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CBL — EGF

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: CBL → EGF (increases) Kassenbrock et al., J Biol Chem 2002*
  Evidence: Stimulation of T47D cells with epidermal growth factor (EGF) results in the activation of the intrinsic tyrosine kinases of the receptor and the phosphorylation of multiple cellular proteins including the receptor, scaffold molecules such as c-Cbl, adapter molecules such as Shc, and the serine/threonine protein kinase Akt.
• BioCarta cbl mediated ligand-induced downregulation of egf receptors pathway: EGF R/SRC/EGF complex (EGFR-SRC-EGF) → CBL (protein ubiquitination, collaborate)
• NCI Pathway Database Internalization of ErbB1: CBL/Ubc4-5 family complex (CBL-UBE2D2_UBE2D3_UBE2D1) → EGFR/EGFR/EGF/EGF complex (EGFR-EGF) (modification, activates)
  Grøvdal et al., Exp Cell Res 2004, Umebayashi et al., Mol Biol Cell 2008
  Evidence: physical interaction
• NCI Pathway Database Internalization of ErbB1: EGFR/EGFR/EGF/EGF/GRB2/CBL complex (EGFR-EGF-GRB2-CBL) → EGFR/EGFR/EGF/EGF complex (EGFR-EGF) (modification, collaborate)
  
• NCI Pathway Database Internalization of ErbB1: EGFR/EGFR/EGF/EGF/GRB2/CBL complex (EGFR-EGF-GRB2-CBL) → GRB2/CBL complex (GRB2-CBL) (modification, collaborate)
  
• NCI Pathway Database Internalization of ErbB1: EGFR/EGFR/EGF/EGF complex (EGFR-EGF) → GRB2/CBL complex (GRB2-CBL) (modification, collaborate)
  
• NCI Pathway Database Internalization of ErbB1: EGFR/EGFR/EGF/EGF complex (EGFR-EGF) → EGFR/EGFR/EGF/EGF/GRB2/CBL complex (EGFR-EGF-GRB2-CBL) (modification, collaborate)
  Levkowitz et al., Mol Cell 1999, Waterman et al., EMBO J 2002, Jiang et al., Mol Biol Cell 2003*, Jiang et al., Traffic 2003*, Huang et al., Mol Biol Cell 2005, Huang et al., Proc Natl Acad Sci U S A 2007*
  Evidence: physical interaction
• NCI Pathway Database Internalization of ErbB1: EGFR/EGFR/EGF/EGF complex (EGFR-EGF) → GRB2/CBL complex (GRB2-CBL) (modification, collaborate)
  Levkowitz et al., Mol Cell 1999, Waterman et al., EMBO J 2002, Jiang et al., Mol Biol Cell 2003*, Jiang et al., Traffic 2003*, Huang et al., Mol Biol Cell 2005, Huang et al., Proc Natl Acad Sci U S A 2007*
  Evidence: physical interaction
• NCI Pathway Database Internalization of ErbB1: EGFR/EGFR/EGF/EGF/GRB2/CBL complex (EGFR-EGF-GRB2-CBL) → GRB2/CBL complex (GRB2-CBL) (modification, collaborate)
  Levkowitz et al., Mol Cell 1999, Waterman et al., EMBO J 2002, Jiang et al., Mol Biol Cell 2003*, Jiang et al., Traffic 2003*, Huang et al., Mol Biol Cell 2005, Huang et al., Proc Natl Acad Sci U S A 2007*
  Evidence: physical interaction
• Reactome Reaction: CBL → EGF (reaction) Joazeiro et al., Science 1999, Waterman et al., EMBO J 2002, Haglund et al., Proc Natl Acad Sci U S A 2002, Hall et al., Curr Biol 2003, Marmor et al., Oncogene 2004, Kassenbrock et al., J Biol Chem 2004, Sordella et al., Science 2004, Grøvdal et al., Exp Cell Res 2004, Greulich et al., PLoS Med 2005, Schmidt et al., Oncogene 2006, Yang et al., Cancer Res 2006, Choi et al., Oncogene 2007, Han et al., Cancer Biol Ther 2006, Lee et al., PLoS Med 2006, Grandal et al., Carcinogenesis 2007*, Padrón et al., Cancer Res 2007, Xu et al., Br J Cancer 2007, Galisteo et al., J Biol Chem 1995*
• Reactome Reaction: CBL → EGF (direct_complex) Joazeiro et al., Science 1999, Rosenthal et al., J Biol Chem 1999, Soubeyran et al., Nature 2002, Klapisz et al., J Biol Chem 2002, Haglund et al., Proc Natl Acad Sci U S A 2002, Marmor et al., Oncogene 2004, Kassenbrock et al., J Biol Chem 2004, Grøvdal et al., Exp Cell Res 2004, Sigismund et al., Proc Natl Acad Sci U S A 2005, Haglund et al., EMBO Rep 2005, Schmidt et al., Oncogene 2006, Galisteo et al., J Biol Chem 1995*
• Reactome Reaction: CBL → EGF (indirect_complex) Joazeiro et al., Science 1999, Waterman et al., EMBO J 2002, Marmor et al., Oncogene 2004, Sordella et al., Science 2004, Greulich et al., PLoS Med 2005, Yang et al., Cancer Res 2006, Choi et al., Oncogene 2007, Han et al., Cancer Biol Ther 2006, Lee et al., PLoS Med 2006, Grandal et al., Carcinogenesis 2007*, Padrón et al., Cancer Res 2007, Xu et al., Br J Cancer 2007

