◀ Back to MAPK14
GFAP — MAPK14
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Aberg et al., Mol Cell Neurosci 2001
(MAP Kinase Signaling System) :
Activation of the mitogen activated protein kinase (
MAPK ) signaling pathway
induced only a transient increase in
glial fibrillary acidic protein (GFAP) expression, and inhibition of this signaling pathway did not block the induction by CNTF of glial differentiation in progenitor cells
Tang et al., Hum Mol Genet 2008
(Alexander Disease) :
The
activation of p38
MAPK by
GFAP accumulation is in part responsible for the down-regulation of phosphorylated-mTOR and the subsequent activation of autophagy
Romão et al., J Neurochem 2008
:
MAPK ( PD98059 ) and PI3K ( LY294002 ) inhibitors fully
prevented activation of
GFAP gene promoter by all treatments
Liu et al., Biomaterials 2013
(Brain Ischemia) :
Furthermore, CBSA-PEG-TIIA-NPs significantly decreased the mRNA expressions of iNOS and
p38MAPK , upregulated PPAR? expression, and
inhibited the protein levels of iNOS,
GFAP and p38MAPK phosphorylation