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Titolo:
Erythropoiesis in the absence of janus-kinase 2: BCR-ABL induces red cell formation in JAK2(-/-) hematopoietic progenitors
Autore:
Ghaffari, S; Kitidis, C; Fleming, MD; Neubauer, H; Pfeffer, K; Lodish, HF;
Indirizzi:
Whitehead Inst Biomed Res, Cambridge, MA 02142 USA Whitehead Inst Biomed Res Cambridge MA USA 02142 Cambridge, MA 02142 USA MIT, Cambridge, MA 02139 USA MIT Cambridge MA USA 02139MIT, Cambridge, MA 02139 USA Harvard Univ, Sch Med, Boston, MA USA Harvard Univ Boston MA USAHarvard Univ, Sch Med, Boston, MA USA Childrens Hosp, Dept Pathol, Boston, MA USA Childrens Hosp Boston MA USAChildrens Hosp, Dept Pathol, Boston, MA USA Tech Univ Munich, D-8000 Munich, Germany Tech Univ Munich Munich GermanyD-8000 iv Munich, D-8000 Munich, Germany
Titolo Testata:
BLOOD
fascicolo: 10, volume: 98, anno: 2001,
pagine: 2948 - 2957
SICI:
0006-4971(20011115)98:10<2948:EITAOJ>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHRONIC MYELOGENOUS LEUKEMIA; ACUTE LYMPHOBLASTIC-LEUKEMIA; BCR/ABL-TRANSFORMED CELLS; DNA-BINDING ACTIVITY; TYROSINE KINASE; SH2 DOMAIN; PHOSPHATIDYLINOSITOL 3-KINASE; DEFINITIVE HEMATOPOIESIS; TRANSCRIPTION FACTOR; SIGNAL-TRANSDUCTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Lodish, HF Whitehead Inst Biomed Res, 9 Cambridge Ctr, Cambridge, MA 02142USA Whitehead Inst Biomed Res 9 Cambridge Ctr Cambridge MA USA 02142
Citazione:
S. Ghaffari et al., "Erythropoiesis in the absence of janus-kinase 2: BCR-ABL induces red cell formation in JAK2(-/-) hematopoietic progenitors", BLOOD, 98(10), 2001, pp. 2948-2957

Abstract

The receptor-associated protein tyrosine kinase janus-kinase 2 (JAK2) is essential for normal red cell development and for erythropoietin receptor (EpoR) signaling. JAK2(-/-) embryos are severely deficient in erythropoiesis and die at an early stage of development from fetal anemia. The binding of erythropoietin (Epo) to the EpoR triggers the activation of JAK2, the phosphorylation of the EpoR, and the initiation of the EpoR signaling cascade. In addition to Epo binding to its receptor, signaling pathways downstream ofthe EpoR can also be stimulated by the BCR-ABL oncoprotein. This study explored whether JAK2 is required for BCR-ABL-mediated stimulation of erythropoiesis. Here, it is shown that JAK2 is constitutively tyrosine phosphorylated in cultured and primary erythroid cells expressing BCR-ABL. However, BCR-ABL effectively supports normal erythroid proliferation, differentiation, and maturation in JAK2-deficient fetal liver cells. Using mutants of SCR-ABL, this study shows that certain signaling pathways activated by BCR-ABL segments distinct from its tyrosine kinase domain are essential for rescue oferythropoiesis in JAK2(-/-) progenitors. The consequences of these multiple signaling pathways for normal erythroid development are discussed. (C) 2001 by The American Society of Hematology.

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Documento generato il 04/04/20 alle ore 02:58:51