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Titolo:
Nf1 and Gmcsf interact in myeloid leukemogenesis
Autore:
Birnbaum, RA; OMarcaigh, A; Wardak, Z; Zhang, YY; Dranoff, G; Jacks, T; Clapp, DW; Shannon, KM;
Indirizzi:
Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Indiana Univ, Sch Med, Dept Pediat, Indianapolis, IN 46202 USA Indiana Univ Indianapolis IN USA 46202 Pediat, Indianapolis, IN 46202 USA Indiana Univ, Sch Med, Herman B Wells Ctr, Indianapolis, IN 46202 USA Indiana Univ Indianapolis IN USA 46202 ls Ctr, Indianapolis, IN 46202 USA Harvard Univ, Sch Med, Dana Farber Canc Inst, Dept Adult Oncol, Boston, MA02115 USA Harvard Univ Boston MA USA 02115 t, Dept Adult Oncol, Boston, MA02115 USA MIT, Howard Hughes Med Inst, Dept Biol, Cambridge, MA 02139 USA MIT Cambridge MA USA 02139 s Med Inst, Dept Biol, Cambridge, MA 02139 USA
Titolo Testata:
MOLECULAR CELL
fascicolo: 1, volume: 5, anno: 2000,
pagine: 189 - 195
SICI:
1097-2765(200001)5:1<189:NAGIIM>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
COLONY-STIMULATING FACTOR; JUVENILE MYELOMONOCYTIC LEUKEMIA; COMMON BETA-SUBUNIT; BONE-MARROW CELLS; NEUROFIBROMATOSIS TYPE-1; SIGNAL-TRANSDUCTION; TRANSGENIC MICE; GM-CSF; RAS; GROWTH;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Shannon, KM Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143USA Univ Calif San Francisco San Francisco CA USA 94143 94143 USA
Citazione:
R.A. Birnbaum et al., "Nf1 and Gmcsf interact in myeloid leukemogenesis", MOL CELL, 5(1), 2000, pp. 189-195

Abstract

The NF1 tumor suppressor gene encodes neurofibromin, a GTPase-activating protein (GAP) for p21(ras) (Ras). Children with NF1 are predisposed to juvenile myelomonocytic leukemia (JMML). Some heterozygous Nf1 mutant mice develop a similar myeloproliferative disorder (MPD), and adoptive transfer of Nf1-deficient fetal liver cells consistently induces this MPD. Human JMML andmurine Nf1-deficient cells are hypersensitive to granulocyte-macrophage colony-stimulating factor (GM-CSF) in methylcellulose cultures. We generated hematopoietic cells deficient in both Nf1 and Gmcsf to test whether GM-CSF is required to drive excessive proliferation of Nf1(-/-) cells in vivo. Here we show that GM-CSF plays a central role in establishing and maintaining the MPD and that recipients engrafted with Nf1(-/-) Gmcsf(-/-) hematopoietic cells are hypersensitive to exogenous GM-CSF.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/05/20 alle ore 15:16:26