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Article: Bcl11a is essential for lymphoid development and negatively regulates p53

TitleBcl11a is essential for lymphoid development and negatively regulates p53
Authors
Issue Date2012
Citation
Journal of Experimental Medicine, 2012, v. 209, n. 13, p. 2467-2483 How to Cite?
AbstractTranscription factors play important roles in lymphopoiesis. We have previously demonstrated that Bcl11a is essential for normal lymphocyte development in the mouse embryo. We report here that, in the adult mouse, Bcl11a is expressed in most hematopoietic cells and is highly enriched in B cells, early T cell progenitors, common lymphoid progenitors (CLPs), and hematopoietic stem cells (HSCs). In the adult mouse, Bcl11a deletion causes apoptosis in early B cells and CLPs and completely abolishes the lymphoid development potential of HSCs to B, T, and NK cells. Myeloid development, in contrast, is not obviously affected by the loss of Bcl11a. Bcl11a regulates expression of Bcl2, Bcl2-xL, and Mdm2, which inhibits p53 activities. Overexpression of Bcl2 and Mdm2, or p53 deficiency, rescues both lethality and proliferative defects in Bcl11a-deficient early B cells and enables the mutant CLPs to differentiate to lymphocytes. Bcl11a is therefore essential for lymphopoiesis and negatively regulates p53 activities. Deletion of Bcl11a may represent a new approach for generating a mouse model that completely lacks an adaptive immune system. © 2012 Yu et al.
Persistent Identifierhttp://hdl.handle.net/10722/249071
ISSN
2017 Impact Factor: 10.79
2015 SCImago Journal Rankings: 10.762
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYu, Yong-
dc.contributor.authorWang, Juexuan-
dc.contributor.authorKhaled, Walid-
dc.contributor.authorBurke, Shannon-
dc.contributor.authorLi, Peng-
dc.contributor.authorChen, Xiongfeng-
dc.contributor.authorYang, Wei-
dc.contributor.authorJenkins, Nancy A.-
dc.contributor.authorCopeland, Neal G.-
dc.contributor.authorZhang, Shujun-
dc.contributor.authorLiu, Pentao-
dc.date.accessioned2017-10-27T05:59:01Z-
dc.date.available2017-10-27T05:59:01Z-
dc.date.issued2012-
dc.identifier.citationJournal of Experimental Medicine, 2012, v. 209, n. 13, p. 2467-2483-
dc.identifier.issn0022-1007-
dc.identifier.urihttp://hdl.handle.net/10722/249071-
dc.description.abstractTranscription factors play important roles in lymphopoiesis. We have previously demonstrated that Bcl11a is essential for normal lymphocyte development in the mouse embryo. We report here that, in the adult mouse, Bcl11a is expressed in most hematopoietic cells and is highly enriched in B cells, early T cell progenitors, common lymphoid progenitors (CLPs), and hematopoietic stem cells (HSCs). In the adult mouse, Bcl11a deletion causes apoptosis in early B cells and CLPs and completely abolishes the lymphoid development potential of HSCs to B, T, and NK cells. Myeloid development, in contrast, is not obviously affected by the loss of Bcl11a. Bcl11a regulates expression of Bcl2, Bcl2-xL, and Mdm2, which inhibits p53 activities. Overexpression of Bcl2 and Mdm2, or p53 deficiency, rescues both lethality and proliferative defects in Bcl11a-deficient early B cells and enables the mutant CLPs to differentiate to lymphocytes. Bcl11a is therefore essential for lymphopoiesis and negatively regulates p53 activities. Deletion of Bcl11a may represent a new approach for generating a mouse model that completely lacks an adaptive immune system. © 2012 Yu et al.-
dc.languageeng-
dc.relation.ispartofJournal of Experimental Medicine-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleBcl11a is essential for lymphoid development and negatively regulates p53-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1084/jem.20121846-
dc.identifier.pmid23230003-
dc.identifier.scopuseid_2-s2.0-84871851852-
dc.identifier.volume209-
dc.identifier.issue13-
dc.identifier.spage2467-
dc.identifier.epage2483-
dc.identifier.eissn1540-9538-
dc.identifier.isiWOS:000312539900012-

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