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v-erbA specifically suppresses transcription of the avian erythrocyte anion transporter (band 3) gene.

作者信息

Zenke M, Kahn P, Disela C, Vennström B, Leutz A, Keegan K, Hayman M J, Choi H R, Yew N, Engel J D

机构信息

European Molecular Biology Laboratory Differentiation Program, Heidelberg, Federal Republic of Germany.

出版信息

Cell. 1988 Jan 15;52(1):107-19. doi: 10.1016/0092-8674(88)90535-1.

DOI:10.1016/0092-8674(88)90535-1
PMID:2830979
Abstract

Previous work has established that the v-erbA oncogene inhibits the temperature-induced differentiation of chick erythroblasts transformed with temperature-sensitive oncogene mutants. Here we demonstrate that v-erbA in differentiating erythroblasts specifically arrests expression of the erythrocyte anion transporter (band 3) gene at the transcriptional level. The v-erbA-induced differentiation block can be overcome by inducing cells to differentiate at alkaline pH. Under these conditions, which possibly impair biological activity of v-erbA, the maturing cells now express the anion transporter gene at high levels. However, its transcription is specifically and rapidly suppressed if v-erbA activity is restored by culturing the cells at neutral pH. Similar but less pronounced inhibition of gene expression by v-erbA was observed for the delta-amino-levulinic acid synthase gene. Additional evidence obtained with an inhibitor of band 3 activity suggests that the v-erbA-induced inhibition of band 3 gene expression is at least partly responsible for the differentiation block caused by this oncogene.

摘要

相似文献

1
v-erbA specifically suppresses transcription of the avian erythrocyte anion transporter (band 3) gene.
Cell. 1988 Jan 15;52(1):107-19. doi: 10.1016/0092-8674(88)90535-1.
2
Transcriptional repression of band 3 and CAII in v-erbA transformed erythroblasts accounts for an important part of the leukaemic phenotype.v-erbA转化的成红细胞中带3蛋白和碳酸酐酶II的转录抑制是白血病表型的重要组成部分。
EMBO J. 1992 Sep;11(9):3355-65. doi: 10.1002/j.1460-2075.1992.tb05414.x.
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v-erbA oncogene activation entails the loss of hormone-dependent regulator activity of c-erbA.
Cell. 1990 Jun 15;61(6):1035-49. doi: 10.1016/0092-8674(90)90068-p.
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Transforming capacities of avian erythroblastosis virus mutants deleted in the erbA or erbB oncogenes.在erbA或erbB癌基因中缺失的禽成红细胞增多症病毒突变体的转化能力。
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v-erbA cooperates with sarcoma oncogenes in leukemic cell transformation.v-erbA在白血病细胞转化中与肉瘤癌基因协同作用。
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6
Phosphorylation of the v-erbA protein is required for its function as an oncogene.
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7
The avian erythroblastosis virus erbA oncogene encodes a DNA-binding protein exhibiting distinct nuclear and cytoplasmic subcellular localizations.禽成红细胞增多症病毒erbA癌基因编码一种具有独特核定位和胞质定位的DNA结合蛋白。
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Biological effects of the v-erbA oncogene in transformation of avian erythroid cells.v-erbA癌基因在禽类红细胞转化中的生物学效应。
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A single point mutation in erbA restores the erythroid transforming potential of a mutant avian erythroblastosis virus (AEV) defective in both erbA and erbB oncogenes.erbA基因中的单个点突变可恢复一种在erbA和erbB癌基因均有缺陷的突变禽成红细胞增多症病毒(AEV)的红细胞转化潜能。
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10
Defective v-erbB genes can be complemented by v-erbA in erythroblast and fibroblast transformation.
Oncogene. 1987 May;1(2):167-73.

引用本文的文献

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Thyroid hormone receptor mutations in cancer and resistance to thyroid hormone: perspective and prognosis.癌症中的甲状腺激素受体突变与甲状腺激素抵抗:现状与预后
J Thyroid Res. 2011;2011:361304. doi: 10.4061/2011/361304. Epub 2011 Jun 8.
2
Large-scale analysis by SAGE reveals new mechanisms of v-erbA oncogene action.SAGE的大规模分析揭示了v-erbA癌基因作用的新机制。
BMC Genomics. 2007 Oct 26;8:390. doi: 10.1186/1471-2164-8-390.
3
Multiple mutations contribute to repression by the v-Erb A oncoprotein.多种突变导致v-Erb A癌蛋白发挥抑制作用。
Oncogene. 2005 Oct 13;24(45):6737-52. doi: 10.1038/sj.onc.1208826.
4
In vivo repression of an erythroid-specific gene by distinct corepressor complexes.不同的共抑制复合物对红系特异性基因的体内抑制作用。
EMBO J. 2002 Mar 15;21(6):1389-97. doi: 10.1093/emboj/21.6.1389.
5
Leukemic transformation by the v-ErbA oncoprotein entails constitutive binding to and repression of an erythroid enhancer in vivo.v-ErbA癌蛋白导致的白血病转化在体内需要与红系增强子持续结合并对其进行抑制。
EMBO J. 1998 Dec 15;17(24):7382-94. doi: 10.1093/emboj/17.24.7382.
6
Cooperation of Spi-1/PU.1 with an activated erythropoietin receptor inhibits apoptosis and Epo-dependent differentiation in primary erythroblasts and induces their Kit ligand-dependent proliferation.Spi-1/PU.1与活化的促红细胞生成素受体协同作用,可抑制原代成红细胞的凋亡和促红细胞生成素依赖性分化,并诱导其Kit配体依赖性增殖。
EMBO J. 1997 Sep 15;16(18):5639-53. doi: 10.1093/emboj/16.18.5639.
7
The estrogen receptor cooperates with the TGF alpha receptor (c-erbB) in regulation of chicken erythroid progenitor self-renewal.雌激素受体与转化生长因子α受体(c-erbB)协同调节鸡红细胞祖细胞的自我更新。
EMBO J. 1993 Mar;12(3):951-60. doi: 10.1002/j.1460-2075.1993.tb05736.x.
8
Thyroid hormone receptor/c-erbA: control of commitment and differentiation in the neuronal/chromaffin progenitor line PC12.甲状腺激素受体/c-erbA:对神经母细胞/嗜铬细胞祖系PC12中细胞定向分化的调控
J Cell Biol. 1993 Apr;121(2):423-38. doi: 10.1083/jcb.121.2.423.
9
Structure and regulation of the chicken erythroid delta-aminolevulinate synthase gene.鸡红细胞δ-氨基乙酰丙酸合酶基因的结构与调控
Nucleic Acids Res. 1994 Apr 11;22(7):1226-33. doi: 10.1093/nar/22.7.1226.
10
A conserved C-terminal sequence that is deleted in v-ErbA is essential for the biological activities of c-ErbA (the thyroid hormone receptor).在v-ErbA中缺失的保守C末端序列对c-ErbA(甲状腺激素受体)的生物学活性至关重要。
Mol Cell Biol. 1993 Jun;13(6):3675-85. doi: 10.1128/mcb.13.6.3675-3685.1993.