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EGF — HBEGF

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: Complex of EGF-EGFR → HBEGF (decreases)
  Evidence: HB-EGF and TGFA, although immunologically distinct from EGF, reportedly inhibit the binding of EGF to its own receptor
• Reactome Reaction: EGF → HBEGF (indirect_complex) Cohen et al., J Biol Chem 1996
• Reactome Reaction: EGF → HBEGF (reaction) Vijapurkar et al., Exp Cell Res 2003, Walton et al., J Biol Chem 1990, Li et al., Cell Signal 2007, Xu et al., Mol Cell Biol 2007, Hazan et al., Cell Growth Differ 1990, Kaushansky et al., Chem Biol 2008, Helin et al., J Biol Chem 1991, Margolis et al., J Biol Chem 1989, Ricci et al., Oncogene 1995, Wallasch et al., EMBO J 1995, Prigent et al., EMBO J 1994, Soler et al., Oncogene 1994, Segatto et al., Oncogene 1993, Cohen et al., J Biol Chem 1996, Pinkas-Kramarski et al., EMBO J 1996

Text-mined interactions from Literome

Hayashida et al., Int J Mol Med 1999 : These results indicate that EGF and HB-EGF possess different functions in RGM-1 cells and that EGF acts as a mediator of both cell maturation and apoptosis in these cells
Eguchi et al., J Biol Chem 2001 : BB2116 as well as HB-EGF neutralizing antibody inhibited the EGF receptor transactivation by AngII, suggesting a critical role of HB-EGF in the metalloprotease dependent EGF receptor transactivation
Martínez-Lacaci et al., J Cell Physiol 2001 : However, the Ha-ras transformed MCF-10A cells were more refractory to inhibition by these agents and only a combination of the 225 MAb and PD153035 was able to significantly abrogate HB-EGF induction by EGF ... The anti-erbB2 MAb L26 which interferes with heterodimer formation was able to block HB-EGF induction in response to EGF in MCF-10A cells and in the Ha-ras transformed cells only when used in combination with either the 225 MAb or PD153035 ... The MEK inhibitor PD90859 completely blocked EGF induction of HB-EGF mRNA levels in the nontransformed and Ha-ras transformed MCF-10A cells, which indicates that MAPK is involved in the signaling pathway of HB-EGF induction by EGF
Miyazaki et al., Gastroenterology 2001 : We determined the role of EGF receptor (EGFR) in stress induced expression of heparin binding EGF-like growth factor ( HB-EGF ) in a rat gastric epithelial cell line ( RGM1 cells )
Reynolds et al., Hypertension 2002 : HB-EGF induced phosphorylation of the EGF receptor (EGFR) with maximum phosphorylation at 0.5 to 1 minute, whereas erbB4, the other receptor to which HB-EGF binds, was not activated on HB-EGF stimulation
Wallasch et al., Biochem Biophys Res Commun 2002 (Stomach Neoplasms) : Helicobacter pylori stimulated EGF receptor transactivation requires metalloprotease cleavage of HB-EGF
Li et al., Dev Cell 2003 : Lack of c-Jun prevents EGF induced expression of HB-EGF , indicating that c-jun controls formation of the epidermal leading edge through its control of an EGF receptor autocrine loop
Besner et al., Growth Factors 1992 (Endometrial Neoplasms) : The inhibitory effect of HB-EGF on 125I-EGF binding was reversed either in the presence of heparin ( but not by chondroitin sulfate ) or by pre treating the cells with heparinase
Hao et al., Circ Res 2004 (Hypertension) : Matrix metalloproteinase ( MMP ) -dependent shedding of heparin binding epidermal growth factor ( HB-EGF ) and subsequent activation of the EGF receptor (EGFR) in the cardiovasculature is emerging as a unique mechanism signaling growth effects of diverse G protein coupled receptors ( GPCRs )
Takashima et al., Nihon Yakurigaku Zasshi 2004 : Recently, similar transactivation of EGF receptor by a GPCR agonist has been reported in various organs, indicating that EGF receptor transactivation by HB-EGF might play the general role of pharmacological reaction by AGII
Yoshioka et al., Proc Natl Acad Sci U S A 2005 (Hypertrophy, Left Ventricular...) : Recent evidence indicates that EGF receptor transactivation by heparin binding EGF (HB-EGF) contributes to hypertrophic signaling in cardiomyocytes
Iwamoto et al., Cell Struct Funct 2006 : The heparin binding EGF-like growth factor ( HB-EGF ) is a member of the EGF family of growth factors that binds to and activates the EGF receptor ( EGFR/ErbB1 ) and ErbB4
