Gene interactions and pathways from curated databases and text-mining

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MAPK1 — PTK2

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

Zubiaur et al., J Biol Chem 1999 : However, in cells expressing chimerical CD25-zeta or CD25-epsilon receptors or in a TCR-beta- Jurkat T cell line, CD38 ligation did not result in tyrosine phosphorylation of the chimeric receptors, or CD3 subunits, or protein-tyrosine kinase or mitogen activated protein kinase activation
Aoki et al., Stroke 2000 (Calcium Signaling...) : Extracellular ATP produced [ Ca ( 2+ ) ] ( i ) elevation and MAPK phosphorylation in RBASMCs, and the effect was regulated by PTK
Yu et al., Am J Physiol Gastrointest Liver Physiol 2000 : Caco-2 motility was inhibited by transfection of FRNK ( the COOH-terminal region of FAK ) and PD-98059, a mitogen activated protein kinase-ERK kinase inhibitor , but not by SB-203580, a p38 inhibitor, suggesting that FAK and ERK modulate Caco-2 migration
Robinson et al., Eur J Pharmacol 2001 : The broad range protein tyrosine kinase inhibitors genistein and tyrphostin A47 ( alpha-cyano- ( 3,4-dihydroxy ) thiocinnamide ) did not block adenosine A(1) receptor stimulation of p42/p44 MAPK
Xiao et al., Clin Exp Immunol 2001 : Secretion of IL-8 by C1q-IC stimulated HUVEC was completely blocked by the PTK inhibitor, genistein or the MAPK inhibitor , UO126
Lu et al., Chin Med J (Engl) 2000 (Arthritis, Rheumatoid) : Role of protein tyrosine kinase in IL-1 beta induced activation of mitogen activated protein kinase in fibroblast-like synoviocytes of rheumatoid arthritis
Secondo et al., J Neurochem 2003 : The receptor and non-receptor protein tyrosine kinase ( PTK ) inhibitors, genistein ( 10 microm ), the Src-specific tyrosine kinase inhibitor PP2 ( 100 microm ), the MAPK inhibitor PD 098059 ( 50 nm ) and the two PI3'-K inhibitors, wortmannin ( 300 nm ) and LY-294002 ( 25 microm ) prevented both basal and exogenous PRL induced expression of nNOSalpha and nNOSbeta isoforms
Ogasawara et al., Int J Hematol 2003 (Leukemia, B-Cell...) : We found that Lyn protein tyrosine kinase was constitutively phosphorylated on tyrosine, and that ERK and p38 MAPK were constitutively active in all cases of the B-cell tumor
Xenaki et al., Cell Signal 2004 : Activation of Bcr-Abl PTK does not phosphorylate or activate either ERK-1/2 or JAK-2/STAT-5b, suggesting that these signal transduction pathways are not involved in Abl PTK mediated suppression of apoptosis in FDCP-Mix cells
Zubkov et al., J Cardiovasc Pharmacol 2004 : The following results were observed : ( 1 ) endothelin-1 produced phosphorylation of MAPK and RhoA and contraction by activation of endothelin-A but not endothelin-B receptors ; ( 2 ) MAPK inhibitors, PD 98059 and U0126, PTK inhibitor , genistein, Src kinase inhibitor, damnacanthal, and Janus tyrosine kinase ( JAK2 ) inhibitor, AG-490, abolished endothelin-1 induced contraction and MAPK immunoreactivity ; ( 3 ) PTK inhibitor, staurosporine, and phosphatidylinositol 3-kinase (PI- 3K) inhibitor wortmannin abolished endothelin-1 induced contraction but not MAPK immunoreactivity ; ( 4 ) Rho-kinase inhibitor, Y-27632, reduced endothelin-1 induced contraction ; ( 5 ) PI-3K inhibitor, wortmannin, but not PKC and PTK inhibitors, reduced endothelin-1 induced RhoA activation ; ( 6 ) endothelin-1 increased the level of myosin light chain ( MLC ) phosphorylation, and Rho-kinase inhibitor, Y-27632, reduced the effect of endothelin- 1 on MLC phosphorylation
Hess et al., Cancer Res 2005 (Melanoma...) : Moreover, we found that FRNK expression resulted in a down-regulation of Erk1/2 phosphorylation resulting in a decrease in urokinase activity
Park et al., World J Gastroenterol 2006 : Bombesin induced circular muscle cell contraction in cat esophagus is madiated via a PKC or a PTK dependent pathway or p44/p42 MAPK pathway
Babilonia et al., J Am Soc Nephrol 2006 : This study explored the role of mitogen activated protein kinase ( MAPK ) in mediating the effect of superoxide anions on PTK expression and ROMK ( Kir 1.1 ) channel activity
Hisaoka et al., Brain Res 2008 (Glioma) : The amitriptyline induced phosphorylation of CREB was completely blocked by U0126 [ a mitogen activated protein ( MAP) kinase kinase 1 inhibitor ] and genistein ( a PTK inhibitor ), but not by inhibitors of protein kinase A, p38 MAP kinase, or Ca ( 2+ ) /calmodulin dependent kinase
Ding et al., J Biol Chem 2008 (Disease Models, Animal...) : FRNK overexpression blocks TGF-beta1 induced ERK or p38 MAPK activation in the presence, and surprisingly, in the absence of FAK
Rao et al., J Biol Chem 1995 : In contrast, however, inhibition of protein-tyrosine kinase activity had no effect on thrombin activation of MAPK
Hawes et al., J Biol Chem 1995 : The Gi-coupled alpha 2A adrenergic receptor (AR) stimulates MAPK activation which is blocked by expression of beta ARKct, RasN17, or N delta Raf, or by PTK inhibitors, but unaffected by cellular depletion of PKC
Kawauchi et al., Mol Immunol 1996 : However, when signaling through the BCR was bypassed by direct stimulation of the Raf1/MEK/MAPK module via a rise in [ Ca2+ ] i and phorbol ester induced PKC activation, the phosphotransferase activities of Raf1, MEK and MAPK were still regulated in a PTK dependent manner that was also partially sensitive to the PTPase inhibitor PAO
Eguchi et al., J Biol Chem 1998 : We have recently reported that angiotensin II (Ang II) induced mitogen activated protein kinase ( MAPK ) activation is mainly mediated by Ca2+ dependent activation of a protein tyrosine kinase through Gq-coupled Ang II type 1 receptor in cultured rat vascular smooth muscle cells ( VSMC )
Iwasaki et al., Endocrinology 1998 : AM-induced MAPK activation and cell proliferation were completely blocked by protein tyrosine kinase inhibitors ( genistein and ST638 ) ... These data suggest that in addition to its vasodilatory effect through the cAMP dependent pathway, AM exerts its mitogenic activity via protein tyrosine kinase mediated MAPK activation in quiescent rat VSMC