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Titolo:
ERYTHROPOIETIN RECEPTOR AND STAT5-SPECIFIC PATHWAYS PROMOTE SKT6 CELLHEMOGLOBINIZATION
Autore:
GREGORY RC; JIANG N; TODOKORO K; CROUSE J; PACIFICI RE; WOJCHOWSKI DM;
Indirizzi:
PENN STATE UNIV,DEPT BIOCHEM & MOL BIOL,CTR GENE REGULAT,GRAD PROGRAMGENET UNIVERSITY PK PA 16802 PENN STATE UNIV,DEPT BIOCHEM & MOL BIOL,CTR GENE REGULAT,GRAD PROGRAMGENET UNIVERSITY PK PA 16802 PENN STATE UNIV,DEPT VET SCI UNIVERSITY PK PA 16802 AMGEN INC THOUSAND OAKS CA 91320 INST PHYS & CHEM RES,TSUKUBA LIFE SCI CTR TSUKUBA IBARAKI 305 JAPAN
Titolo Testata:
Blood
fascicolo: 4, volume: 92, anno: 1998,
pagine: 1104 - 1118
SICI:
0006-4971(1998)92:4<1104:ERASPP>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
ERYTHROID PROGENITOR CELLS; SIGNAL-TRANSDUCTION; C-KIT; STAT5 ACTIVATION; COLONY FORMATION; DNA-BINDING; FACTOR-I; DIFFERENTIATION; PROLIFERATION; MOUSE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
63
Recensione:
Indirizzi per estratti:
Citazione:
R.C. Gregory et al., "ERYTHROPOIETIN RECEPTOR AND STAT5-SPECIFIC PATHWAYS PROMOTE SKT6 CELLHEMOGLOBINIZATION", Blood, 92(4), 1998, pp. 1104-1118

Abstract

Erythrocyte production in mammals is known to depend on the exposure of committed progenitor cells to the glycoprotein hormone erythropoietin (Epo), In chimeric mice, gene disruption experiments have demonstrated a critical role for Epo signaling in development beyond the erythroid colony-forming unit (CFU-e) stage. However, whether this might include the possible Epo-specific induction of red blood cell differentiation events is largely unresolved. To address this issue, mechanisms of induced globin expression in Eporesponsive SKT6 cells have been investigated. Chimeric receptors containing an epidermal growth factor (EGF) receptor extracellular domain and varied Epo receptor cytoplasmic domains first were expressed stably at physiological levels in SKT6 cells, and their activities in mediating induced hemoglobinization were assayed. While activity was exerted by a full-length chimera (EE483), truncation to remove 7 of 8 carboxyl-terminal tyrosine sites (EE372) markedly enhanced differentiation signaling. Moreover, mutation of a STATE binding site in this construct (EE372-Y343F) inhibited induced globin expression and SKT6 cell hemoglobinization, as did the ectopic expression of dominant-negative forms of STAT5 in parental SKT6 cells. As in normal CFU-e, SKT6 cells also were shown to express functional receptors for stem cell factor (SCF), To further define possible specific requirements for differentiation signaling, effects of SCF on SKT6 cell hemoglobinization were tested, Interestingly, SCF not only failed topromote globin expression but inhibited this Epo-induced event in a dose-dependent, STAT5-independent fashion. Thus, effects of Epo on globin expression may depend specifically on STAT5-dependent events, and SCF normally may function to attenuate terminal differentiation while promoting CFU-e expansion. (C) 1998 by The American Society of Hematology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 23:47:48