DC Field | Value | Language |
---|---|---|
dc.contributor.author | Choi, Juhyun | ko |
dc.contributor.author | Oh, Sangphil | ko |
dc.contributor.author | Lee, Dongjun | ko |
dc.contributor.author | Oh, Hyun Jung | ko |
dc.contributor.author | Park, Jik Young | ko |
dc.contributor.author | Lee, Sean Bong | ko |
dc.contributor.author | Lim, Dae-Sik | ko |
dc.date.accessioned | 2013-03-09T20:36:46Z | - |
dc.date.available | 2013-03-09T20:36:46Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2009-11 | - |
dc.identifier.citation | PLOS ONE, v.4, no.11 | - |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | http://hdl.handle.net/10203/97418 | - |
dc.description.abstract | Background: The Ste-20 family kinase Hippo restricts cell proliferation and promotes apoptosis for proper organ development in Drosophila. In C. elegans, Hippo homolog also regulates longevity. The mammalian Ste20-like protein kinase, Mst1, plays a role in apoptosis induced by various types of apoptotic stress. Mst1 also regulates peripheral naive T cell trafficking and proliferation in mice. However, its functions in mammals are not fully understood. Methodology/Principal Findings: Here, we report that the Mst1-FoxO signaling pathway plays a crucial role in survival, but not apoptosis, of naive T cells. In Mst1(-/-) mice, peripheral T cells showed impaired FoxO1/3 activation and decreased FoxO protein levels. Consistently, the FoxO targets, Sod2 and catalase, were significantly down-regulated in Mst1(-/-) T cells, thereby resulting in elevated levels of intracellular reactive oxygen species (ROS) and induction of apoptosis. Expression of constitutively active FoxO3a restored Mst1(-/-) T cell survival. Crossing Mst1 transgenic mice (Mst1 Tg) with Mst1(-/-) mice reduced ROS levels and restored normal numbers of peripheral naive T cells in Mst1 Tg; Mst1(-/-) progeny. Interestingly, peripheral T cells from Mst1(-/-) mice were hypersensitive to gamma-irradiation and paraquat-induced oxidative stresses, whereas those from Mst1 Tg mice were resistant. Conclusions/Significance: These data support the hypothesis that tolerance to increased levels of intracellular ROS provided by the Mst1-FoxOs signaling pathway is crucial for the maintenance of naive T cell homeostasis in the periphery. | - |
dc.language | English | - |
dc.publisher | PUBLIC LIBRARY SCIENCE | - |
dc.subject | STERILE-20 KINASE | - |
dc.subject | HISTONE H2B | - |
dc.subject | IN-VIVO | - |
dc.subject | CELLS | - |
dc.subject | APOPTOSIS | - |
dc.subject | RECEPTOR | - |
dc.subject | MST1 | - |
dc.subject | PHOSPHORYLATION | - |
dc.subject | PROLIFERATION | - |
dc.subject | TRANSLOCATION | - |
dc.title | Mst1-FoxO Signaling Protects Naive T Lymphocytes from Cellular Oxidative Stress in Mice | - |
dc.type | Article | - |
dc.identifier.wosid | 000272827500034 | - |
dc.identifier.scopusid | 2-s2.0-71049155850 | - |
dc.type.rims | ART | - |
dc.citation.volume | 4 | - |
dc.citation.issue | 11 | - |
dc.citation.publicationname | PLOS ONE | - |
dc.identifier.doi | 10.1371/journal.pone.0008011 | - |
dc.contributor.localauthor | Lim, Dae-Sik | - |
dc.contributor.nonIdAuthor | Choi, Juhyun | - |
dc.contributor.nonIdAuthor | Park, Jik Young | - |
dc.contributor.nonIdAuthor | Lee, Sean Bong | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | STERILE-20 KINASE | - |
dc.subject.keywordPlus | HISTONE H2B | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | CELLS | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | RECEPTOR | - |
dc.subject.keywordPlus | MST1 | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | PROLIFERATION | - |
dc.subject.keywordPlus | TRANSLOCATION | - |
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