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CRK — EPHB2

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

Studies that report less than 10 interactions are marked with *

• IRef Biogrid Interaction: CRK — EPHB2 (direct interaction, pull down) Zisch et al., Oncogene 2000

Text-mined interactions from Literome

Blaukat et al., J Biol Chem 1999 : Grb2 with a deleted carboxyl-terminal Src homology 3 domain partially blocked Pyk2 induced ERK and JNK pathways, whereas expression of dominant interfering mutants of p130Cas or Crk specifically inhibited JNK but not ERK activation by Pyk2
Zimmermann et al., J Biol Chem 2001 (MAP Kinase Signaling System) : The results indicate that ERK3 expression is a consequence of p38 pathway activation and most probably represents an intracellular defense or rescue mechanism against cell stress and damage induced by proteasome inhibition
Choi et al., Cancer Res 2001 (Glioblastoma...) : Herein, we demonstrate that : ( a ) stimulation with agonistic anti-Fas monoclonal antibody CH-11 and human recombinant soluble Fas ligand induces expression of the CC chemokine MCP-1 and the CXC chemokine interleukin-8 by human glioma cell lines at the mRNA and protein levels in a dose- and time dependent manner ; ( b ) selective pharmacological inhibitors of MEK1 ( U0126 and PD98059 ) and p38 mitogen activated protein kinase ( MAPK ) ( SB202190 ) suppress Fas mediated chemokine expression in a dose dependent manner ; ( c ) Fas ligation on human glioma cells leads to activation of both extracellular signal regulated kinases ERK1/ERK2 and p38 MAPK ; and ( d ) GBM samples express higher levels of Fas compared with normal control brain, which correlates with increased interleukin 8 expression
Chen et al., J Biol Chem 2001 (MAP Kinase Signaling System) : We found that the catalytic activity of MKP-2 was enhanced dramatically by ERK and JNK but was affected only minimally by p38
Miyazaki et al., Ann Hematol 2001 : These results indicate that activation of extracellular-signal regulated kinase ( ERK ) is required for TPO induced megakaryocyte differentiation and that p38 is required for TPO induced erythroid differentiation
Singh et al., Carcinogenesis 2002 (Skin Neoplasms) : Together, the data suggest that an inhibition of ERK1/2 activation and an increased activation of JNK1/2 and p38 by silibinin could be possible underlying molecular events involved in inhibition of proliferation and induction of apoptosis in A431 cells
Park et al., Hepatology 2002 (Carcinoma, Hepatocellular...) : Inhibition of ERK activity enhanced TGF-beta1 induced p38 and JNK activation
Nagashima et al., Mol Biol Cell 2002 : We especially focused on the role of Crk adaptor protein in EphB mediated signaling
Aguirre-Ghiso et al., Cancer Res 2003 (Breast Neoplasms...) : Modulation of ERK/p38 activity ratio by multiple pharmacological and genetic interventions confirms that high ERK/p38 ratio favors tumor growth, whereas high p38/ERK ratio induces tumor growth arrest ( dormancy ) in vivo and that ERK is negatively regulated by p38
Maroni et al., Mol Cell Endocrinol 2003 : ERK1 , ERK2 and p38 MAP kinase phosphorylation significantly increased , even if the latter only in wild-type animals
Faisal et al., J Biol Chem 2004 : In a quest for molecules upstream of ShcA in this signaling, we found that CSR induced ShcA tyrosine phosphorylation, its association with Grb2, Erk activation, and uPA gene expression were all dependent on Rho kinase, p38 mitogen activated protein kinase, and Src
Williamson et al., J Biol Chem 2004 (Sarcoma, Ewing) : This hypothesis is supported by observations in the A673 cell line ; bFGF induced sustained activation of ERK and transient activation of p38 ( MAPK ), which was not associated with cell death
