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Bcr-Abl是造血干细胞生长和分化决策中的一个“分子开关”。

Bcr-Abl is a "molecular switch" for the decision for growth and differentiation in hematopoietic stem cells.

作者信息

Era Takumi

机构信息

Stem Cell Biology Group, RIKEN Center for Development Biology, Kobe City, Hyogo, Japan.

出版信息

Int J Hematol. 2002 Jul;76(1):35-43. doi: 10.1007/BF02982716.

Abstract

Chronic myeloid leukemia (CML) is a clonal disorder originating in the pluripotent hematopoietic stem cell (HSC), the hallmark of which is the constitutively activated p210-type of Bcr-Abl tyrosine kinase protein. Studies in recent years have helped us to understand the molecular processes involved in the initiation and progression of CML. Although a great amount of knowledge has been accumulated, the effect of Bcr-Abl on the HSC is still unclear. We have developed an in vitro system that mirrors the chronic phase of CML with a combination of in vitro embryonic stem cell differentiation and tetracycline-inducible Bcr-Abl expression. Enforced Bcr-Abl expression was sufficient to increase the number of both multilineage progenitors and myeloid progenitors. The current system is powerful for analyzing the genetic changes in hematopoietic development. This review focuses on how Bcr-Abl affects HSCs and how Bcr-Abl expression alters the properties of HSCs.

摘要

慢性髓性白血病(CML)是一种起源于多能造血干细胞(HSC)的克隆性疾病,其标志是持续激活的p210型Bcr-Abl酪氨酸激酶蛋白。近年来的研究帮助我们了解了CML发生和发展过程中涉及的分子机制。尽管已经积累了大量知识,但Bcr-Abl对HSC的影响仍不清楚。我们开发了一种体外系统,该系统通过体外胚胎干细胞分化和四环素诱导的Bcr-Abl表达相结合来模拟CML的慢性期。强制表达Bcr-Abl足以增加多谱系祖细胞和髓系祖细胞的数量。当前系统对于分析造血发育中的基因变化非常有效。本综述重点关注Bcr-Abl如何影响HSC以及Bcr-Abl表达如何改变HSC的特性。

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