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The estrogen receptor cooperates with the TGF alpha receptor (c-erbB) in regulation of chicken erythroid progenitor self-renewal.

1993; Springer Nature; Volume: 12; Issue: 3 Linguagem: Inglês

10.1002/j.1460-2075.1993.tb05736.x

1460-2075

Christian Schroeder, Leonie Gibson, Camilla Nordström, Hartmut Beug,

Growth Hormone and Insulin-like Growth Factors

Research Article1 March 1993free access The estrogen receptor cooperates with the TGF alpha receptor (c-erbB) in regulation of chicken erythroid progenitor self-renewal. C. Schroeder C. Schroeder IMP, Vienna, Austria. Search for more papers by this author L. Gibson L. Gibson IMP, Vienna, Austria. Search for more papers by this author C. Nordström C. Nordström IMP, Vienna, Austria. Search for more papers by this author H. Beug H. Beug IMP, Vienna, Austria. Search for more papers by this author C. Schroeder C. Schroeder IMP, Vienna, Austria. Search for more papers by this author L. Gibson L. Gibson IMP, Vienna, Austria. Search for more papers by this author C. Nordström C. Nordström IMP, Vienna, Austria. Search for more papers by this author H. Beug H. Beug IMP, Vienna, Austria. Search for more papers by this author Author Information C. Schroeder1, L. Gibson1, C. Nordström1 and H. Beug1 1IMP, Vienna, Austria. The EMBO Journal (1993)12:951-960https://doi.org/10.1002/j.1460-2075.1993.tb05736.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info A unique combination of growth promoting factors is described that allows growth of large amounts (10(10)-10(11)) of normal erythroid progenitors from chick bone marrow. These erythroid progenitors express the estrogen receptor (ER) as well as the receptor tyrosine kinase TGF alpha R/c-erbB. They require both TGF alpha and estradiol for sustained self-renewal in vitro, but terminally differentiate upon withdrawal of TGF alpha and inactivation of the ER by an antagonist (ICI 164.384). Overexpression of the human ER in erythroblasts devoid of endogenous ER revealed that the hormone-activated ER alone arrested erythroid differentiation and repressed a large group of erythrocyte genes. When similarly overexpressed, TGF alpha R/c-erbB inhibited the expression of a distinct, but overlapping, set of genes. The endogenous ER and TGF alpha R/c-erbB affect erythrocyte gene expression in a similar, but less pronounced fashion. Surprisingly, suppression of ER function by antagonist efficiently inhibited erythroblast transformation by tyrosine kinase oncogenes, suggesting a role of the endogenous ER in leukemogenesis. We speculate that the oncogenes v-erbB and v-erbA cooperate in erythroleukemia induction by a mechanism that is employed by TGF alpha R/c-erbB and ER to regulate normal progenitor self-renewal in response to external signals. Previous ArticleNext Article Volume 12Issue 31 March 1993In this issue RelatedDetailsLoading ...