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dc.contributor.authorIglesias, Teresa-
dc.contributor.authorLlanos, Susana-
dc.contributor.authorLópez-Barahona, Mónica-
dc.contributor.authorRodríguez-Peña, Ángeles-
dc.contributor.authorBernal, Juan-
dc.contributor.authorSeliger, Barbara-
dc.contributor.authorMuñoz Terol, Alberto-
dc.date.accessioned2010-05-07T07:21:10Z-
dc.date.available2010-05-07T07:21:10Z-
dc.date.issued1994-07-
dc.identifier.citationCell Growth and Differentiation 5(7): 697-704 (1994)en_US
dc.identifier.issn1044-9523-
dc.identifier.urihttp://hdl.handle.net/10261/24013-
dc.description8 pages, 7 figures.-- et al.en_US
dc.description.abstractThe c-erbAa protooncogene coding for the thyroid hormone (T3) receptor (TRa1 ) and the viral, mutated v-erbA oncogene were expressed in an immortal mouse glial cell line (B3.1 ) using retroviral vedors. c-erbAa expression led to a decrease in cell proliferation in high and low serum conditions, both in the presence and in the absence of T3. In serum-free medium, c-erbAexpressing cells (B3.1 + TRa1 ) were completely arrested, whereas cells expressing v-erbA (B3.1 + v-erbA) showed a higher DNA synthesis rate than normal B3.1 cells. Although proliferation of all three cell types was stimulated by platelet-derived growth factor and basic fibroblast growth factor, differences were also observed in the response to these agents. B3.1 + TRa1 cells were more sensitive to platelet-derived growth factor than B3.1 and B3.1 + v-erbA cells. In contrast, B3.1 cells responded to basic fibroblast growth factor better than B3.1 + TRa1 or B3.1 + v-erbA cells. Insulinlike growth factor I potentiated the action of plateletderived growth factor and basic fibroblast growth factor. Again, different responses to treatment with insulin-like growth factor I alone were observed; B3.1 + TRa1 cells did not respond to it, whereas B3.1 + v-erbA cells showed a dramatic stimulation by this agent. Interestingly, in the presence of 13, the blockade in B3.1 + TRa1 cell proliferation was accompanied by the down-regulation of the typical astrocytic genes, glial fibrillary acidic protein and vimentin. These hormone effects were not found in v-erbA-expressing cells. In addition, v-erbA inhibited the basal expression of the cyclic nucleotide phosphodiesterase gene, an oligodendrocytic marker. In summary, our results show that c-erbAa inhibits cell proliferation, whereas v-erbA has the opposite effect, causing an increased cell growth. Both genes also affect distinctly gene expression in B3.1 cells. Together, these data suggest a role for erbA genes in glial cell proliferation and differentiation.en_US
dc.description.sponsorshipThis work was supported by grants from the Plan Nacional de l+D (SAF92- 0396) and Fundación Ramón Areces. T. I. was supported by a postdoctoral fellowship from the Gobierno Vasco and S. L. from the Programa de Formación del Personal Investigador del Ministerio de Educación y ciencia.en_US
dc.format.extent1573748 bytes-
dc.format.mimetypeapplication/pdf-
dc.language.isoengen_US
dc.publisherAmerican Association for Cancer Researchen_US
dc.rightsclosedAccessen_US
dc.titleC-erbA and v-erbA modulate growth and gene expression of a mouse glial precursor cell lineen_US
dc.typeartículoen_US
dc.description.peerreviewedPeer revieweden_US
dc.relation.publisherversionhttp://cgd.aacrjournals.org/cgi/content/abstract/5/7/697en_US
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