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This Article Full Text Full Text (PDF) All Versions of this Article: ERC-08-0281v1 16/2/351    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Dressing, G. E Articles by Lange, C. A Search for Related Content PubMed PubMed Citation Articles by Dressing, G. E Articles by Lange, C. A

Department of Medicine (Division of Hematology, Oncology, and Transplantation) and Pharmacology, Masonic Cancer Center, University of Minnesota, MMC 806, 420 Delaware Street, Minneapolis, Minnesota 55455, USA

(Correspondence should be addressed to C A Lange; Email: lange047{at}umn.edu)

Progesterone receptors (PR), members of the nuclear receptor superfamily, function as ligand-activated transcription factors and initiators of c-Src kinase and mitogen-activated protein kinase signaling. Bidirectional cross-talk between PR and mitogenic protein kinases results in changes in PR post-translational modification, leading to alterations in PR transcriptional activity and promoter selectivity. PR-induced rapid activation of cytoplasmic protein kinases insures precise regulatory input to downstream cellular processes that are dependent upon nuclear PR, such as cell-cycle progression, and pro-survival signaling. Here, we review interactions between PR and mitogenic protein kinases and discuss the consequences of specific post-translational modifications on PR action in breast cancer cell-line models.