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Article: 14-3-3σ regulates B-cell homeostasis through stabilization of FOXO1

Title14-3-3σ regulates B-cell homeostasis through stabilization of FOXO1
Authors
Issue Date2011
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2011, v. 108, n. 4, p. 1555-1560 How to Cite?
Abstract14-3-3σ regulates cytokinesis and cell cycle arrest induced by DNA damage but its role in the immune system is unknown. Using gene-targeted 14-3-3σ-deficient (i.e., KO) mice, we studied the role of 14-3-3σ in B-cell functions. Total numbers of B cells were reduced by spontaneous apoptosis of peripheral B cells. Upon B-cell antigen receptor engagement in vitro, KO B cells did not proliferate properly or up-regulate CD86. In response to T cell-independent antigens, KO B cells showed poor secretion of antigen-specific IgM. This deficit led to increased lethality of KO mice after vesicular stomatitis virus infection. KO B cells showed elevated total FOXO transcriptional activity but also increased FOXO1 degradation. Coimmunoprecipitation revealed that endogenous 14-3-3σ protein formed a complex with FOXO1 protein. Our results suggest that 14-3-3σ maintains FOXO1 at a consistent level critical for normal B-cell antigen receptor signaling and B-cell survival.
Persistent Identifierhttp://hdl.handle.net/10722/292019
ISSN
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 3.737
PubMed Central ID
ISI Accession Number ID
Errata

 

DC FieldValueLanguage
dc.contributor.authorSu, Yu Wen-
dc.contributor.authorHao, Zhenyue-
dc.contributor.authorHirao, Atsushi-
dc.contributor.authorYamamoto, Kazuo-
dc.contributor.authorLin, Wen Jye-
dc.contributor.authorYoung, Ashley-
dc.contributor.authorDuncan, Gordon S.-
dc.contributor.authorYoshida, Hiroki-
dc.contributor.authorWakeham, Andrew-
dc.contributor.authorLang, Philipp A.-
dc.contributor.authorMurakami, Kiichi-
dc.contributor.authorHeremeking, Heiko-
dc.contributor.authorVogelstein, Bert-
dc.contributor.authorOhashi, Pamela-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:55:36Z-
dc.date.available2020-11-17T14:55:36Z-
dc.date.issued2011-
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2011, v. 108, n. 4, p. 1555-1560-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/292019-
dc.description.abstract14-3-3σ regulates cytokinesis and cell cycle arrest induced by DNA damage but its role in the immune system is unknown. Using gene-targeted 14-3-3σ-deficient (i.e., KO) mice, we studied the role of 14-3-3σ in B-cell functions. Total numbers of B cells were reduced by spontaneous apoptosis of peripheral B cells. Upon B-cell antigen receptor engagement in vitro, KO B cells did not proliferate properly or up-regulate CD86. In response to T cell-independent antigens, KO B cells showed poor secretion of antigen-specific IgM. This deficit led to increased lethality of KO mice after vesicular stomatitis virus infection. KO B cells showed elevated total FOXO transcriptional activity but also increased FOXO1 degradation. Coimmunoprecipitation revealed that endogenous 14-3-3σ protein formed a complex with FOXO1 protein. Our results suggest that 14-3-3σ maintains FOXO1 at a consistent level critical for normal B-cell antigen receptor signaling and B-cell survival.-
dc.languageeng-
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America-
dc.title14-3-3σ regulates B-cell homeostasis through stabilization of FOXO1-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.1017729108-
dc.identifier.pmid21205887-
dc.identifier.pmcidPMC3029705-
dc.identifier.scopuseid_2-s2.0-79952119593-
dc.identifier.volume108-
dc.identifier.issue4-
dc.identifier.spage1555-
dc.identifier.epage1560-
dc.identifier.eissn1091-6490-
dc.identifier.isiWOS:000286594800065-
dc.relation.erratumdoi:10.1073/pnas.1104407108-
dc.relation.erratumeid:eid_2-s2.0-79955575355-
dc.relation.erratumdoi:10.1073/pnas.1316144110-
dc.relation.erratumeid:eid_2-s2.0-84884633770-
dc.identifier.issnl0027-8424-

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