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AuthorWang, Jianweidc.contributor.author
Date of accession2016-03-15T06:24:12Zdc.date.accessioned
Available in OPARU since2016-03-15T06:24:12Zdc.date.available
Year of creation2011dc.date.created
AbstractCheckpoints that limit stem cell self-renewal in response to DNA damage can contribute to cancer protection but may also promote tissue aging. Molecular components that control stem cell responses to DNA damage remain to be delineated. Using in vivo RNAi screens, we identified “Basic leucine zipper transcription factor, ATF-like” (BATF) as a major component limiting self-renewal of hematopoietic stem cells (HSCs) in response to telomere dysfunction and -irradiation. DNA damage induces BATF in a G-CSF/STAT3-dependent manner resulting in lymphoid differentiation of HSCs. BATF deletion improves HSC self-renewal and function in response to -irradiation or telomere shortening but results in accumulation of DNA damage in HSCs. Analysis of bone marrow from patients with myelodysplastic syndrome supports the conclusion that DNA damage dependent induction of BATF is conserved in human HSCs. Together, these results provide experimental evidence that a BATF-dependent differentiation checkpoint limits self-renewal of HSCs in response to DNA damage.dc.description.abstract
Languageendc.language.iso
PublisherUniversität Ulmdc.publisher
LicenseStandarddc.rights
Link to license texthttps://oparu.uni-ulm.de/xmlui/license_v3dc.rights.uri
Dewey Decimal GroupDDC 570 / Life sciencesdc.subject.ddc
MeSHAgingdc.subject.mesh
MeSHCell differentiationdc.subject.mesh
MeSHDNA damagedc.subject.mesh
MeSHHematopoietic stem cellsdc.subject.mesh
TitleBatf defines a differentiation checkpoint limiting hematopoietic stem cell self renewal in response to DNA damagedc.title
Resource typeDissertationdc.type
DOIhttp://dx.doi.org/10.18725/OPARU-1953dc.identifier.doi
PPN718911857dc.identifier.ppn
URNhttp://nbn-resolving.de/urn:nbn:de:bsz:289-vts-79063dc.identifier.urn
GNDBlutstammzelledc.subject.gnd
GNDDNS-Schädigungdc.subject.gnd
FacultyFakultät für Naturwissenschaftenuulm.affiliationGeneral
Date of activation2012-06-19T13:33:52Zuulm.freischaltungVTS
Peer reviewneinuulm.peerReview
Shelfmark print versionW: W-H 12.923uulm.shelfmark
DCMI TypeTextuulm.typeDCMI
VTS-ID7906uulm.vtsID
CategoryPublikationenuulm.category
University Bibliographyjauulm.unibibliographie


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