Glucose transport regulation by p210 Bcr-Abl in a chronic myeloid leukaemia model

被引:39
作者
Bentley, J
Walker, I
McIntosh, E
Whetton, AD
Owen-Lynch, PJ
Baldwin, SA
机构
[1] Univ Leeds, Sch Biochem & Mol Biol, Leeds, W Yorkshire, England
[2] Univ Manchester, Dept Biochem & Appl Mol Biol, LRF Unit, Manchester M60 1QD, Lancs, England
关键词
Bcr-Abl; CML; multipotent stem cells; glucose transport; PI3-kinase;
D O I
10.1046/j.1365-2141.2001.02428.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The regulation of nutrient transport by both cytokines and oncogenes has been linked to haemopoietic cell survival. In this study, we found that activation of Bcr-Abl protein tyrosine kinase was associated with the stimulation of glucose transport in the multipotent haemopoietic cell line FDCP-mix, a cell model for chronic-phase chronic myeloid leukaemia (CML). Bcr-Abl upregulation of glucose transport was mediated by phosphatidylinositol-3-kinase. The observation that Bcr-Abl can regulate glucose transport in a CML cell model raises the possibility that glucose transport regulation may have a role to play in the aberrant survival of stem cells in the chronic phase of CML.
引用
收藏
页码:212 / 215
页数:4
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