Literature DB >> 8144631

SH-PTP2/Syp SH2 domain binding specificity is defined by direct interactions with platelet-derived growth factor beta-receptor, epidermal growth factor receptor, and insulin receptor substrate-1-derived phosphopeptides.

R D Case1, E Piccione, G Wolf, A M Benett, R J Lechleider, B G Neel, S E Shoelson.   

Abstract

Signaling by tyrosine kinases involves direct associations between proteins with Src homology 2 (SH2) domains and sites of tyrosine phosphorylation. Specificity in signaling pathways results in part from inherent selectivity in interactions between particular SH2 domains and phosphopeptide sequences. The cytoplasmic phosphotyrosine phosphatase SH-PTP2 (Syp, PTP 1D, PTP-2C) contains two SH2 domains (N and C) which mediate its association with and activation by the platelet-derived growth factor (PDGF) and epidermal growth factor receptors and IRS-1. We have developed a competitive phosphopeptide binding assay to analyze specificity of the SH-PTP2 N-SH2 domain for phosphorylation sites of these phosphoproteins. The sequence surrounding Tyr1009 bound with greatest affinity (ID50 = 14 microM) of eight PDGF receptor-derived phosphopeptides tested. No peptides corresponding to known epidermal growth factor receptor phosphorylation sites bound with high affinity. However, an alternative sequence surrounding Tyr954 bound tightly (ID50 = 21 microM). Of the 13 IRS-1-related peptides analyzed, sequences surrounding Tyr546, Tyr895, and Tyr1172 bound with highest affinity (ID50 = 11, 4, and 1 microM, respectively). Alternative phosphopeptides generally bound with much weaker affinity (ID50 > 150 microM). These findings are consistent with recent mutational analyses of the PDGF receptor and predict site-specific interactions between SH-PTP2 and each of these phosphoproteins. Comparisons between peptide sequences suggest that the N-terminal SH2 domain of SH-PTP2 binds with highest affinity to phosphotyrosine (pY) followed by a beta-branched residue (Val, Ile, Thr) at pY+1 and a hydrophobic residue (Val, Leu, Ile) at pY+3 positions. Peptide truncation studies also indicate that residues outside of the pY-1 to pY+4 motif are required for high affinity interactions.

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Year:  1994        PMID: 8144631

Source DB:  PubMed          Journal:  J Biol Chem        ISSN: 0021-9258            Impact factor:   5.157


  22 in total

1.  A quantitative study of the recruitment potential of all intracellular tyrosine residues on EGFR, FGFR1 and IGF1R.

Authors:  Alexis Kaushansky; Andrew Gordus; Bryan Chang; John Rush; Gavin MacBeath
Journal:  Mol Biosyst       Date:  2008-04-08

2.  Cellular effects of phosphotyrosine-binding domain inhibitors on insulin receptor signaling and trafficking.

Authors:  S Giorgetti-Peraldi; E Ottinger; G Wolf; B Ye; T R Burke; S E Shoelson
Journal:  Mol Cell Biol       Date:  1997-03       Impact factor: 4.272

3.  Tyrosine phosphatase SHP-2 dephosphorylates the platelet-derived growth factor receptor but enhances its downstream signalling.

Authors:  R Zhao; Z J Zhao
Journal:  Biochem J       Date:  1999-02-15       Impact factor: 3.857

Review 4.  Regulation of the insulin signalling pathway by cellular protein-tyrosine phosphatases.

Authors:  B J Goldstein; F Ahmad; W Ding; P M Li; W R Zhang
Journal:  Mol Cell Biochem       Date:  1998-05       Impact factor: 3.396

5.  Interaction between cAMP-dependent and insulin-dependent signal pathways in tyrosine phosphorylation in primary cultures of rat hepatocytes.

Authors:  Y Ito; Y Uchijima; M Ariga; T Seki; A Takenaka; F Hakuno; S I Takahashi; T Ariga; T Noguchi
Journal:  Biochem J       Date:  1997-06-01       Impact factor: 3.857

6.  Abnormal mesoderm patterning in mouse embryos mutant for the SH2 tyrosine phosphatase Shp-2.

Authors:  T M Saxton; M Henkemeyer; S Gasca; R Shen; D J Rossi; F Shalaby; G S Feng; T Pawson
Journal:  EMBO J       Date:  1997-05-01       Impact factor: 11.598

7.  Protein tyrosine phosphatase 2 (SHP-2) moderates signaling by gp130 but is not required for the induction of acute-phase plasma protein genes in hepatic cells.

Authors:  H Kim; T S Hawley; R G Hawley; H Baumann
Journal:  Mol Cell Biol       Date:  1998-03       Impact factor: 4.272

Review 8.  Interleukin-6-type cytokine signalling through the gp130/Jak/STAT pathway.

Authors:  P C Heinrich; I Behrmann; G Müller-Newen; F Schaper; L Graeve
Journal:  Biochem J       Date:  1998-09-01       Impact factor: 3.857

9.  Activation of the protein tyrosine phosphatase SHP2 via the interleukin-6 signal transducing receptor protein gp130 requires tyrosine kinase Jak1 and limits acute-phase protein expression.

Authors:  F Schaper; C Gendo; M Eck; J Schmitz; C Grimm; D Anhuf; I M Kerr; P C Heinrich
Journal:  Biochem J       Date:  1998-11-01       Impact factor: 3.857

10.  Identification of canonical tyrosine-dependent and non-canonical tyrosine-independent STAT3 activation sites in the intracellular domain of the interleukin 23 receptor.

Authors:  Doreen M Floss; Simone Mrotzek; Tobias Klöcker; Jutta Schröder; Joachim Grötzinger; Stefan Rose-John; Jürgen Scheller
Journal:  J Biol Chem       Date:  2013-05-14       Impact factor: 5.157

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