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1
Nuclear localization of v-Abl leads to complex formation with cyclic AMP response element (CRE)-binding protein and transactivation through CRE motifs.v-Abl的核定位导致其与环磷酸腺苷反应元件（CRE）结合蛋白形成复合物，并通过CRE基序进行反式激活。
Mol Cell Biol. 1995 Nov;15(11):6088-99. doi: 10.1128/MCB.15.11.6088.
2
The p120-v-Abl protein interacts with E2F-1 and regulates E2F-1 transcriptional activity.p120-v-Abl蛋白与E2F-1相互作用并调节E2F-1的转录活性。
J Biol Chem. 1997 Apr 4;272(14):8905-11. doi: 10.1074/jbc.272.14.8905.
3
v-Abl activates c-myc transcription through the E2F site.v-Abl 通过 E2F 位点激活 c-myc 转录。
Mol Cell Biol. 1995 Dec;15(12):6535-44. doi: 10.1128/MCB.15.12.6535.
4
Genetic characterization of transactivation of the human T-cell leukemia virus type 1 promoter: Binding of Tax to Tax-responsive element 1 is mediated by the cyclic AMP-responsive members of the CREB/ATF family of transcription factors.人类1型T细胞白血病病毒启动子反式激活的遗传学特征：Tax与Tax反应元件1的结合由转录因子CREB/ATF家族的环磷酸腺苷反应成员介导。
Mol Cell Biol. 1996 May;16(5):2174-82. doi: 10.1128/MCB.16.5.2174.
5
Transcription of the rat glucagon gene by the cyclic AMP response element-binding protein CREB is modulated by adjacent CREB-associated proteins.环磷酸腺苷反应元件结合蛋白（CREB）对大鼠胰高血糖素基因的转录受到相邻CREB相关蛋白的调节。
Mol Cell Biol. 1993 Nov;13(11):7080-90. doi: 10.1128/mcb.13.11.7080-7090.1993.
6
Transcriptional induction of the human renin gene by cyclic AMP requires cyclic AMP response element-binding protein (CREB) and a factor binding a pituitary-specific trans-acting factor (Pit-1) motif.环磷酸腺苷（cAMP）对人肾素基因的转录诱导需要环磷酸腺苷反应元件结合蛋白（CREB）以及一个与垂体特异性反式作用因子（Pit-1）基序结合的因子。
Biochem J. 1996 May 15;316 ( Pt 1)(Pt 1):107-13. doi: 10.1042/bj3160107.
7
Molecular interactions involved in the transactivation of the human T-cell leukemia virus type 1 promoter mediated by Tax and CREB-2 (ATF-4).由Tax和CREB-2（ATF-4）介导的人类1型T细胞白血病病毒启动子反式激活中涉及的分子相互作用。
Mol Cell Biol. 2000 May;20(10):3470-81. doi: 10.1128/MCB.20.10.3470-3481.2000.
8
Grb4/Nckbeta acts as a nuclear repressor of v-Abl-induced transcription from c-jun/c-fos promoter elements.Grb4/Nckbeta作为v-Abl诱导的从c-jun/c-fos启动子元件转录的核阻遏物。
J Biol Chem. 2001 Nov 16;276(46):43419-27. doi: 10.1074/jbc.M107030200. Epub 2001 Aug 20.
9
Ischemia and reperfusion enhance ATF-2 and c-Jun binding to cAMP response elements and to an AP-1 binding site from the c-jun promoter.缺血再灌注增强了ATF-2和c-Jun与cAMP反应元件以及c-jun启动子的AP-1结合位点的结合。
J Biol Chem. 1995 Dec 15;270(50):30084-92. doi: 10.1074/jbc.270.50.30084.
10
Transactivation by the human T-cell leukemia virus Tax protein is mediated through enhanced binding of activating transcription factor-2 (ATF-2) ATF-2 response and cAMP element-binding protein (CREB).人类T细胞白血病病毒Tax蛋白的反式激活作用是通过增强激活转录因子2（ATF-2）、ATF-2反应元件和环磷酸腺苷反应元件结合蛋白（CREB）的结合来介导的。
J Biol Chem. 1993 Oct 5;268(28):21225-31.

引用本文的文献

1
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.
2
The BCR-ABL oncoprotein potentially interacts with the xeroderma pigmentosum group B protein.BCR-ABL癌蛋白可能与着色性干皮病B组蛋白相互作用。
Proc Natl Acad Sci U S A. 1999 Jan 5;96(1):203-7. doi: 10.1073/pnas.96.1.203.
3
Identification of a binding site in c-Ab1 tyrosine kinase for the C-terminal repeated domain of RNA polymerase II.鉴定RNA聚合酶II C末端重复结构域在c-Ab1酪氨酸激酶中的结合位点。
Mol Cell Biol. 1996 Jul;16(7):3361-9. doi: 10.1128/MCB.16.7.3361.
4
The cytostatic function of c-Abl is controlled by multiple nuclear localization signals and requires the p53 and Rb tumor suppressor gene products.c-Abl的细胞生长抑制功能受多个核定位信号的控制，并且需要p53和Rb肿瘤抑制基因产物。
EMBO J. 1996 Apr 1;15(7):1583-95.

