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Bmi1在小鼠睾丸中的表达定位

Expression localization of Bmi1 in mice testis.

作者信息

Zhang Shiqing, Li Dexue, Li Enzhong, Li Lan, Wang Junjun, Wang Changyong, Lu Jingyan, Zhang Xueming

机构信息

Institute of Basic Medical Sciences, Beijing 100850, People's Republic of China.

出版信息

Mol Cell Endocrinol. 2008 Jun 11;287(1-2):47-56. doi: 10.1016/j.mce.2008.01.008. Epub 2008 Jan 29.

DOI:10.1016/j.mce.2008.01.008
PMID:18359150
Abstract

B cell-specific Moloney murine leukaemia virus integration site 1 (Bmi1), known as the first functional member of PcG (Polycomb Group) family, is supposed to be a key regulator of stem cell self-proliferation. In this study, we investigated its expression in testis and its impact on spermatogonia proliferation for better understanding of its role in spermatogenesis. Results showed that Bmi1 was expressed in undifferentiated spermatogonia (A(s), A(pr) and A(al) spermatogonia). Overexpression of BMI1 could promote spermatogonia proliferation, while repression of endogenous Bmi1 by RNAi resulted in inhibition of the proliferation.

摘要

B细胞特异性莫洛尼鼠白血病病毒整合位点1(Bmi1),作为聚梳蛋白家族(PcG)的首个功能性成员,被认为是干细胞自我增殖的关键调节因子。在本研究中,我们调查了其在睾丸中的表达及其对精原细胞增殖的影响,以更好地了解其在精子发生中的作用。结果显示,Bmi1在未分化的精原细胞(A(s)、A(pr)和A(al)精原细胞)中表达。BMI1的过表达可促进精原细胞增殖,而RNA干扰对内源性Bmi1的抑制则导致增殖受到抑制。

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Expression localization of Bmi1 in mice testis.Bmi1在小鼠睾丸中的表达定位
Mol Cell Endocrinol. 2008 Jun 11;287(1-2):47-56. doi: 10.1016/j.mce.2008.01.008. Epub 2008 Jan 29.
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Bcl-w forms complexes with Bax and Bak, and elevated ratios of Bax/Bcl-w and Bak/Bcl-w correspond to spermatogonial and spermatocyte apoptosis in the testis.Bcl-w与Bax和Bak形成复合物,睾丸中Bax/Bcl-w和Bak/Bcl-w比例升高与精原细胞和精母细胞凋亡相关。
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Polycomb group protein Bmi1 is overexpressed and essential in anchorage-independent colony formation, cell proliferation and repression of cellular senescence in cholangiocarcinoma: tissue and culture studies.多梳蛋白家族蛋白Bmi1在胆管癌的非锚定依赖性集落形成、细胞增殖及细胞衰老抑制过程中过表达且发挥重要作用:组织及细胞培养研究
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[Cloning of Bmi1 cDNA from mouse testis and its expression in E. coli BL21].[小鼠睾丸Bmi1 cDNA的克隆及其在大肠杆菌BL21中的表达]
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BMI1 promotes spermatogonial stem cell maintenance by epigenetically repressing Wnt10b/β-catenin signaling.
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