| pubmed-article:17090653 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17090653 | lifeskim:mentions | umls-concept:C0330390 | lld:lifeskim |
| pubmed-article:17090653 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17090653 | lifeskim:mentions | umls-concept:C0027022 | lld:lifeskim |
| pubmed-article:17090653 | lifeskim:mentions | umls-concept:C0085113 | lld:lifeskim |
| pubmed-article:17090653 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
| pubmed-article:17090653 | lifeskim:mentions | umls-concept:C1514761 | lld:lifeskim |
| pubmed-article:17090653 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:17090653 | lifeskim:mentions | umls-concept:C0205214 | lld:lifeskim |
| pubmed-article:17090653 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:17090653 | pubmed:dateCreated | 2007-2-7 | lld:pubmed |
| pubmed-article:17090653 | pubmed:abstractText | 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. | lld:pubmed |
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| pubmed-article:17090653 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17090653 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17090653 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:17090653 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17090653 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17090653 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:17090653 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:LargaespadaDa... | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:DiersMiechale... | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:WiesnerStephe... | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:KoganScott... | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:ParadaLuis... | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:ShannonKevinK | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:LeDoan TDT | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:LauchleJennif... | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:MorganKellyK | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:KimAndrewA | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:HaszDiane EDE | lld:pubmed |
| pubmed-article:17090653 | pubmed:author | pubmed-author:GeurtsJennife... | lld:pubmed |
| pubmed-article:17090653 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17090653 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:17090653 | pubmed:volume | 109 | lld:pubmed |
| pubmed-article:17090653 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17090653 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17090653 | pubmed:pagination | 1687-91 | lld:pubmed |
| pubmed-article:17090653 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:17090653 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17090653 | pubmed:articleTitle | Beta common receptor inactivation attenuates myeloproliferative disease in Nf1 mutant mice. | lld:pubmed |
| pubmed-article:17090653 | pubmed:affiliation | Department of Pediatrics, University of California San Francisco, USA. | lld:pubmed |
| pubmed-article:17090653 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17090653 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:17090653 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17090653 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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