Literature DB >> 8195176

SH2-containing phosphotyrosine phosphatase Syp is a target of p210bcr-abl tyrosine kinase.

T Tauchi1, G S Feng, R Shen, H Y Song, D Donner, T Pawson, H E Broxmeyer.   

Abstract

The phosphorylation of proteins at tyrosine residues is critical in cellular signal transduction and neoplastic transformation. These mechanisms are regulated by the activities of both protein-tyrosine kinases and protein-tyrosine phosphatases. Recent studies have identified a novel protein-tyrosine phosphatase, termed Syp, that is widely expressed in various tissues. Syp encodes a cytoplasmic phosphatase that contains two Src homology 2 (SH2) domains. Since SH2 domains have been shown to target the association of signal-transducing molecules to activated tyrosine kinases, experiments were performed to determine whether Syp might form specific complexes with p210bcr-abl, a fusion protein believed to be involved in the pathogenesis of chronic myelogenous leukemia and, thus, possibly alter or mediate p210bcr-abl tyrosine kinase activity. We found that Syp was highly and constitutively tyrosine phosphorylated in three different murine cell lines transfected with a p210bcr-abl expression vector. Furthermore, p210bcr-abl, Syp, and Grb2 formed stable complexes in BCR-ABL-expressing cells. Complex formation between p210bcr-abl and Syp was mediated in vitro by the NH2-terminal SH2 domain of Syp. Last, p210bcr-abl tyrosine kinase was effectively dephosphorylated by Syp in vitro. These results suggest an interaction between Syp and BCR-ABL protein, which might play a role in cellular transformation of BCR-ABL.

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Year:  1994        PMID: 8195176

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


  14 in total

1.  H-2Dd engagement of Ly49A leads directly to Ly49A phosphorylation and recruitment of SHP1.

Authors:  M R Daws; M Eriksson; L Oberg; A Ullén; C L Sentman
Journal:  Immunology       Date:  1999-08       Impact factor: 7.397

2.  The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells.

Authors:  Agata Klejman; Steven J Schreiner; Malgorzata Nieborowska-Skorska; Artur Slupianek; Matthew Wilson; Thomas E Smithgall; Tomasz Skorski
Journal:  EMBO J       Date:  2002-11-01       Impact factor: 11.598

3.  Protein tyrosine phosphatase 1B antagonizes signalling by oncoprotein tyrosine kinase p210 bcr-abl in vivo.

Authors:  K R LaMontagne; A J Flint; B R Franza; A M Pandergast; N K Tonks
Journal:  Mol Cell Biol       Date:  1998-05       Impact factor: 4.272

Review 4.  ABL tyrosine kinases: evolution of function, regulation, and specificity.

Authors:  John Colicelli
Journal:  Sci Signal       Date:  2010-09-14       Impact factor: 8.192

Review 5.  Src kinase signaling in leukaemia.

Authors:  Shaoguang Li
Journal:  Int J Biochem Cell Biol       Date:  2007-02-09       Impact factor: 5.085

6.  SHP-2 phosphatase is required for hematopoietic cell transformation by Bcr-Abl.

Authors:  Jing Chen; Wen-Mei Yu; Hanako Daino; Hal E Broxmeyer; Brian J Druker; Cheng-Kui Qu
Journal:  Blood       Date:  2006-09-26       Impact factor: 22.113

Review 7.  Mechanisms of transformation by the BCR/ABL oncogene.

Authors:  M Sattler; J D Griffin
Journal:  Int J Hematol       Date:  2001-04       Impact factor: 2.490

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.  Mutant forms of growth factor-binding protein-2 reverse BCR-ABL-induced transformation.

Authors:  M L Gishizky; D Cortez; A M Pendergast
Journal:  Proc Natl Acad Sci U S A       Date:  1995-11-21       Impact factor: 11.205

10.  SHP-2 is a novel target of Abl kinases during cell proliferation.

Authors:  Sayan Mitra; Carol Beach; Gen-Sheng Feng; Rina Plattner
Journal:  J Cell Sci       Date:  2008-09-30       Impact factor: 5.285

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