RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/20826722http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20826722http://www.w3.org/2000/01/rdf-schema#comment"Progressive bone marrow failure is a major cause of morbidity and mortality in human Fanconi Anemia patients. In an effort to develop a Fanconi Anemia murine model to study bone marrow failure, we found that Fancd2(-/-) mice have readily measurable hematopoietic defects. Fancd2 deficiency was associated with a significant decline in the size of the c-Kit(+)Sca-1(+)Lineage(-) (KSL) pool and reduced stem cell repopulation and spleen colony-forming capacity. Fancd2(-/-) KSL cells showed an abnormal cell cycle status and loss of quiescence. In addition, the supportive function of the marrow microenvironment was compromised in Fancd2(-/-) mice. Treatment with Sirt1-mimetic and the antioxidant drug, resveratrol, maintained Fancd2(-/-) KSL cells in quiescence, improved the marrow microenvironment, partially corrected the abnormal cell cycle status, and significantly improved the spleen colony-forming capacity of Fancd2(-/-) bone marrow cells. We conclude that Fancd2(-/-) mice have readily quantifiable hematopoietic defects, and that this model is well suited for pharmacologic screening studies."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.org/dc/terms/identifier"doi:10.1182/blood-2010-04-278226"xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Grompe M."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Fleming W.H."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Goldman D.C."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Bagby G.C."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Duncan A.W."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Zhang Q.S."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Rathbun R.K."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Eaton L."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Anur P."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Marquez-Loza L."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/author"Watanabe-Smith K."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/name"Blood"xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/pages"5140-5148"xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/title"Fancd2-/- mice have hematopoietic defects that can be partially corrected by resveratrol."xsd:string
http://purl.uniprot.org/citations/20826722http://purl.uniprot.org/core/volume"116"xsd:string
http://purl.uniprot.org/citations/20826722http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20826722
http://purl.uniprot.org/citations/20826722http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/20826722
http://purl.uniprot.org/uniprot/#_A0A0N4SV29-mappedCitation-20826722http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20826722
http://purl.uniprot.org/uniprot/#_A0A0N4SVS0-mappedCitation-20826722http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20826722
http://purl.uniprot.org/uniprot/#_E9QAE8-mappedCitation-20826722http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20826722
http://purl.uniprot.org/uniprot/#_E0CYC3-mappedCitation-20826722http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20826722