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GRAP2 — JUN

Text-mined interactions from Literome

Itaya et al., Thromb Haemost 2001 : These results suggest that the LPS induced VEGF expression depends on the p38 mediated expression of c-Jun , which constitutes the AP-1 complex and binds to the AP-1 site in the VEGF promoter
Linseman et al., J Biol Chem 2001 : However, pyridyl imidazole inhibitors of JNK/p38 attenuated c-Jun phosphorylation
Yu et al., Cancer Res 2001 (Breast Neoplasms...) : Expression of dominant negative mutants of ERK1, MAPK/ERK activator-1, or JNK1 but not p38 blocked phosphorylation of the substrate glutathione S-transferase-c-Jun and inhibited VES induced apoptosis
Granet et al., Cell Signal 2002 : Downregulation of protein kinase C ( PKC ) and COX1/2 or inhibition of ERK1/2, p38 ( MAPK ) or src kinases had no major effect on AP-1 mRNA expression in the Flexcell
Silvers et al., Neoplasia (New York, N.Y.) 2003 (Skin Neoplasms) : To examine the role of p38 and JNK MAPKs in UVA induced AP-1 and c-fos transactivations, the selective pharmacologic MAPK inhibitors, SB202190 ( p38 inhibitor ) and SP600125 ( JNK inhibitor ), were used to independently treat stably transfected HaCaT cells in luciferase reporter assays
Cameron et al., Br J Pharmacol 2003 : 2. Both VT1 and VT2 stimulated a weak, transient increase in c-Jun-N-terminal kinase (JNK) activity and a strong activation of both p38 mitogen activated protein kinase ( MAP kinase ) and extracellular regulated kinase (ERK) activity in human monocytes, which was sustained in the case of p38 MAP kinase
Park et al., Biochem Biophys Res Commun 2004 (MAP Kinase Signaling System) : Taken together, these results demonstrate that naturally occurring furosin has an inhibitory activity on both osteoclast differentiation and function through mechanisms involving inhibition of the RANKL induced p38MAPK and JNK/AP-1 activation as well as actin ring formation
Muthumani et al., Blood 2005 : Loss-of-function experiments through dominant negative p38 isoform, p38 siRNA, and chemical inhibitors of p38 activation suggest that p38 is necessary for Nef induced activator protein-1 (AP-1) activation, as inhibition leads to an attenuation of AP-1 dependent transcription
Kumasawa et al., Eur J Pharmacol 2005 : We examined the effect LTD ( 4 ) on AP-1 activation in human airway smooth muscle cells and analyzed a role of apoptosis signal regulating kinase1 ( ASK1 ), an upstream kinase kinase of c-Jun-NH ( 2 ) -terminal kinase ( JNK ) and p38 mitogen activated protein kinase ( MAPK ) in LTD ( 4 ) -induced AP-1 activation to clarify the signaling molecule regulating AP-1 activation
Kobayashi et al., Exp Dermatol 2005 : We show ( i ) UV induced up-regulation of TNF-alpha mRNA and protein expression in keratinocytes ; ( ii ) cells treated with KTI before UV irradiation showed a significantly lower accumulation of TNF-alpha protein in a dose dependent manner and a reduced UV-induced up-regulation of TNF-alpha mRNA expression ; ( iii ) KTI inhibited the induction of TNF-alpha target molecules interleukin-1beta (IL-1beta) and IL-6 proteins ; ( iv ) UV irradiation transiently activated c-Jun N-terminal kinase (JNK) and Akt signaling but only weakly activated extracellular signal regulated kinase ( ERK ) and p38 ; ( v ) KTI specifically inhibited UV-induced activation of ERK, JNK, and p38 , but not Akt ; ( vi ) treatment of cells with SP600125, a pharmacological inhibitor of JNK, predominantly suppressed UV-induced up-regulation of TNF-alpha expression ; and ( vii ) KTI did not enhance suppression of UV-induced JNK phosphorylation by SP600125
Dziembowska et al., Biochem Biophys Res Commun 2007 (Glioblastoma) : In parallel, a selective activation of p38 MAPK, and phosphorylation of its substrates : ATF2 and c-Jun proteins were followed by a transient activation of AP-1 transcription factor
Humar et al., Int J Biochem Cell Biol 2007 : This demonstrates that the protein kinase p38 plays a unique and non-redundant role in posttranslational c-Jun regulation ... Different cell lines show p38 dependent c-Jun phosphorylation upon phorbol ester induction but there is evidence that the simian virus 40 large T-antigen may interfere with this pathway
Muniyappa et al., Cell Signal 2008 (MAP Kinase Signaling System) : Activation of c-Jun N-terminal kinase (JNK) by widely used specific p38 MAPK inhibitors SB202190 and SB203580 : a MLK-3-MKK7 dependent mechanism
Dolinay et al., PloS one 2008 (Edema...) : We characterize the role of p38 mitogen activated protein kinase/mitogen activated protein kinase kinase-3 and c-Jun-NH ( 2 ) -terminal kinase-1 in ventilator induced lung injury and investigate novel independent mechanisms contributing to lung injury during mechanical ventilation
Ding et al., Stem Cells Dev 2008 : Although p38MAPK ( mitogen activated protein kinase ), extracellular signal regulated kinase ( ERK ), and c-Jun N-terminal protein kinase (JNK) were spontaneously activated in early differentiation, only the phosphorylation of p38MAPK was enhanced and prolonged when icariin was present, whereas both ERK and JNK showed no response to icariin treatment
Kino et al., Science signaling 2009 (Dehydration) : This process required the activity of p38 mitogen activated protein kinase ( MAPK ) and NFAT5 and involved a physical interaction between Brx and c-Jun N-terminal kinase (JNK) interacting protein 4 ( JIP4 ), a scaffold molecule specific to activation of the p38 MAPK cascade
Chang et al., J Neurochem 2010 (Alzheimer Disease) : Importantly, Cdk5 mediated p38 activation increases c-Jun expression, thereby revealing a mechanistic link between deregulated Cdk5 and c-Jun level in AD brains
Ibrahim et al., Diabetes 2011 (Diabetes Mellitus, Experimental...) : The results showed that formation of reactive oxygen species and subsequent activation of ERK and P38 , but not Jun NH2-terminal kinase, are molecular events underpinning retinal microglial TNF-a release during AGA treatment
Nito et al., J Neurotrauma 2012 (Hypoxia-Ischemia, Brain...) : Treatment with SB203580, a selective p38 MAPK inhibitor, or SP600125, a selective c-Jun N-terminal kinase inhibitor , significantly attenuated the return of AQP4 to its normal level, and SB203580, but not SP600125, significantly decreased cell death
Torsney et al., Arterioscler Thromb Vasc Biol 2012 (Aortic Aneurysm, Abdominal...) : We found that HDLs reduced extracellular signal related kinases 1/2 activation in the suprarenal segment, while having no effect on p38 mitogen associated protein kinase activation in any aortic segment and inhibiting c-Jun N-terminal kinase activation in all aortic segments
Johnston et al., J Diabetes Complications 2013 (Diabetes Mellitus, Type 1...) : To examine the role of placental protein tyrosine nitration and p38-Mitogen Activated Protein Kinase a ( p38-MAPKa ), Extra Cellular-Signal Regulated Kinase ( ERK ) and c-Jun NH2-Terminal Kinase (JNK) activity, in the pathogenesis of type 1 diabetic pre-eclampsia, and the putative modulation of these indices by maternal vitamin C and E supplementation