Gene interactions and pathways from curated databases and text-mining

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CRK — GRAP2

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Aghdasi et al., Proc Natl Acad Sci U S A 2001 : By contrast, activated phosphorylated p38 is markedly augmented in FKBP12 ( -/- ) cells and the p21 up-regulation is prevented by an inhibitor of p38
Lee et al., Mol Cell Biol 2003 (MAP Kinase Signaling System) : In transfection studies, RIP1 and TRAF2 stimulate p38 MAP kinase activation, and dominant negative forms of RIP1 and TRAF2 inhibit TNF-alpha induced p38 MAP kinase activation
Salvador et al., Nat Immunol 2005 (MAP Kinase Signaling System) : TCR activation of p38 lacking Tyr323 was diminished, and blocking of p38 activity prevented p38 dual phosphorylation in normal T cells but not in B cells
Supinski et al., Am J Respir Cell Mol Biol 2010 (Sepsis) : This study determined whether : ( 1 ) endotoxin administration elicits p38 activation in the diaphragm ; ( 2 ) cytokines activate p38 in isolated muscle cells ; ( 3 ) activation of p38 is accompanied by caspase 8 activation ; ( 4 ) inhibition of p38 prevents caspase 8 activation and ; ( 5 ) inhibition of p38 prevents diaphragm dysfunction in endotoxin treated animals
Rakkestad et al., Inhal Toxicol 2010 (Inflammation) : MEHP also induced phosphorylation of MAPK p38 , while the p38 inhibitor SB 202190 reduced MEHP induced TNF-alpha, suggesting a p38 dependent cytokine production
He et al., Sichuan Da Xue Xue Bao Yi Xue Ban 2010 : Compared with the nomoxia control, hypoxia enhanced the proliferation of MRC-5 and the expressions of pro-collal, p-p38 and p-AKT ( P < 0.05 ). Curcumin inhibited the hypoxia induced proliferation of MRC and the expression of pro-collal and p-p38 ( P < 0.05 ), but not the expression of p-AKT ( P > 0.05 )
Cai et al., Fish Shellfish Immunol 2011 (DNA Virus Infections...) : The tissue distribution patterns of Ec-p38a, p38b and p38ß were different, and Ec-p38ß was up-regulated most obviously in head kidney after Singapore grouper iridovirus ( SGIV ) infection