BCR-ABL癌蛋白可能与着色性干皮病B组蛋白相互作用。
The BCR-ABL oncoprotein potentially interacts with the xeroderma pigmentosum group B protein.
作者信息
Takeda N, Shibuya M, Maru Y
机构信息
Department of Genetics, Institute of Medical Science, University of Tokyo, Tokyo 108, Japan.
出版信息
Proc Natl Acad Sci U S A. 1999 Jan 5;96(1):203-7. doi: 10.1073/pnas.96.1.203.
Abstract
The previously uncharacterized CDC24 homology domain of BCR, which is missing in the P185 BCR-ABL oncogene of Philadelphia chromosome (Ph1)-positive acute lymphocytic leukemia but is retained in P210 BCR-ABL of chronic myelogeneous leukemia, was found to bind to the xeroderma pigmentosum group B protein (XPB). The binding appeared to be required for XPB to be tyrosine-phosphorylated by BCR-ABL. The interaction not only reduced both the ATPase and the helicase activities of XPB purified in the baculovirus system but also impaired XPB-mediated cross-complementation of the repair deficiency in rodent UV-sensitive mutants of group 3. The persistent dysfunction of XPB may in part underlie genomic instability in blastic crisis.
摘要
在费城染色体（Ph1）阳性急性淋巴细胞白血病的P185 BCR-ABL癌基因中缺失但在慢性粒细胞白血病的P210 BCR-ABL中保留的BCR的先前未被表征的CDC24同源结构域，被发现与着色性干皮病B组蛋白（XPB）结合。这种结合似乎是XPB被BCR-ABL酪氨酸磷酸化所必需的。这种相互作用不仅降低了在杆状病毒系统中纯化的XPB的ATP酶和螺旋酶活性，而且还损害了XPB介导的对3组啮齿动物紫外线敏感突变体修复缺陷的交叉互补作用。XPB的持续功能障碍可能部分是 blast危机中基因组不稳定的基础。
相似文献
1
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.
2
BCR binds to the xeroderma pigmentosum group B protein.BCR与着色性干皮病B组蛋白结合。
Biochem Biophys Res Commun. 1999 Jul 5;260(2):309-12. doi: 10.1006/bbrc.1999.0822.
3
FTY720, a new alternative for treating blast crisis chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphocytic leukemia.FTY720，一种治疗急变期慢性粒细胞白血病和费城染色体阳性急性淋巴细胞白血病的新选择。
J Clin Invest. 2007 Sep;117(9):2408-21. doi: 10.1172/JCI31095.
4
TFIIH functions are altered by the P210BCR-ABL oncoprotein produced on the Philadelphia chromosome.
Mutat Res. 2001 Nov 1;483(1-2):83-8. doi: 10.1016/s0027-5107(01)00229-9.
5
P210 BCR-ABL is complexed to P160 BCR and ph-P53 proteins in K562 cells.在K562细胞中，P210 BCR-ABL与P160 BCR和磷酸化P53蛋白形成复合物。
Oncogene. 1990 May;5(5):773-6.
6
The RhoGEF domain of p210 Bcr-Abl activates RhoA and is required for transformation.p210 Bcr-Abl的RhoGEF结构域激活RhoA，是细胞转化所必需的。
Oncogene. 2008 Mar 27;27(14):2064-71. doi: 10.1038/sj.onc.1210841. Epub 2007 Oct 8.
7
p210 BCR/ABL kinase regulates nucleotide excision repair (NER) and resistance to UV radiation.p210 BCR/ABL激酶调节核苷酸切除修复（NER）以及对紫外线辐射的抗性。
Blood. 2003 Oct 1;102(7):2632-7. doi: 10.1182/blood-2002-10-3207. Epub 2003 Jun 26.
8
Molecular characterization and sensitivity of STI-571 (imatinib mesylate, Gleevec)-resistant, Bcr-Abl-positive, human acute leukemia cells to SRC kinase inhibitor PD180970 and 17-allylamino-17-demethoxygeldanamycin.对STI-571（甲磺酸伊马替尼，格列卫）耐药、Bcr-Abl阳性的人急性白血病细胞对SRC激酶抑制剂PD180970和17-烯丙基氨基-17-去甲氧基格尔德霉素的分子特征及敏感性
Cancer Res. 2002 Oct 15;62(20):5761-9.
9
Bcr: a negative regulator of the Bcr-Abl oncoprotein.Bcr：Bcr-Abl癌蛋白的负调控因子。
Oncogene. 1999 Aug 5;18(31):4416-24. doi: 10.1038/sj.onc.1202828.
10
An actin-binding function contributes to transformation by the Bcr-Abl oncoprotein of Philadelphia chromosome-positive human leukemias.肌动蛋白结合功能有助于费城染色体阳性人类白血病的Bcr-Abl癌蛋白介导的细胞转化。
EMBO J. 1993 Apr;12(4):1533-46. doi: 10.1002/j.1460-2075.1993.tb05797.x.
引用本文的文献
1
The Coiled Coil and C2 Domains Modulate BCR Localization and BCR-ABL1 Compartmentalization, Transforming Activity and TKI Responsiveness.卷曲螺旋结构域和C2结构域调节BCR定位以及BCR-ABL1的区室化、转化活性和TKI反应性。
Int J Mol Sci. 2025 Jul 9;26(14):6591. doi: 10.3390/ijms26146591.
