Coordination of erythropoiesis by the transcription factor c-Myb

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Coordination of erythropoiesis by the transcription factor c-Myb. / Vegiopoulos, Alexandros; Garcia, Paloma; Emambokus, M; Frampton, Jonathan.

In: Blood, Vol. 107, No. 12, 15.06.2006, p. 4703-10.

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@article{d0bf1372b8fb4ae9a8fece227741ab15,
title = "Coordination of erythropoiesis by the transcription factor c-Myb",
abstract = "The involvement of the transcription factor c-Myb in promoting the proliferation and inhibition of erythroid cell differentiation has been established in leukemia cell models. The anemia phenotype observed in c-myb knockout and knockdown mice highlights a critical role for c-Myb in erythropoiesis. However, determining the reason for the failure of erythropoiesis in these mice and the precise function of c-Myb in erythroid progenitors remains elusive. We examined erythroid development under conditions of reduced c-Myb protein levels and report an unexpected role for c-Myb in the promotion of commitment to the erythroid lineage and progression to erythroblast stages. c-myb knockdown erythroid colony-forming unit (CFU-E) stage progenitors displayed an immature phenotype and aberrant expression of several hematopoietic regulators. To extend our findings, we analyzed the response of normal enriched erythroid progenitors to inducible disruption of a floxed c-myb allele. In agreement with the c-myb knockdown phenotype, we show that c-Myb is strictly required for expression of the c-Kit receptor in erythroid cells.",
author = "Alexandros Vegiopoulos and Paloma Garcia and M Emambokus and Jonathan Frampton",
year = "2006",
month = jun,
day = "15",
doi = "10.1182/blood-2005-07-2968",
language = "English",
volume = "107",
pages = "4703--10",
journal = "Blood",
issn = "0006-4971",
publisher = "American Society of Hematology",
number = "12",

}

RIS

TY - JOUR

T1 - Coordination of erythropoiesis by the transcription factor c-Myb

AU - Vegiopoulos, Alexandros

AU - Garcia, Paloma

AU - Emambokus, M

AU - Frampton, Jonathan

PY - 2006/6/15

Y1 - 2006/6/15

N2 - The involvement of the transcription factor c-Myb in promoting the proliferation and inhibition of erythroid cell differentiation has been established in leukemia cell models. The anemia phenotype observed in c-myb knockout and knockdown mice highlights a critical role for c-Myb in erythropoiesis. However, determining the reason for the failure of erythropoiesis in these mice and the precise function of c-Myb in erythroid progenitors remains elusive. We examined erythroid development under conditions of reduced c-Myb protein levels and report an unexpected role for c-Myb in the promotion of commitment to the erythroid lineage and progression to erythroblast stages. c-myb knockdown erythroid colony-forming unit (CFU-E) stage progenitors displayed an immature phenotype and aberrant expression of several hematopoietic regulators. To extend our findings, we analyzed the response of normal enriched erythroid progenitors to inducible disruption of a floxed c-myb allele. In agreement with the c-myb knockdown phenotype, we show that c-Myb is strictly required for expression of the c-Kit receptor in erythroid cells.

AB - The involvement of the transcription factor c-Myb in promoting the proliferation and inhibition of erythroid cell differentiation has been established in leukemia cell models. The anemia phenotype observed in c-myb knockout and knockdown mice highlights a critical role for c-Myb in erythropoiesis. However, determining the reason for the failure of erythropoiesis in these mice and the precise function of c-Myb in erythroid progenitors remains elusive. We examined erythroid development under conditions of reduced c-Myb protein levels and report an unexpected role for c-Myb in the promotion of commitment to the erythroid lineage and progression to erythroblast stages. c-myb knockdown erythroid colony-forming unit (CFU-E) stage progenitors displayed an immature phenotype and aberrant expression of several hematopoietic regulators. To extend our findings, we analyzed the response of normal enriched erythroid progenitors to inducible disruption of a floxed c-myb allele. In agreement with the c-myb knockdown phenotype, we show that c-Myb is strictly required for expression of the c-Kit receptor in erythroid cells.

UR - http://www.scopus.com/inward/record.url?scp=33745061675&partnerID=8YFLogxK

U2 - 10.1182/blood-2005-07-2968

DO - 10.1182/blood-2005-07-2968

M3 - Article

VL - 107

SP - 4703

EP - 4710

JO - Blood

JF - Blood

SN - 0006-4971

IS - 12

ER -