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JUN — POLDIP2

Text-mined interactions from Literome

Harada et al., Jpn J Pharmacol 1999 : These results suggest that activation of c-Jun by p38 and/or JNK mediates the activation of caspase in the low KCl induced apoptosis in cerebellar granule neurons
Munshi et al., J Biol Chem 1999 (Sarcoma, Kaposi) : KSHV encodes a G protein coupled receptor ( GPCR ) that acts as an oncogene and constitutively activates two protein kinases, c-Jun amino-terminal kinase (JNK)/stress activated protein kinase ( SAPK ) and p38 mitogen activated protein kinase
Chen et al., Mol Carcinog 2000 : In the present study, we further examined the role of p38 in UVB induced AP-1 activation ... These results suggested, for the first time, that activation of p38 is required for UVB induced AP-1 activation in human keratinocytes
Oh et al., J Biol Chem 2001 : This Lf-induced AP-1 DNA binding activity was reduced by a p38 MAPK inhibitor
Onodera et al., J Biol Chem 2002 : Consistent with these results, MIF stimulated phosphorylation of tyrosine, autophosphorylation of Src, activation of Ras, activation of extracellular signal regulated kinases ( ERK ) 1/2, a MAPK, but not c-Jun N-terminal kinase or p38 , and phosphorylation of c-Jun
Kolfschoten et al., Biochem Pharmacol 2002 (Ovarian Neoplasms) : The mitogen activated protein kinase pathway ( JNKs/SAPKs or c-Jun N-terminal kinases/stress activated protein kinases, JNK1/2 ; extracellular response kinase, ERK1/2 ; p38 ) did not seem to be directly involved in Bcl-2 phosphorylation or apoptosis
Heijink et al., Immunology 2002 : This is not the case for the short-term IL-6 effect on IL-5 secretion, where the p38 mitogen activated protein kinase dependent induction of activator protein-1 DNA binding activity is involved, independent of signal transducer and activator of transcription 3 phosphorylation
Mori et al., J Gen Virol 2003 : Differential activation of the c-Jun N-terminal kinase/stress activated protein kinase and p38 mitogen activated protein kinase signal transduction pathways in the mouse brain upon infection with neurovirulent influenza A virus
Tian et al., Blood 2005 (Lymphoma, B-Cell) : Induction of Bcl10 activity caused rapid activation of nuclear factor-kappaB (NF-kappaB) and c-Jun N-terminal kinase (JNK) , but not activation of extracellular signal regulated kinase ( ERK ) or p38 mitogen activated protein ( MAP ) kinases
Oyama et al., J Periodontal Res 2007 : Roxithromycin significantly inhibited TNF-alpha induced c-Jun N-terminal kinase activation ( JNP ) and marginally inhibited extracellular signal regulated kinase ( ERK ) 1/2 activation, but not p38 mitogen activated protein kinase activation
Qi et al., J Biol Chem 2007 (Breast Neoplasms) : Analyses of MAPK kinase 6 ( MKK6 ) -p38 fusion proteins showed that constitutively active p38alpha ( MKK6-p38alpha ) and p38gamma ( MKK6-p38gamma ) stimulates and inhibits c-Jun phosphorylation respectively, leading to a distinct AP-1 regulation ... Analyses of MAPK kinase 6 ( MKK6 ) -p38 fusion proteins showed that constitutively active p38alpha ( MKK6-p38alpha ) and p38gamma ( MKK6-p38gamma ) stimulates and inhibits c-Jun phosphorylation respectively, leading to a distinct AP-1 regulation ... Mechanistic analyses show that p38alpha requires c-Jun activation to deplete p38gamma proteins by ubiquitin-proteasome pathways
Shim et al., Planta Med 2008 (MAP Kinase Signaling System) : Moreover, inhibition of ERK, JNK and p38 by panduratin A resulted in decreased c-Fos expression and c-Jun phosphorylation induced by UV, which led to inhibition of activator protein-1 (AP-1) DNA binding activity
Brown et al., J Endocrinol 2009 (Disease Models, Animal...) : T supplementation not only triggered p38 mitogen activated protein kinase ( MAPK ) activation but also concurrently inhibited c-Jun NH ( 2 ) -terminal kinase ( JNK ) activation within 2 weeks of treatment
Persichini et al., Neurosci Lett 2010 : Moreover, we have observed that IL-1ß regulates the expression of Cp and Fpn genes through ( i ) p38 MAPK mediated activation of C/EBP transcription factor, ( ii ) ERK1/2-, JNK1- and partially p38 MAPK dependent activation of AP-1 , and through ( iii ) activation of NF-?B partially mediated by p38 MAPK
Huang et al., Toxicol Appl Pharmacol 2013 (Inflammation) : Moreover, LTA induced increases of ?B-DNA and AP-1-DNA binding activity were inhibited by p38 , JNK, and PI3-kinase inhibitors
Ganju et al., Blood 1998 (Lymphoma) : Macrophage inflammatory protein 1 beta ( MIP 1 beta ) binding to its cognate receptor CCR5 resulted in activation of the related adhesion focal tyrosine kinase ( RAFTK ), with subsequent activation of the cytoskeletal protein paxillin and the down-stream transcriptional activators, c-Jun N-terminal kinase (JNK)/stress activated protein kinase ( SAPK ) and p38 mitogen activated protein ( MAP ) kinase