2
Modeling Blast Crisis Using Mutagenized Chronic Myeloid Leukemia-Derived Induced Pluripotent Stem Cells (iPSCs).利用突变的慢性髓性白血病源性诱导多能干细胞（iPSCs）建立急变期白血病模型。
Cells. 2023 Feb 12;12(4):598. doi: 10.3390/cells12040598.
3
Secondary Resistant Mutations to Small Molecule Inhibitors in Cancer Cells.癌细胞中对小分子抑制剂的继发性耐药突变
Cancers (Basel). 2020 Apr 9;12(4):927. doi: 10.3390/cancers12040927.
4
BCR: a promiscuous fusion partner in hematopoietic disorders.BCR：造血系统疾病中一个混杂的融合伙伴。
Oncotarget. 2019 Apr 12;10(28):2738-2754. doi: 10.18632/oncotarget.26837.
5
Loss of the xeroderma pigmentosum group B protein binding site impairs p210 BCR/ABL1 leukemogenic activity.丧失着色性干皮病 B 组蛋白结合位点会损害 p210 BCR/ABL1 白血病发病活性。
Blood Cancer J. 2013 Aug 16;3(8):e135. doi: 10.1038/bcj.2013.36.
6
Polymorphisms of ERCC1 genotype associated with response to imatinib therapy in chronic phase chronic myeloid leukemia.ERCC1 基因型多态性与慢性期慢性髓性白血病伊马替尼治疗反应相关。
Int J Hematol. 2012 Sep;96(3):327-33. doi: 10.1007/s12185-012-1142-6. Epub 2012 Jul 21.
7
XPB induces C1D expression to counteract UV-induced apoptosis.XPB 诱导 C1D 表达以拮抗 UV 诱导的细胞凋亡。
Mol Cancer Res. 2010 Jun;8(6):885-95. doi: 10.1158/1541-7786.MCR-09-0467. Epub 2010 Jun 8.
8
BCR-ABL: a multi-faceted promoter of DNA mutation in chronic myelogeneous leukemia.BCR-ABL：慢性髓性白血病中多种促 DNA 突变的因素。
Leukemia. 2010 Jun;24(6):1105-12. doi: 10.1038/leu.2010.67. Epub 2010 May 6.
9
Stem cell and kinase activity-independent pathway in resistance of leukaemia to BCR-ABL kinase inhibitors.白血病对BCR-ABL激酶抑制剂耐药中的干细胞及激酶活性非依赖途径
J Cell Mol Med. 2007 Nov-Dec;11(6):1251-62. doi: 10.1111/j.1582-4934.2007.00108.x.
10
The RhoGEF domain of p210 Bcr-Abl activates RhoA and is required for transformation.p210 Bcr-Abl的RhoGEF结构域激活RhoA，是细胞转化所必需的。
Oncogene. 2008 Mar 27;27(14):2064-71. doi: 10.1038/sj.onc.1210841. Epub 2007 Oct 8.
本文引用的文献
1
2
Typical chronic myelogenous leukemia with e19a2 junction BCR/ABL transcript.伴有e19a2连接区BCR/ABL转录本的典型慢性髓性白血病
Blood. 1997 Dec 15;90(12):5024-5.
3
4
TFIIH: a key component in multiple DNA transactions.TFIIH：多种DNA事务中的关键成分。
Curr Opin Genet Dev. 1996 Feb;6(1):26-33. doi: 10.1016/s0959-437x(96)90006-4.
5
A 3' --> 5' XPB helicase defect in repair/transcription factor TFIIH of xeroderma pigmentosum group B affects both DNA repair and transcription.B组着色性干皮病的修复/转录因子TFIIH中3'→5' XPB解旋酶缺陷影响DNA修复和转录。
J Biol Chem. 1996 Jul 5;271(27):15898-904. doi: 10.1074/jbc.271.27.15898.
6
The dimerization property of glutathione S-transferase partially reactivates Bcr-Abl lacking the oligomerization domain.谷胱甘肽S-转移酶的二聚化特性可部分重新激活缺乏寡聚化结构域的Bcr-Abl。
J Biol Chem. 1996 Jun 28;271(26):15353-7. doi: 10.1074/jbc.271.26.15353.
7
BCR/ABL P210 and P190 cause distinct leukemia in transgenic mice.BCR/ABL P210和P190在转基因小鼠中引发不同类型的白血病。
Blood. 1995 Dec 15;86(12):4603-11.
8
Subcellular localization of Bcr, Abl, and Bcr-Abl proteins in normal and leukemic cells and correlation of expression with myeloid differentiation.Bcr、Abl和Bcr-Abl蛋白在正常细胞和白血病细胞中的亚细胞定位以及表达与髓系分化的相关性。
J Clin Invest. 1993 Oct;92(4):1925-39. doi: 10.1172/JCI116786.
9
Generation of the AML1-EVI-1 fusion gene in the t(3;21)(q26;q22) causes blastic crisis in chronic myelocytic leukemia.t(3;21)(q26;q22)中AML1-EVI-1融合基因的产生导致慢性粒细胞白血病发生原始细胞危象。
EMBO J. 1994 Feb 1;13(3):504-10. doi: 10.1002/j.1460-2075.1994.tb06288.x.
10
Mutational analysis of ERCC3, which is involved in DNA repair and transcription initiation: identification of domains essential for the DNA repair function.参与DNA修复和转录起始的ERCC3的突变分析：鉴定DNA修复功能所必需的结构域。
Mol Cell Biol. 1994 Jun;14(6):4126-34. doi: 10.1128/mcb.14.6.4126-4134.1994.
Zotero 插件