Wang et al., Oncogene 2007 (Neoplasms) : Induction of HB-EGF expression and ectodomain shedding synergistically led to robust epidermal growth factor receptor (EGFR) phosphorylation, whereas inhibition of HB-EGF expression by use of the HB-EGF inhibitor ( CRM197 ) or siRNA resulted in the suppression of chemotherapy induced EGFR phosphorylation
Xu et al., Invest Ophthalmol Vis Sci 2007 : The release of HB-EGF assessed by AP activity increased significantly in response to wounding, LPA, or both, and the release of HB-EGF-AP induced by LPA was inhibited by PP2 and GM6001
Koide et al., Am J Physiol Heart Circ Physiol 2007 : Here we have tested the hypothesis that shedding of heparin binding EGF-like growth factor ( HB-EGF ) and the resulting activation of the tyrosine kinase EGF receptor (EGFR) underlie OxyHb induced K ( V ) channel suppression in the cerebral vasculature
Tse et al., Comp Biochem Physiol A Mol Integr Physiol 2009 : Differential regulation of betacellulin and heparin binding EGF-like growth factor in cultured zebrafish ovarian follicle cells by EGF family ligands
Hirata et al., Br J Cancer 2009 (Neoplasm Invasiveness...) : The HB-EGF-CTF nuclear translocation leads to the interaction of BCL6 with HB-EGF-CTF and the nuclear export of BCL6, and after that BCL6 degradation was mediated by ubiquitin/proteasome pathway
Chen et al., Growth Factors 2010 : Since HB-EGF activates EGF receptors which have been implicated in tumor development, we examined the effects of HB-EGF overexpression in the intestine
Smirnova et al., Tsitologiia 2010 : [ Metalloprotease mediated HB-EGF release regulates EGF receptor transactivation in A431 cells under oxidative stress ] ... H2O2 induced EGF receptor phosphorylation was inhibited by HB-EGF , but not TGF-alpha, neutralizing antibody
Yokoyama et al., Int J Oncol 1996 : These findings suggest that HB-EGF activates the EGF receptor in human pancreatic cancer cells, but that it is not involved in enhancing the biological aggressiveness of this malignancy in vivo
Akool et al., Biochem Pharmacol 2012 (MAP Kinase Signaling System) : Moreover, neutralizing antibodies against heparin binding-epidermal growth factor ( HB-EGF ), and inhibition of the EGF receptor by either small interfering ( si ) RNA or AG1478, demonstrate that ERK activation by both PPIase inhibitors is mediated via HB-EGF induced EGF receptor (EGFR) tyrosine kinase activation
Aviezer et al., Proc Natl Acad Sci U S A 1994 : These results directly demonstrate that HB-EGF but not EGF requires heparin or cell surface HSPG for binding and activation of the EGF receptor and that HB-EGF receptor interactions can be tightly regulated by the available local concentration of heparin-like molecules
Kobrin et al., Biochem Biophys Res Commun 1994 (Pancreatic Neoplasms) : Several cell lines expressed HB-EGF mRNA transcripts, and the transcript level was enhanced by HB-EGF , as well as by 12-O-tetradecanoylphorbol-13-acetate and transforming growth factor-alpha ( TGF-alpha )
Ushiro et al., Jpn J Cancer Res 1996 : HB-EGF inhibited the binding of ( 125 ) I-EGF to the EGF receptor and induced autophosphorylation of the receptor on endothelial cells
Freeman et al., J Clin Invest 1997 (Urinary Bladder Diseases) : This conclusion is based on demonstration of HB-EGF synthesis and secretion by primary culture HUC, identification of HER1 as an activatable HB-EGF receptor on HUC surfaces, stimulation of HUC clonal growth by HB-EGF , inhibition of HB-EGF stimulated growth by heparin and of log-phase growth by CRM 197, a specific inhibitor of HB-EGF/HER1 interaction, and identification of human urothelium as a site of HB-EGF precursor ( proHB-EGF ) synthesis in vivo
Stoll et al., J Clin Invest 1997 : Amphiregulin and heparin binding EGF-like growth factor ( HB-EGF ) transcripts were rapidly and markedly induced , whereas EGF and TGF-alpha mRNAs were undetectable or only slightly increased
Romano et al., J Clin Invest 1998 (Adenocarcinoma...) : Inhibition of AR- or HB-EGF- induced stimulation of cell growth was not mediated by downregulation of the EGF receptor since EGF receptor protein levels, EGF binding affinity, number of specific binding sites for EGF, or HB-EGF- or AR-dependent tyrosine phosphorylation of the EGF receptor were not significantly altered by incubation with H. pylori broth culture filtrates