Literature DB >> 2852893

The viral and cellular forms of the Abelson (abl) oncogene.

N Rosenberg1, O N Witte.   

Abstract

The precision of molecular biology has allowed a better definition of the components of the Abelson system. We know the gene structures and gene products for the cellular and viral forms of this family of related tyrosine kinases. However, many basic issues first identified in the early biological observations of Abelson, Rabstein, and others remain unanswered. The precise pathway for transformation in biochemical terms remains unknown for Ab-MLV and all of its relatives. Relatively little can be said to explain the preferential growth stimulation for certain hematopoietic cell types by the viral and other altered forms of the oncogene, and no clear insights into the function of the normal cellular forms of the abl oncogene are available. Future progress will certainly depend on the intensive efforts by many workers in the broader field of cellular growth control mechanisms.

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Year:  1988        PMID: 2852893     DOI: 10.1016/s0065-3527(08)60708-3

Source DB:  PubMed          Journal:  Adv Virus Res        ISSN: 0065-3527            Impact factor:   9.937


  57 in total

Review 1.  Lessons learned from the development of an abl tyrosine kinase inhibitor for chronic myelogenous leukemia.

Authors:  B J Druker; N B Lydon
Journal:  J Clin Invest       Date:  2000-01       Impact factor: 14.808

2.  Point mutations in the abl SH2 domain coordinately impair phosphotyrosine binding in vitro and transforming activity in vivo.

Authors:  B J Mayer; P K Jackson; R A Van Etten; D Baltimore
Journal:  Mol Cell Biol       Date:  1992-02       Impact factor: 4.272

3.  The noncatalytic src homology region 2 segment of abl tyrosine kinase binds to tyrosine-phosphorylated cellular proteins with high affinity.

Authors:  B J Mayer; P K Jackson; D Baltimore
Journal:  Proc Natl Acad Sci U S A       Date:  1991-01-15       Impact factor: 11.205

4.  Gag influences transformation by Abelson murine leukemia virus and suppresses nuclear localization of the v-Abl protein.

Authors:  Chae-Ryun Yi; Naomi Rosenberg
Journal:  J Virol       Date:  2007-06-27       Impact factor: 5.103

5.  Early pre-B-cell transformation induced by the v-fms oncogene in long-term mouse bone marrow cultures.

Authors:  G V Borzillo; C J Sherr
Journal:  Mol Cell Biol       Date:  1989-09       Impact factor: 4.272

6.  TYK2 is a key regulator of the surveillance of B lymphoid tumors.

Authors:  Dagmar Stoiber; Boris Kovacic; Christian Schuster; Carola Schellack; Marina Karaghiosoff; Rita Kreibich; Eva Weisz; Michaela Artwohl; Olaf C Kleine; Mathias Muller; Sabina Baumgartner-Parzer; Jacques Ghysdael; Michael Freissmuth; Veronika Sexl
Journal:  J Clin Invest       Date:  2004-12       Impact factor: 14.808

7.  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

8.  Transcriptional activation of a ras-like gene (kir) by oncogenic tyrosine kinases.

Authors:  L Cohen; R Mohr; Y Y Chen; M Huang; R Kato; D Dorin; F Tamanoi; A Goga; D Afar; N Rosenberg
Journal:  Proc Natl Acad Sci U S A       Date:  1994-12-20       Impact factor: 11.205

9.  Protein tyrosine phosphatase PTP1B suppresses p210 bcr-abl-induced transformation of rat-1 fibroblasts and promotes differentiation of K562 cells.

Authors:  K R LaMontagne; G Hannon; N K Tonks
Journal:  Proc Natl Acad Sci U S A       Date:  1998-11-24       Impact factor: 11.205

10.  A 41-kilodalton protein is a potential substrate for the p210bcr-abl protein-tyrosine kinase in chronic myelogenous leukemia cells.

Authors:  E Freed; T Hunter
Journal:  Mol Cell Biol       Date:  1992-03       Impact factor: 4.272

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