Chen et al., Life Sci 2005 : Furthermore, the A549 cells were pretreated with 50 microM PD98059, a specific inhibitor of the upstream regulator of ERK1/2 , or with the p38 kinase inhibitor 20 microM SB203580 or JNK inhibitor 20 microM SP600125 for 30 min, followed by 24 h of incubation with AE-BS, PD98059 can inhibit K8-Ser-73 hyperphosphorylation and prevented cell apoptosis which was induced by AE-BS significantly
Peng et al., Circulation 2005 (Cardiomyopathies) : NADH oxidase activation by LPS increased ERK1/2 and p38 phosphorylation, and inhibition of ERK1/2 and p38 phosphorylation blocked the effect of NADH oxidase on TNF-alpha expression
Kakisis et al., Int J Biochem Cell Biol 2005 : Pretreating the cells with SB202190, a specific inhibitor of p38 , resulted in an increase in basal phosphorylation of ERK1/2 and a subsequent increase in basal serine phosphorylation of STAT-3
Ren et al., J Neurochem 2005 : ERK1/2 but not JNK and p38 were activated by GTS-21, and the ERK phosphorylation inhibitors PD98059 and U0126 blocked protection
Hagiwara et al., Nephrol Dial Transplant 2006 (Diabetes Mellitus, Type 2...) : EPA and specific inhibitors of ERK1/2 , JNK and PI3K decreased levels of MCP-1 in MMCs. EPA suppressed phosphorylation of ERK1/2 and p38 in MMCs, and decreased p-ERK positive cells in glomeruli of KKAy/Ta mice
Jiang et al., J Ocul Pharmacol Ther 2006 : EGF induced cell migration in a dose dependent manner ; EGF induced EGFR phosphorylation and downstream activation of c-Jun N-terminal protein kinase (JNK), p38 MAP kinase ( p38 ) , extracellular signal regulated kinase ( ERK1/2 ) and AKT, were inhibited by PD153035 ( EGFR inhibitor ), JNKi ( JNK inhibitor ), SB203580 ( p38 inhibitor ), U0126 ( MEK/ERK inhibitor ), and LY294002 ( PI3K/AKT inhibitor ), respectively
Zanin-Zhorov et al., J Clin Invest 2006 : The enhancing effects of HSP60 costimulation on Tregs involved innate signaling via TLR2, led to activation of PKC, PI3K, and p38 , and were further enhanced by inhibition of ERK
Deleault et al., Mol Immunol 2008 (MAP Kinase Signaling System) : These data establish that TTP mediated TNF-alpha mRNA decay is inhibited by the combined activation of ERK and p38 and not by p38 activation alone
Park et al., FEBS Lett 2007 (Prostatic Neoplasms) : Under senescence inducing condition, decreased Erk phosphorylation was detected in caRhoA transfected cells and inactivation of Erk, but not p38 , prevented doxorubicin induced cell senescence
Bouchard et al., Apoptosis 2008 : Hence, beta1 integrin/Fak/Src signaling translates into integrated mediating functions of p38beta activation and regulation of Bcl-2 homologs by PI3-K/Akt-1 and MEK/Erk , consequently determining their requirement ( or not ) for survival
Ding et al., J Gastroenterol Hepatol 2008 (Helicobacter Infections...) : We also detected MAPK cross-talk in AGS cells : p38 and JNK inhibitors increased ERK activation
Kawahara et al., Int J Mol Med 2008 (Atherosclerosis...) : HMGB1 induced the activation of p38MAPK , ERK1/2 and Akt
Liu et al., J Cell Physiol 2009 (MAP Kinase Signaling System) : Activated ERK suppressed p38 MAPK activation and Fas/FasL protein expression
Cheng et al., Mol Cell Biochem 2009 : After administration of inhibitors including U0126 ( ERK1/2 inhibitor ), SB203580 ( p38 MAPK inhibitor ), SP600125 ( JNK1/2 inhibitor ), CsA ( calcineurin inhibitor ), and QNZ ( NFkappaB inhibitor ), the LPS upregulated expression and/or activity of uPA, MMP-2, and MMP-9 in H9c2 cardiomyoblasts are markedly inhibited only by ERK1/2 inhibitors, U0126
Hassan et al., Hepatology 2009 (Hepatitis C, Chronic...) : In addition, regulated expression of core protein in HepG2 or Huh7 cells was found to induce expression and activation of the transcription factor E2F1 and apoptosis signal regulating kinase 1 ( ASK1 ), activation of c-jun-N-terminal kinase ( JNK ) and p38 , and extracellular regulated kinase (ERK) , and transcription factors activator protein 1 (AP-1), activating transcription factor 2 ( ATF-2 ), cyclic adenosine monophosphate response element binding ( CREB ), E2F1, hypoxia inducing factor 1 alpha ( HIF-1alpha ), and specificity protein 1
