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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Trouche, D. Articles by Harel-Bellan, A. Search for Related Content PubMed PubMed Citation Articles by Trouche, D. Articles by Harel-Bellan, A. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  The dyad symmetry element is the molecular target for c-fos induction and inhibition during K 562 differentiation along mutually exclusive lineages D Trouche, P Robin, P Sassone-Corsi, WL Farrar and A Harel-Bellan Laboratoire d'Immunologie, CNRS URA 1156, Institut Gustave Roussy, Villejuif, France. The c-fos proto-oncogene seems to play an important role during differentiation and activation of cells from the hematopoietic lineage. Therefore, it is of interest to investigate the mechanism underlying its transcriptional activation in these cells. To delineate the sequences and factors involved in c-fos transcriptional activation during the course of myeloid cell differentiation, we have used the K 562 chronic leukemic cell line as a model. K 562 cells were transfected with chloramphenicol transacetylase (CAT) reporter constructs, including various regions of the human c-fos promoter, and induced to differentiate by two distinct agents: 12-O-tetradecanoyl phorbol-13- acetate (TPA), which activates a differentiation program along the megakaryoblastic pathway; and hemin, which induces erythroid differentiation. We show here that TPA treatment of K 562 cells induces fos CAT reporter constructs activation, whereas treatment with hemin does not. Furthermore, predifferentiation of the cells with hemin blocks a subsequent induction by TPA, in correlation with the inhibition by hemin of megakaryoblastic differentiation markers appearance. Both the induction by TPA and the inhibition by hemin are mediated by a dyad symmetry element (DSE) located in the upstream regulatory region, between -318 and -296. These results suggest that the protein complex binding to the DSE regulatory element is the target for c-fos activation by TPA and inhibition by hemin in K 562 cells. However, no modulation of protein affinity for the DSE sequence was detected by gel shift assay during the course of induction or inhibition, suggesting that the structural change responsible for the transcriptional modulation is too unstable or too subtle to be detected by this method. Volume 77, Issue 1, pp. 55-63, 01/01/1991 Copyright © 1991 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. M. Zutter, A. D. Painter, and X. Yang The Megakaryocyte/Platelet-Specific Enhancer of the alpha 2beta 1 Integrin Gene: Two Tandem AP1 Sites and the Mitogen-Activated Protein Kinase Signaling Cascade Blood, March 1, 1999; 93(5): 1600 - 1611. [Abstract] [Full Text] [PDF]

	Copyright © 1991 by American Society of Hematology         Online ISSN: 1528-0020