BMI1 represses Ink4a/Arf and Hox genes to regulate stem cells in the rodent incisor

被引：0
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作者：
Brian Biehs
Jimmy Kuang-Hsien Hu
Nicolas B. Strauli
Eugenio Sangiorgi
Heekyung Jung
Ralf-Peter Heber
Sunita Ho
Alice F. Goodwin
Jeremy S. Dasen
Mario R. Capecchi
Ophir D. Klein
机构：
[1] University of California San Francisco,Department of Orofacial Sciences and Program in Craniofacial and Mesenchymal Biology
[2] University of California San Francisco,Department of Pediatrics and Institute for Human Genetics
[3] University of Utah School of Medicine,Howard Hughes Medical Institute and Department of Human Genetics
[4] Smilow Neuroscience Program,Department of Physiology and Neuroscience
[5] Howard Hughes Medical Institute,Department of Preventative and Restorative Dental Sciences
[6] NYU School of Medicine,undefined
[7] University of California San Francisco,undefined
[8] Present addresses: Department of Molecular Biology,undefined
[9] Genentech Inc.,undefined
[10] 1 DNA Way,undefined
[11] South San Francisco,undefined
[12] California 94080,undefined
[13] USA (B.B.); Istituto di Genetica Medica,undefined
[14] Università Cattolica del Sacro Cuore,undefined
[15] Rome,undefined
[16] Italy (E.S.),undefined
来源：
Nature Cell Biology | 2013年 / 15卷
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摘要：
The polycomb protein BMI1 has been linked to maintenance of adult stem cells. Klein and colleagues find that BMI1 is also required for the maintenance of stem cells in the continuously growing mouse incisor, through repression of the Ink4a/Arf locus to modulate the proliferation of stem cells and repression of Hox genes to prevent inappropriate lineage decisions in stem cell progeny.
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页码：846 / 852
页数：6
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