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http://purl.uniprot.org/citations/17090653http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17090653http://www.w3.org/2000/01/rdf-schema#comment"Neurofibromatosis type 1 (NF1) syndrome is caused by germline mutations in the NF1 tumor suppressor, which encodes neurofibromin, a GTPase activating protein for Ras. Children with NF1 are predisposed to juvenile myelomonocytic leukemia (JMML) and lethally irradiated mice given transplants with homozygous Nf1 mutant (Nf1-/-) hematopoietic stem cells develop a fatal myeloproliferative disorder (MPD) that models JMML. We investigated the requirement for signaling through the GM-CSF receptor to initiate and sustain this MPD by generating Nf1 mutant hematopoietic cells lacking the common beta chain (Beta c) of the GM-CSF receptor. Mice reconstituted with Nf1-/-, beta c-/-stem cells did not develop evidence of MPD despite the presence of increased number of immature hematopoietic progenitors in the bone marrow. Interestingly, when the Mx1-Cre transgene was used to inactivate a conditional Nf1 mutant allele in hematopoietic cells, concomitant loss of beta c-/-reduced the severity of the MPD, but did not abrogate it. Whereas inhibiting GM-CSF signaling may be of therapeutic benefit in JMML, our data also demonstrate aberrant proliferation of Nf1-/-myeloid progenitors that is independent of signaling through the GM-CSF receptor."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.org/dc/terms/identifier"doi:10.1182/blood-2006-05-025395"xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Kim A."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Largaespada D.A."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Morgan K."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Wiesner S.M."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Le D.T."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Kogan S.C."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Shannon K."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Lauchle J.O."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Hasz D.E."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Parada L.F."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Geurts J.L."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/author"Diers M.D."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/date"2007"xsd:gYear
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/name"Blood"xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/pages"1687-1691"xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/title"Beta common receptor inactivation attenuates myeloproliferative disease in Nf1 mutant mice."xsd:string
http://purl.uniprot.org/citations/17090653http://purl.uniprot.org/core/volume"109"xsd:string
http://purl.uniprot.org/citations/17090653http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/17090653
http://purl.uniprot.org/citations/17090653http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/17090653
http://purl.uniprot.org/uniprot/#_A0A2R8VHF2-mappedCitation-17090653http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17090653
http://purl.uniprot.org/uniprot/#_A0A1W2P863-mappedCitation-17090653http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17090653
http://purl.uniprot.org/uniprot/#_A0A2R8VK01-mappedCitation-17090653http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/17090653