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Molecular and Cellular Biology Volume 19, 1999 - Issue 10
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Cell Growth and Development

Bcr-Abl with an SH3 Deletion Retains the Ability To Induce a Myeloproliferative Disease in Mice, yet c-Abl Activated by an SH3 Deletion Induces Only Lymphoid Malignancy

Alec W. Gross1 Rosenstiel Basic Medical Sciences Research Center, Department of Biology
,
Xiaowu Zhang2 Department of Biochemistry, Brandeis University, Waltham, Massachusetts02454-9110
&
Ruibao Ren1 Rosenstiel Basic Medical Sciences Research Center, Department of BiologyCorrespondence[email protected]
Pages 6918-6928 | Received 09 Apr 1999, Accepted 19 Jul 1999, Published online: 28 Mar 2023

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Gui Xiaomin, Zhang Yong, Pan Jinlan, Qiu Huiying, Cen Jiannong, Xue Yongquan, Chen Suning, Shen Hongjie, Yao Li, Zhang Jun, Wu Yafang & Chen Yan. (2015) Chronic myeloid leukemia with e14a3 BCR-ABL transcript: analysis of characteristics and prognostic significance. Leukemia & Lymphoma 56:12, pages 3343-3347.
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Ryan P. Million, Nari Harakawa, Sergei Roumiantsev, Lyuba Varticovski & Richard A. Van Etten. (2004) A Direct Binding Site for Grb2 Contributes to Transformation and Leukemogenesis by the Tel-Abl (ETV6-Abl) Tyrosine Kinase. Molecular and Cellular Biology 24:11, pages 4685-4695.
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Xiaowu Zhang, Ramesh Subrahmanyam, Ray Wong, Alec W. Gross & Ruibao Ren. (2001) The NH2-Terminal Coiled-Coil Domain and Tyrosine 177 Play Important Roles in Induction of a Myeloproliferative Disease in Mice by Bcr-Abl. Molecular and Cellular Biology 21:3, pages 840-853.
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Sheryl X. Hao & Ruibao Ren. (2000) Expression of Interferon Consensus Sequence Binding Protein (ICSBP) Is Downregulated in Bcr-Abl-Induced Murine Chronic Myelogenous Leukemia-Like Disease, and Forced Coexpression of ICSBP Inhibits Bcr-Abl-Induced Myeloproliferative Disorder. Molecular and Cellular Biology 20:4, pages 1149-1161.
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