本文引用的文献

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The activation domain of transcription factor PU.1 binds the retinoblastoma (RB) protein and the transcription factor TFIID in vitro: RB shows sequence similarity to TFIID and TFIIB.转录因子PU.1的激活结构域在体外与视网膜母细胞瘤（RB）蛋白和转录因子TFIID结合：RB与TFIID和TFIIB表现出序列相似性。
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Distinct activation domains within cAMP response element-binding protein (CREB) mediate basal and cAMP-stimulated transcription.环磷酸腺苷反应元件结合蛋白（CREB）内不同的激活结构域介导基础转录和环磷酸腺苷刺激的转录。
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A C-terminal protein-binding domain in the retinoblastoma protein regulates nuclear c-Abl tyrosine kinase in the cell cycle.视网膜母细胞瘤蛋白中的C末端蛋白结合结构域在细胞周期中调节核c-Abl酪氨酸激酶。
Cell. 1993 Nov 19;75(4):779-90. doi: 10.1016/0092-8674(93)90497-e.
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E1A-associated p300 and CREB-associated CBP belong to a conserved family of coactivators.与E1A相关的p300和与CREB相关的CBP属于一个保守的共激活因子家族。
Cell. 1994 Jun 17;77(6):799-800. doi: 10.1016/0092-8674(94)90127-9.
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The cAMP-regulated transcription factor CREB interacts with a component of the TFIID complex.环磷酸腺苷（cAMP）调节的转录因子CREB与TFIID复合物的一个组分相互作用。
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Biologic properties of factor-independent nonadherent hematopoietic and adherent preadipocyte cell lines derived from continuous bone marrow culture.源自连续骨髓培养的不依赖因子的非贴壁造血细胞系和贴壁前脂肪细胞系的生物学特性
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Nucleotide sequence of Abelson murine leukemia virus genome: structural similarity of its transforming gene product to other onc gene products with tyrosine-specific kinase activity.阿贝尔逊鼠白血病病毒基因组的核苷酸序列：其转化基因产物与其他具有酪氨酸特异性激酶活性的癌基因产物的结构相似性。
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Transfection of fibroblasts by cloned Abelson murine leukemia virus DNA and recovery of transmissible virus by recombination with helper virus.通过克隆的阿贝尔逊鼠白血病病毒DNA转染成纤维细胞，并通过与辅助病毒重组回收可传播病毒。
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v-Abl的核定位导致其与环磷酸腺苷反应元件（CRE）结合蛋白形成复合物，并通过CRE基序进行反式激活。

Nuclear localization of v-Abl leads to complex formation with cyclic AMP response element (CRE)-binding protein and transactivation through CRE motifs.

作者信息

Birchenall-Roberts M C, Ruscetti F W, Kasper J J, Bertolette D C, Yoo Y D, Bang O S, Roberts M S, Turley J M, Ferris D K, Kim S J

机构信息

Biological Carcinogenesis and Development Program, Science Applications International Corporation Frederick, Maryland.

出版信息

Mol Cell Biol. 1995 Nov;15(11):6088-99. doi: 10.1128/MCB.15.11.6088.

DOI:10.1128/MCB.15.11.6088
PMID:7565761
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC230860/
Abstract

Deregulated expression of v-abl and BCR/abl genes has been associated with myeloproliferative syndromes and myelodysplasia, both of which can progress to acute leukemia. These studies identify the localization of the oncogenic form of the abl gene product encoded by the Abelson murine leukemia virus in the nuclei of myeloid cells and the association of the v-Abl protein with the transcriptional regulator cyclic AMP response element-binding protein (CREB). We have mapped the specific domains within each of the proteins responsible for this interaction. We have shown that complex formation is a prerequisite for transcriptional potentiation of CREB. Transient overexpression of the homologous cellular protein c-Abl also results in the activation of promoters containing an intact CRE. These observations identify a novel function for v-Abl, that of a transcriptional activator that physically interacts with a transcription factor.

摘要

v-abl和BCR/abl基因的表达失调与骨髓增殖综合征和骨髓发育异常有关，这两种病症都可能发展为急性白血病。这些研究确定了由Abelson小鼠白血病病毒编码的abl基因产物的致癌形式在髓样细胞核中的定位，以及v-Abl蛋白与转录调节因子环磷酸腺苷反应元件结合蛋白（CREB）的关联。我们已经绘制了每种蛋白质中负责这种相互作用的特定结构域。我们已经表明，复合物的形成是CREB转录增强的先决条件。同源细胞蛋白c-Abl的瞬时过表达也会导致含有完整CRE的启动子的激活。这些观察结果确定了v-Abl的一种新功能，即作为一种与转录因子发生物理相互作用的转录激活因子。