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本文引用的文献

1
Selective pyrrolo-pyrimidine inhibitors reveal a necessary role for Src family kinases in Bcr-Abl signal transduction and oncogenesis.选择性吡咯并嘧啶抑制剂揭示了Src家族激酶在Bcr-Abl信号转导和肿瘤发生中的必要作用。
Oncogene. 2002 Nov 21;21(53):8075-88. doi: 10.1038/sj.onc.1206008.
2
Phosphatidylinositol-3 kinase inhibitors enhance the anti-leukemia effect of STI571.磷脂酰肌醇-3激酶抑制剂增强STI571的抗白血病作用。
Oncogene. 2002 Aug 29;21(38):5868-76. doi: 10.1038/sj.onc.1205724.
3
Complementary functions of the antiapoptotic protein A1 and serine/threonine kinase pim-1 in the BCR/ABL-mediated leukemogenesis.抗凋亡蛋白A1和丝氨酸/苏氨酸激酶pim-1在BCR/ABL介导的白血病发生中的互补功能。
Blood. 2002 Jun 15;99(12):4531-9. doi: 10.1182/blood.v99.12.4531.
4
SH3-dependent stimulation of Src-family kinase autophosphorylation without tail release from the SH2 domain in vivo.体内SH3依赖性刺激Src家族激酶自身磷酸化，而尾部未从SH2结构域释放。
Nat Struct Biol. 2002 May;9(5):365-9. doi: 10.1038/nsb782.
5
Reduced lymphomyeloid repopulating activity from adult bone marrow and fetal liver of mice lacking expression of STAT5.缺乏STAT5表达的小鼠的成年骨髓和胎肝中淋巴细胞和髓细胞重建活性降低。
Blood. 2002 Jan 15;99(2):479-87. doi: 10.1182/blood.v99.2.479.
6
Functional cooperation among Ras, STAT5, and phosphatidylinositol 3-kinase is required for full oncogenic activities of BCR/ABL in K562 cells.Ras、STAT5和磷脂酰肌醇3激酶之间的功能合作是K562细胞中BCR/ABL完全致癌活性所必需的。
J Biol Chem. 2002 Mar 8;277(10):8076-82. doi: 10.1074/jbc.M111501200. Epub 2002 Jan 4.
7
BCR/ABL regulates mammalian RecA homologs, resulting in drug resistance.BCR/ABL调节哺乳动物RecA同源物，从而导致耐药性。
Mol Cell. 2001 Oct;8(4):795-806. doi: 10.1016/s1097-2765(01)00357-4.
8
Src directly tyrosine-phosphorylates STAT5 on its activation site and is involved in erythropoietin-induced signaling pathway.Src直接在其激活位点对STAT5进行酪氨酸磷酸化，并参与促红细胞生成素诱导的信号通路。
Oncogene. 2001 Oct 4;20(45):6643-50. doi: 10.1038/sj.onc.1204807.
9
Involvement of Jak2 tyrosine phosphorylation in Bcr-Abl transformation.Jak2酪氨酸磷酸化在Bcr-Abl转化中的作用。
Oncogene. 2001 Sep 27;20(43):6188-95. doi: 10.1038/sj.onc.1204834.
10
Molecular biology of chronic myeloid leukemia.慢性髓系白血病的分子生物学
Int J Hematol. 2001 Apr;73(3):308-22. doi: 10.1007/BF02981955.

Src家族激酶Hck在髓系白血病细胞中将BCR/ABL与STAT5激活偶联起来。

The Src family kinase Hck couples BCR/ABL to STAT5 activation in myeloid leukemia cells.

作者信息

Klejman Agata, Schreiner Steven J, Nieborowska-Skorska Malgorzata, Slupianek Artur, Wilson Matthew, Smithgall Thomas E, Skorski Tomasz

机构信息

Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USA.

出版信息

EMBO J. 2002 Nov 1;21(21):5766-74. doi: 10.1093/emboj/cdf562.

DOI:10.1093/emboj/cdf562
PMID:12411494
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC131059/
Abstract

Signal transducer and activator of transcription 5 (STAT5) is constitutively activated by BCR/ABL, the oncogenic tyrosine kinase responsible for chronic myelogenous leukemia. The mechanism of BCR/ABL-mediated STAT5 activation is unknown. We show here that the BCR/ABL SH3 and SH2 domains interact with hematopoietic cell kinase (Hck), leading to the stimulation of Hck catalytic activity. Active Hck phosphorylated STAT5B on Tyr699, which represents an essential step in STAT5B stimulation. Moreover, a kinase-dead Hck mutant and Hck inhibitor PP2 abrogated BCR/ABL-dependent activation of STAT5 and elevation of expression of STAT5 downstream effectors A1 and pim-1. These data identify a novel BCR/ABL-Hck-STAT5 signaling pathway, which plays an important role in BCR/ABL-mediated transformation of myeloid cells.

摘要

信号转导子和转录激活子5（STAT5）被BCR/ABL组成性激活，BCR/ABL是一种致癌酪氨酸激酶，与慢性粒细胞白血病有关。BCR/ABL介导的STAT5激活机制尚不清楚。我们在此表明，BCR/ABL的SH3和SH2结构域与造血细胞激酶（Hck）相互作用，导致Hck催化活性的刺激。活性Hck在Tyr699处磷酸化STAT5B，这是STAT5B激活的关键步骤。此外，激酶失活的Hck突变体和Hck抑制剂PP2消除了STAT5的BCR/ABL依赖性激活以及STAT5下游效应物A1和pim-1表达的升高。这些数据确定了一条新的BCR/ABL-Hck-STAT5信号通路，该通路在BCR/ABL介导的髓系细胞转化中起重要作用。