Text-mined interactions from Literome

Take et al., Biochem Biophys Res Commun 2000 : Our results suggest that CIN85 may play a specific role in the EGF receptor mediated signaling cascade via its interaction with c-Cbl
Ettenberg et al., J Biol Chem 2001 : Epidermal growth factor (EGF) induced Cbl-b degradation requires intact RING finger and tyrosine kinase binding domains and requires binding of the Cbl-b protein to the activated EGF receptor (EGFR)
Tvorogov et al., Exp Cell Res 2002 : EGF dependent association of phospholipase C-gamma1 with c-Cbl ... c-Cbl is shown to associate with tyrosine phosphorylated PLC-gamma1 in an EGF dependent manner, but no association was detected with the PLC-gamma1DeltaSH3 mutant
Huang et al., J Biol Chem 2003 : Finally, we observed augmentation of early aspects of EGF signaling ( EGF induced ERK2 activation and EGF induced Cbl tyrosine phosphorylation ) by GH cotreatment ; the GH effect on EGF induced Cbl tyrosine phosphorylation was also prevented by MEK1 inhibition
Choi et al., Mol Cells 2003 : Association of Cbl with PLC-gamma1 was induced by epidermal growth factor (EGF) but not by nerve growth factor (NGF) ... Mutation of the SH2 domains of either Cbl or PLC-gamma1 abrogated the EGF induced interaction of PLC-gamma1 with Cbl , indicating that SH2 mediated translocation is essential for the association of PLC-gamma1 and Cbl
Fong et al., J Biol Chem 2003 (MAP Kinase Signaling System) : In this study it is demonstrated that hSpry2 is tyrosine phosphorylated upon stimulation by either FGFR or EGF and subsequently binds endogenous c-Cbl with high affinity
Alwan et al., J Biol Chem 2003 : Here we evaluated EGFR activation, Cbl recruitment, EGFR ubiquitination and degradation in response to EGF , TGF alpha, and E4T ... In contrast, lactacystin treatment blocks EGF induced c-Cbl degradation but does not block EGFR degradation, even though lactacystin causes a minor delay in EGFR degradation
Kowanetz et al., J Biol Chem 2003 : Identification of a novel proline-arginine motif involved in CIN85 dependent clustering of Cbl and down-regulation of epidermal growth factor receptors
Samet et al., Toxicol Appl Pharmacol 2003 : PD153035 abolished EGF induced phosphorylation of the EGFR substrate Cbl , but had no effect on levels of phospho-Cbl caused by Zn ( 2+ )
Kowanetz et al., Mol Biol Cell 2004 : CIN85 is a multidomain adaptor protein involved in Cbl mediated down-regulation of epidermal growth factor (EGF) receptors
Feshchenko et al., Oncogene 2004 : Functional studies in a model system based on co-expression of TULA, c-Cbl, and EGF receptor in 293T cells demonstrate that TULA is capable of inhibiting c-Cbl mediated downregulation of EGF receptor
de Melker et al., J Cell Sci 2004 : c-Cbl directs EGF receptors into an endocytic pathway that involves the ubiquitin interacting motif of Eps15
Row et al., Biochem J 2005 : Consistent with this, expression of a dominant negative form of the E3 ubiquitin ligase, c-Cbl , inhibits EGF- and HGF dependent Hrs phosphorylation
Yang et al., Cancer Res 2006 (Lung Neoplasms) : Association with HSP90 inhibits Cbl mediated down-regulation of mutant epidermal growth factor receptors
