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Titolo:
Abnormal stat activation, hematopoietic homeostasis, and innate immunity in c-fes(-/-) mice
Autore:
Hackenmiller, R; Kim, J; Feldman, RA; Simon, MC;
Indirizzi:
Univ Chicago, Comm Genet, Chicago, IL 60637 USA Univ Chicago Chicago IL USA 60637 cago, Comm Genet, Chicago, IL 60637 USA Univ Chicago, Howard Hughes Med Inst, Chicago, IL 60637 USA Univ Chicago Chicago IL USA 60637 Hughes Med Inst, Chicago, IL 60637 USA Univ Maryland, Sch Med, Dept Microbiol & Immunol, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 l & Immunol, Baltimore, MD 21201 USA
Titolo Testata:
IMMUNITY
fascicolo: 3, volume: 13, anno: 2000,
pagine: 397 - 407
SICI:
1074-7613(200009)13:3<397:ASAHHA>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
COLONY-STIMULATING FACTOR; PROTEIN-TYROSINE KINASE; FES-RELATED PROTEIN; C-FOS PROMOTER; MYELOID DIFFERENTIATION; PROTOONCOGENE PRODUCT; SIGNAL-TRANSDUCTION; BINDING PROTEINS; CELL-POPULATIONS; TRANSGENIC MICE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Simon, MC Univ Chicago, Comm Genet, Chicago, IL 60637 USA Univ Chicago Chicago IL USA 60637 Genet, Chicago, IL 60637 USA
Citazione:
R. Hackenmiller et al., "Abnormal stat activation, hematopoietic homeostasis, and innate immunity in c-fes(-/-) mice", IMMUNITY, 13(3), 2000, pp. 397-407

Abstract

The c-fes protooncogene encodes a nonreceptor tyrosine kinase (Fes) implicated in cytokine receptor signal transduction, neutrophil survival, and myeloid differentiation. To determine the role of Fes in embryonic developmentand hematopoiesis, we engineered a null mutation of the murine c-fes locus. c-fes(-/-) mice are viable but not born in the expected Mendelian ratios. Live born c-fes(-/-) mice exhibit lymphoid/myeloid homeostasis defects, compromised innate immunity, and increased Stat activation in response to GM-CSF and IL-6 signaling. Therefore, increased cytokine responsiveness in theabsence of Fes leads to abnormal myeloid proliferation and functional defects in the macrophage lineage.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/09/20 alle ore 10:13:02