Liu et al., Amino Acids 2010 : Preptin induced activation of ERK mitogen activated protein kinase ( MAPK ), but not p38 or JNK in human osteoblasts
Yao et al., Am J Chin Med 2009 (MAP Kinase Signaling System) : Moreover, magnolol attenuated the deactivation of ERK/MAPK ( extracellular signal regulated kinase/mitogen activated protein kinase ) and the enhanced activation of p38 , JNK ( c-Jun N-terminal kinase ) induced by H2O2
Kozono et al., Biochem Biophys Res Commun 2010 : CP55940 ( CB1/CB2 agonist ) induced phosphorylation of the extracellular regulated kinases (ERK) 1/2, p38 mitogen activated protein kinase ( p38MAPK ), and Akt in HGFs. Wound closure by CP55940 in an in-vitro scratch assay was significantly suppressed by inhibitors of MAP kinase kinase ( MEK ), p38MAPK , and phosphoinositol 3-kinase (PI3-K)
El-Bikai et al., Arthritis Res Ther 2010 (Osteoarthritis) : It inhibited a1ß1 integrin and Col II expression as well as ERK1/2 and NF-?B-p65 phosphorylation, but, in contrast, markedly elicited PGE2 release, COX-2 expression and p38 MAPK phosphorylation
Bros et al., Gene 2011 : Both Cacnb3 isoforms, similar to Fscn1, required JNK and p38 kinase activity for stimulation associated upregulation, and this process was inhibited by ERK and PI(3)K
Peng et al., J Biol Chem 2011 (Latent Tuberculosis) : Incubation of T cells with ESAT-6 induced phosphorylation and increased functional p38 MAPK activity, but not activation of ERK or JNK
Wu et al., Biochem Pharmacol 2011 : In addition, knockdown of NAPA induced the activation of the MAPK kinases ERK, JNK and p38 , but only inhibition of ERK reduced synoviolin ubiquitination and p53 accumulation
Hutchison et al., Mol Endocrinol 2012 (MAP Kinase Signaling System) : Two factors that promote chondrocyte differentiation, brain derived neurotrophic factor (BDNF) and C-type natriuretic peptide, increase p38 activity while decreasing, but not completely inhibiting , ERK activity
Yang et al., Biosci Rep 2012 (Insulin Resistance) : In contrast, saturated fatty acid exposure caused insulin resistance, reducing PI3K ( phosphoinositide 3-kinase ) and ERK ( extracellular-signal regulated kinase ) activation while increasing activation of stress kinases JNK ( c-Jun N-terminal kinase ) and p38
Samoylenko et al., Carcinogenesis 2012 (Adenocarcinoma...) : Thereby, Ruk ( l ) /CIN85 led to a more rapid and prolonged epidermal growth factor dependent activation of Src, Akt and ERK1/2 and treatment with the Src inhibitor PP2 and the PI3K inhibitor LY294002 abolished the Ruk ( l ) /CIN85 dependent changes in cell motility
Bae et al., Biochem Biophys Res Commun 2013 : U0126 ( ERK1/2 inhibitor ) and SB203580 ( p38 MAPK inhibitor ) inhibited IGF-1 induced MUC8 and MUC5B mRNA expression
Park et al., Anticancer Drugs 2013 (Bone Neoplasms...) : Whereas BMP-2 mainly activated ERK1/2 , BMP-9 phosphorylated p38 within 1 h. pBMP-2 did not activate either the Smad or ERK/p38, whereas pBMP-9, like BMP-9, induced both Smad1/5/8 and p38 phosphorylation
Jensen et al., Cell Host Microbe 2013 (Coxsackievirus Infections...) : The kinase ERK5 requires p38 kinase activity and inhibits apoptosis caused by CVB3 infection
Li et al., Retrovirology 2013 : Activation of Erk/Akt suppresses p38 due to CCR5 binding, and allows cell survival
Tanaka et al., Mol Cell Biol 1995 : These results suggest that both Crk and Grb2 may contribute to the activation of Erk by oncogenic Abl, whereas Nck is unlikely to participate in this pathway
McGilvray et al., J Biol Chem 1998 : Moreover, whereas inhibition of ERK had no effect on p38 activity, p38 inhibition consistently increased MHV-3 induced ERK activity