◀ Back to JUN

IFI44 — JUN

Text-mined interactions from Literome

Gao et al., Hepatology 1999 : HGF alone induced moderate levels of c-Jun-N-terminal kinase (JNK) and p44/p42 mitogen activated protein kinase ( MAPK ), resulting in moderate levels of AP-1-DNA binding activity
Mendes et al., Nitric Oxide 2002 : Finally, the p42/44MAPK inhibitor, PD 98059, prevented IL-1 induced AP-1 activation in a concentration that did not inhibit iNOS expression
Darmoul et al., Am J Pathol 2003 (Colonic Neoplasms) : This effect was reversed by the MEK inhibitor PD98059 in consonance with the ability of thrombin or AP1 to induce phosphorylation of p42/p44 extracellular regulated protein kinases
Tu et al., Cardiovasc Toxicol 2003 : Distinct roles of p42/p44 ( ERK ) and p38 MAPK in oxidant induced AP-1 activation and cardiomyocyte hypertrophy
Fradette et al., Curr Drug Metab 2004 (Anoxia...) : The up-regulation of CYP3A6 implies a PTK- and p42/44MAPK dependent stabilization/activation, nuclear translocation of HIF-1 and AP-1 , binding to CYP3A6 promoter, and transactivation of the gene to induce CYP3A6 expression
Chen et al., Immunol Lett 2008 (Genetic Predisposition to Disease...) : Consistent with the activation of JNK/c-Jun pathway by T cell stimulation, forced expression of c-Jun in 2B4 T cells and in mouse embryonic fibroblasts ( MEFs ) also up-regulated the Ifi202 expression
Bisping et al., Clin Cancer Res 2009 (Multiple Myeloma...) : RTKI, bortezomib, and dexamethasone were active as single agents in t ( 4 ; 14 ) + MM. RTK inhibition triggered complementary proapoptotic pathways ( e.g., decrease of Mcl-1, down-regulation of p44/42 mitogen activated protein kinase, and activation of proapoptotic stress activated protein/c-Jun NH ( 2 ) -terminal kinases )
Li et al., ASN neuro 2012 (Demyelinating Diseases) : The activation of p42/p44 MAPK ( mitogen activated protein kinase ) and induction of the transcription factor c-Jun serve as negative regulators of myelination
Englaro et al., J Biol Chem 1995 (Melanoma, Experimental) : In an attempt to connect these molecular events to the control of tyrosinase expression that appears to be the pivotal point of melanogenesis regulation, we hypothesized that following its activation by cAMP, p44mapk activates AP-1