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dc.creatorYalcin, Safak
dc.creatorZhang, Xin
dc.creatorLuciano, Julia P.
dc.creatorMungamuri, Sathish Kumar
dc.creatorMarinković, Dragan
dc.creatorVercherat, Cecile
dc.creatorSarkar, Abby
dc.creatorGrisotto, Marcos
dc.creatorTaneja, Reshma
dc.creatorGhaffari, Saghi
dc.date.accessioned2021-06-09T13:22:33Z
dc.date.available2021-06-09T13:22:33Z
dc.date.issued2008
dc.identifier.issn0021-9258
dc.identifier.urihttp://rfasper.fasper.bg.ac.rs/handle/123456789/193
dc.description.abstractUnchecked accumulation of reactive oxygen species (ROS) compromises maintenance of hematopoietic stem cells. Regulation of ROS by the tumor suppressor protein ataxia telangiectasia mutated (ATM) is critical for preserving the hematopoietic stem cell pool. In this study we demonstrate that the Foxo3 member of the Forkhead Box O (FoxO) family of transcription factors is essential for normal ATM expression. In addition, we show that loss of Foxo3 leads to defects in hematopoietic stem cells, and these defects result from an overaccumulation of ROS. Foxo3 suppression of ROS in hematopoietic stem cells is mediated partly by regulation of ATM expression. We identify ROS-independent modulations of ATM and p16(INK4a) and ROS-mediated activation of p53/p21(CIP1/WAF1/Sdi1) tumor suppressor pathways as major contributors to Foxo3-null hematopoietic stem cells defects. Our studies demonstrate that Foxo3 represses ROS in part via regulation of ATM and that this repression is required for maintenance of the hematopoietic stem cell pool.en
dc.publisherAmer Soc Biochemistry Molecular Biology Inc, Bethesda
dc.relationAmerican Cancer Society Research Scholarship [RSG LIB-110480]
dc.relationCareer Enhancement Award [K18 HL76510-01]
dc.relationBlack Family Stem Cell Institute
dc.relationMount Sinai School of Medicine research funds
dc.rightsopenAccess
dc.sourceJournal of Biological Chemistry
dc.titleFoxo3 is essential for the regulation of ataxia telangiectasia mutated and oxidative stress-mediated homeostasis of hematopoietic stem cellsen
dc.typearticle
dc.rights.licenseARR
dc.citation.epage25705
dc.citation.issue37
dc.citation.other283(37): 25692-25705
dc.citation.rankM21
dc.citation.spage25692
dc.citation.volume283
dc.identifier.doi10.1074/jbc.M800517200
dc.identifier.fulltexthttp://rfasper.fasper.bg.ac.rs/bitstream/id/322/190.pdf
dc.identifier.pmid18424439
dc.identifier.scopus2-s2.0-54449092731
dc.identifier.wos000259012700064
dc.type.versionpublishedVersion


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