The expression of the non‐receptor tyrosine kinases Arg and c‐abl is differently modulated in B lymphoid cells at different stages of differentiation
- 6 September 2002
- journal article
- Published by Wiley in FEBS Letters
- Vol. 527 (1-3) , 216-222
- https://doi.org/10.1016/s0014-5793(02)03233-7
Abstract
The products of the human ARG gene and the human ABL gene characterize the Abelson family of non-receptor tyrosine protein kinases. Both genes are ubiquitously expressed. The interactions of these two similar protein kinases are still not well known, although it has been suggested that they could cooperate, with redundant actions, to provide intracellular signals in the cells. Lymphopenia occurs in mice with homozygous disruption of c-abl, indicating that in certain tissues Arg is unable to substitute c-abl functions. In B and T lymphoid cell lines at different stages of differentiation, we studied, by a reverse transcriptase-competitive polymerase chain reaction and Western blotting, Arg and c-abl in order to evaluate whether the expression pattern of the two genes could give insight as to why they do not exhibit overlapping roles in lymphocytes and whether the product levels of the two genes are related to lymphoid differentiation. The data showed that their expression is differently modified in lymphoid B cell lines. The highest Arg transcript and protein levels are in the mature B cellsKeywords
This publication has 42 references indexed in Scilit:
- Multiple signaling interactions of Abl and Arg kinases with the EphB2 receptorOncogene, 2001
- Inhibition of Cell Migration by Abl Family Tyrosine Kinases through Uncoupling of Crk-CAS ComplexesPublished by Elsevier ,2001
- The ARG Tyrosine Kinase Interacts with Siva-1 in the Apoptotic Response to Oxidative StressJournal of Biological Chemistry, 2001
- Bone Marrow B Lymphocyte Development in c-abl-Deficient MiceCellular Immunology, 1995
- AnnotationBritish Journal of Haematology, 1995
- Abl protein-tyrosine kinase selects the Crk adapter as a substrate using SH3-binding sites.Genes & Development, 1994
- Mice homozygous for the ablm1 mutation show poor viability and depletion of selected B and T cell populationsCell, 1991
- Neonatal lethality and lymphopenia in mice with a homozygous disruption of the c-abl proto-oncogeneCell, 1991
- The mouse type IV c-abl gene product is a nuclear protein, and activation of transforming ability is associated with cytoplasmic localizationCell, 1989
- A Novel Human Gene Closely Related to the abl Proto-OncogeneScience, 1986