Glucose transport regulation by p210 Bcr-Abl in a chronic myeloid leukaemia model
Glucose transport regulation by p210 Bcr-Abl in a chronic myeloid leukaemia model
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DOI：
10.1046/j.1365-2141.2001.02428.x
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发表时间：
2001-01-01
影响因子：
6.5
通讯作者：
Baldwin, SA
中科院分区：
文献类型：
--
作者：
Bentley, J;Walker, I;Baldwin, SA
细胞因子和癌基因对营养物质转运的调节与造血细胞的存活有关。在这项研究中，我们发现BCR-Abl蛋白酪氨酸激酶的激活与刺激多能造血细胞系FDCP-Mix的葡萄糖转运有关，FDCP-Mix是慢性期慢性髓系白血病(CML)的细胞模型。Bcr-Abl上调葡萄糖转运是由磷脂酰肌醇-3-激酶介导的。观察到BCR-Abl可以调节CML细胞模型中的葡萄糖运输，这增加了葡萄糖运输调节可能在CML慢性期干细胞异常存活中发挥作用的可能性。
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.