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本文引用的文献

1
Enhanced delivery efficiency of recombinant adenovirus into tumor and mesenchymal stem cells by a novel PTD.一种新型穿膜肽提高重组腺病毒向肿瘤细胞和间充质干细胞的递送效率
Cancer Gene Ther. 2008 Nov;15(11):703-12. doi: 10.1038/cgt.2008.45. Epub 2008 Jul 4.
2
Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency.p16Ink4a和p19Arf在BubR1功能不足引起的衰老和老化过程中的相反作用。
Nat Cell Biol. 2008 Jul;10(7):825-36. doi: 10.1038/ncb1744. Epub 2008 May 30.
3
Cell specific differences between human adipose-derived and mesenchymal-stromal cells despite similar differentiation potentials.尽管人类脂肪来源细胞与间充质基质细胞具有相似的分化潜能，但它们在细胞特异性上存在差异。
Exp Cell Res. 2008 Apr 15;314(7):1575-84. doi: 10.1016/j.yexcr.2007.12.022. Epub 2008 Jan 12.
4
p53 activation in response to mitotic spindle damage requires signaling via BubR1-mediated phosphorylation.响应有丝分裂纺锤体损伤的p53激活需要通过BubR1介导的磷酸化进行信号传导。
Cancer Res. 2007 Aug 1;67(15):7155-64. doi: 10.1158/0008-5472.CAN-06-3392.
5
Differential promoter methylation may be a key molecular mechanism in regulating BubR1 expression in cancer cells.差异性启动子甲基化可能是调节癌细胞中BubR1表达的关键分子机制。
Exp Mol Med. 2007 Apr 30;39(2):195-204. doi: 10.1038/emm.2007.22.
6
Concise review: adipose tissue-derived stromal cells--basic and clinical implications for novel cell-based therapies.简要综述：脂肪组织来源的基质细胞——基于新型细胞疗法的基础与临床意义
Stem Cells. 2007 Apr;25(4):818-27. doi: 10.1634/stemcells.2006-0589.
7
On the road to cancer: aneuploidy and the mitotic checkpoint.通往癌症之路：非整倍体与有丝分裂检查点
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8
Accelerated growth and prolonged lifespan of adipose tissue-derived human mesenchymal stem cells in a medium using reduced calcium and antioxidants.在使用低钙和抗氧化剂的培养基中脂肪组织来源的人间充质干细胞的加速生长和延长寿命。
Stem Cells Dev. 2005 Feb;14(1):92-102. doi: 10.1089/scd.2005.14.92.
9
The human mitotic checkpoint protein BubR1 regulates chromosome-spindle attachments.人类有丝分裂检查点蛋白BubR1调节染色体与纺锤体的附着。
Nat Cell Biol. 2005 Jan;7(1):93-8. doi: 10.1038/ncb1208. Epub 2004 Dec 12.
10
Ink4a/Arf expression is a biomarker of aging.Ink4a/Arf表达是衰老的一个生物标志物。
J Clin Invest. 2004 Nov;114(9):1299-307. doi: 10.1172/JCI22475.

BubR1 表达与脂肪间充质干细胞分化承诺之间的串扰。

Cross-talk between BubR1 expression and the commitment to differentiate in adipose-derived mesenchymal stem cells.

机构信息

Department of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea.

出版信息

Exp Mol Med. 2009 Dec 31;41(12):873-9. doi: 10.3858/emm.2009.41.12.093.

DOI:10.3858/emm.2009.41.12.093
PMID:19745606
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2802683/
Abstract

BubR1 mitotic checkpoint kinase monitors attachment of microtubules to kinetochores and links regulation of the chromosome-spindle attachment to mitotic checkpoint signaling. Defects in BubR1-mediated signaling severely perturb checkpoint control and are linked to diseases such as cancer. Studies using BubR1 mouse models suggest that BubR1 activities prevent premature aging and infertility. In this study, we show that BubR1 depletion in human adipose-derived mesenchymal stem cells (ASCs) precedes loss of the differentiation potential and induction of replicative senescence. These effects occur independently of p16(INK4A) expression and may involve DNA methylation. Our results reveal a new and unsuspected feature of BubR1 expression in regulation of adult stem cell differentiation.

摘要

BubR1 有丝分裂检查点激酶监测微管与动粒的连接，并将染色体-纺锤体连接的调节与有丝分裂检查点信号联系起来。BubR1 介导的信号缺陷严重扰乱了检查点控制，并与癌症等疾病有关。使用 BubR1 小鼠模型的研究表明，BubR1 活性可预防早衰和不孕。在这项研究中，我们表明 BubR1 在人脂肪间充质干细胞 (ASC) 中的耗竭先于分化潜能的丧失和复制性衰老的诱导。这些影响独立于 p16(INK4A)表达，可能涉及 DNA 甲基化。我们的结果揭示了 BubR1 表达在调节成体干细胞分化中的一个新的、意想不到的特征。