◀ Back to MAPK8

ATF6 — MAPK8

Text-mined interactions from Literome

Mielke et al., Neuroscience 1999 (Seizures) : Our results demonstrate that activation of c-Jun N-terminal kinase 1 , phosphorylation of c-Jun and selective occupation of the c-jun promoter by activating transcription factor-2 or c-Jun are part of the neuronal response following excitotoxicity that is considered as the mechanism for neuronal apoptosis in vivo
Yosimichi et al., Eur J Biochem 2001 : These inhibitors of MAPKK and MAPK suppressed phosphorylation of ets-like gene-1 (Elk-1) and nuclear activating transcription factor-2 ( Atf-2 ) induced by CTGF/Hcs24 in a dose dependent manner, respectively
Faour et al., J Biol Chem 2005 (Arthritis, Rheumatoid) : Initial studies confirmed that PGE2 induces egr-1 mRNA expression and protein synthesis by restricted SAPK2/p38 MAPK dependent activating transcription factor-2 ( ATF-2) dimer transactivation of the egr-1 promoter as judged by studies using wild-type ( WT ) and deletion mutant egr-1 promoter constructs, Northern and Western blotting, and standard and supershift electrophoretic mobility shift analyses
Hisatsune et al., J Immunol 2008 : Molecular characterization of Helicobacter pylori VacA induction of IL-8 in U937 cells reveals a prominent role for p38MAPK in activating transcription factor-2 , cAMP response element binding protein, and NF-kappaB activation
Cho et al., Mol Endocrinol 2009 : The inhibition of MAPK dependent activating transcription factor 2/c-Jun phosphorylation by GR in COX-2 repression was a result of MAPK phosphatase-1 (MKP-1) induction