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Titolo:
Defective stem cell factor expression in c-myb null fetal liver stroma
Autore:
Sicurella, C; Freeman, R; Micallef, S; Mucenski, ML; Bertoncello, I; Ramsay, RG;
Indirizzi:
Peter MacCallum Canc Inst, Differentiat & Transcript Lab, Melbourne, Vic 8006, Australia Peter MacCallum Canc Inst Melbourne Vic Australia 8006 ic 8006, Australia Childrens Hosp, Med Ctr, Div Pulm Biol, Cincinnati, OH 45229 USA ChildrensHosp Cincinnati OH USA 45229 ulm Biol, Cincinnati, OH 45229 USA
Titolo Testata:
BLOOD CELLS MOLECULES AND DISEASES
fascicolo: 2, volume: 27, anno: 2001,
pagine: 470 - 478
SICI:
1079-9796(200103)27:2<470:DSCFEI>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTO-ONCOGENE; GROWTH-FACTOR; IN-VITRO; BINDING; DIFFERENTIATION; PROTOONCOGENE; HEMATOPOIESIS; PROTEINS; TISSUES; LOCUS;
Keywords:
c-Myb; stem cell factor; stromal cells; knock-out mice;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Ramsay, RG Peter MacCallum Canc Inst, Differentiat & Transcript Lab, Locked Bag 1,A Beckett St, Melbourne, Vic 8006, Australia Peter MacCallum Canc Inst Locked Bag 1,A Beckett St Melbourne Vic Australia 8006
Citazione:
C. Sicurella et al., "Defective stem cell factor expression in c-myb null fetal liver stroma", BL CELL M D, 27(2), 2001, pp. 470-478

Abstract

High levels of c-Myb are observed in immature precursor myeloid and lymphoid cells, while downregulation of c-myb accompanies terminal differentiation to a mature phenotype, This has established c-Myb as a crucial transcription factor for hematopoiesis, Further evidence for this is the embryonic death of the c-myb homozygous mutant mouse at ED15 due to defective fetal liver erythropoiesis, Cells from fetal liver of wild-type and c-myb-/- embryoswere examined in detail for their hematopoietic potential and the capacityof the stroma to support wild-type hematopoiesis. The c-myb-/- fetal liverwas shown to harbor sevenfold fewer spleen focus-forming cells and a similarly lower number of cells with long-term repopulating capacity (high proliferative potential cells), However, shorter term repopulating cells were not substantially reduced, c-myb-/- stromal cells were unable to support the proliferation of wild-type bone marrow lineage-negative cells. This was found to be partly due to a decrease in stem cell factor (SCF) expression while partial rescue of the stromal cell cultures was achieved through the addition of exogenous SCF. DNA binding studies for two sites within the SCF promoter demonstrated an in vitro interaction between the SCF promoter and c-Myb and transient transfection studies demonstrated that c-Myb could substantially transactivate the SCF promoter in HEK293 cells. These data explain why the c-myb-/- embryos are so impaired in their ability to establish hematopoiesis. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 20:04:40