ Back to MOK
MOK — RAC1
Text-mined interactions from Literome
Bassi et al., J Neurooncol 2008
(Brain Neoplasms...) :
Moreover, in a wounding model, it induced a significant increase in cell migration, and
RAGE dependent activation of
Rac1 was crucial in giving the tumour cells a motile phenotype
Hudson et al., J Biol Chem 2008
:
Down-regulation of Dia-1 expression by RNA interference blocks
RAGE mediated
activation of
Rac-1 and Cdc42 and, in parallel, RAGE ligand stimulated cellular migration
Bianchi et al., J Biol Chem 2011
(Encephalitis) :
We show here that high S100B stimulates murine microglia migration in Boyden chambers via
RAGE dependent activation of Src kinase, Ras, PI3K, MEK/ERK1/2, RhoA/ROCK, Rac1/JNK/AP-1,
Rac1/NF-?B , and, to a lesser extent, p38 MAPK ... The
S100B/RAGE dependent activation of diaphanous-1/Rac1/JNK/AP-1,
Ras/Rac1/NF-?B and Src/Ras/PI3K/RhoA/diaphanous-1 results in the up-regulation of expression of the chemokines, CCL3, CCL5, and CXCL12, whose release and activity are required for S100B to stimulate microglia migration