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Article: Lung stem cell self-renewal relies on BMI1-dependent control of expression at imprinted loci

TitleLung stem cell self-renewal relies on BMI1-dependent control of expression at imprinted loci
Authors
Issue Date2011
Citation
Cell Stem Cell, 2011, v. 9, n. 3, p. 272-281 How to Cite?
AbstractBMI1 is required for the self-renewal of stem cells in many tissues including the lung epithelial stem cells, Bronchioalveolar Stem Cells (BASCs). Imprinted genes, which exhibit expression from only the maternally or paternally inherited allele, are known to regulate developmental processes, but what their role is in adult cells remains a fundamental question. Many imprinted genes were derepressed in Bmi1 knockout mice, and knockdown of Cdkn1c (p57) and other imprinted genes partially rescued the self-renewal defect of Bmi1 mutant lung cells. Expression of p57 and other imprinted genes was required for lung cell self-renewal in culture and correlated with repair of lung epithelial cell injury in vivo. Our data suggest that BMI1-dependent regulation of expressed alleles at imprinted loci, distinct from imprinting per se, is required for control of lung stem cells. We anticipate that the regulation and function of imprinted genes is crucial for self-renewal in diverse adult tissue-specific stem cells. © 2011 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/262828
ISSN
2023 Impact Factor: 19.8
2023 SCImago Journal Rankings: 10.253
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZacharek, Sima J.-
dc.contributor.authorFillmore, Christine M.-
dc.contributor.authorLau, Allison N.-
dc.contributor.authorGludish, David W.-
dc.contributor.authorChou, Alan-
dc.contributor.authorHo, Joshua W.K.-
dc.contributor.authorZamponi, Raffaella-
dc.contributor.authorGazit, Roi-
dc.contributor.authorBock, Christoph-
dc.contributor.authorJäger, Natalie-
dc.contributor.authorSmith, Zachary D.-
dc.contributor.authorKim, Tae Min-
dc.contributor.authorSaunders, Arven H.-
dc.contributor.authorWong, Janice-
dc.contributor.authorLee, Joo Hyeon-
dc.contributor.authorRoach, Rebecca R.-
dc.contributor.authorRossi, Derrick J.-
dc.contributor.authorMeissner, Alex-
dc.contributor.authorGimelbrant, Alexander A.-
dc.contributor.authorPark, Peter J.-
dc.contributor.authorKim, Carla F.-
dc.date.accessioned2018-10-08T02:47:11Z-
dc.date.available2018-10-08T02:47:11Z-
dc.date.issued2011-
dc.identifier.citationCell Stem Cell, 2011, v. 9, n. 3, p. 272-281-
dc.identifier.issn1934-5909-
dc.identifier.urihttp://hdl.handle.net/10722/262828-
dc.description.abstractBMI1 is required for the self-renewal of stem cells in many tissues including the lung epithelial stem cells, Bronchioalveolar Stem Cells (BASCs). Imprinted genes, which exhibit expression from only the maternally or paternally inherited allele, are known to regulate developmental processes, but what their role is in adult cells remains a fundamental question. Many imprinted genes were derepressed in Bmi1 knockout mice, and knockdown of Cdkn1c (p57) and other imprinted genes partially rescued the self-renewal defect of Bmi1 mutant lung cells. Expression of p57 and other imprinted genes was required for lung cell self-renewal in culture and correlated with repair of lung epithelial cell injury in vivo. Our data suggest that BMI1-dependent regulation of expressed alleles at imprinted loci, distinct from imprinting per se, is required for control of lung stem cells. We anticipate that the regulation and function of imprinted genes is crucial for self-renewal in diverse adult tissue-specific stem cells. © 2011 Elsevier Inc.-
dc.languageeng-
dc.relation.ispartofCell Stem Cell-
dc.titleLung stem cell self-renewal relies on BMI1-dependent control of expression at imprinted loci-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1016/j.stem.2011.07.007-
dc.identifier.pmid21885022-
dc.identifier.scopuseid_2-s2.0-80052289137-
dc.identifier.volume9-
dc.identifier.issue3-
dc.identifier.spage272-
dc.identifier.epage281-
dc.identifier.eissn1875-9777-
dc.identifier.isiWOS:000295024200013-
dc.identifier.f100013360017-
dc.identifier.issnl1875-9777-

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