Stern et al., Mol Cell Biol 2007 : Using an HEK 293 model system, we found that ectopic expression of the protein Cbl enhances Hrs ubiquitination and increases Hrs phosphorylation following cell stimulation with EGF
Bertelsen et al., Exp Cell Res 2007 : The Cbl- and ubiquitin interacting protein T-cell ubiquitin ligand ( TULA ) has been demonstrated to inhibit endocytosis and downregulation of ligand activated EGF receptor (EGFR) by impairing Cbl induced ubiquitination
Stern et al., Biochem J 2008 : EGF and amphiregulin differentially regulate Cbl recruitment to endosomes and EGF receptor fate
Scalabrino et al., Brain Res 2010 (Multiple Sclerosis) : Our results indicate that : ( a ) the positive Cbl mediated regulation of myelino- and oligodendrocyte-trophic EGF is lost in the CSF of RR- or SP-MS patients ; ( b ) the decrease in EGF levels in the CSF may be one factor impeding CNS remyelination in MS ; and ( c ) the PP clinical course may have different pathogenetic mechanism ( s ) also on the basis of the molecules investigated in this study
Duan et al., J Biol Chem 2011 : The E3 ubiquitin ligase Casitas B lymphoma protein (Cbl) controls the ubiquitin dependent degradation of EGF receptor (EGFR) , but its role in regulating downstream signaling elements with which it associates and its impact on biological outcomes of EGFR signaling are less clear
Sévère et al., J Biol Chem 2011 : Analysis of molecular mechanisms revealed that the Cbl mutant increased PDGF receptor a and FGF receptor 2 but not EGF receptor expression in hMSCs, resulting in increased ERK1/2 and PI3K signaling
Fukazawa et al., J Biol Chem 1996 : Phosphorylation of Cbl was EGF dose dependent , rapid ( detectable as early as 5 s and maximal by 2 min ), and relatively sustained ( detectable even after 1 h ) ... Co-immunoprecipitation studies demonstrated that Cbl became associated with the EGF receptor in an EGF dependent manner ... Cbl was basally associated with the adaptor protein growth factor receptor binding protein 2 ( Grb2 ), and this interaction was further enhanced by EGF stimulation ; however, the interaction was entirely mediated via the Grb2 Src homology 3 (SH3) domains, suggesting that binding of Grb2 SH2 domain to EGF receptor provides one mechanism of Cbl 's association with the EGF receptor ... EGF stimulation also induced the association of Cbl with Src homology and collagen (Shc) protein, p85 subunit of the phosphatidylinositol 3-kinase and Crk proteins, in particular with the CrkL isoform
Meisner et al., Mol Cell Biol 1997 : EGF also caused tyrosine phosphorylation of D-Cbl in such cells, but no association of phosphatidylinositol 3-kinase was detected in assays using anti-p85 antibody
Thien et al., Oncogene 1997 (Lymphoma, B-Cell) : Tyrosine kinase activity of the EGF receptor is enhanced by the expression of oncogenic 70Z-Cbl
Li et al., EMBO J 1998 : In PKC depleted cells, EGF receptor-specific tyrosine kinase inhibitors blocked Ang II-dependent EGF receptor and Cbl tyrosine phosphorylation, and ERK activation