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REVIEW |
G Dressing, Medicine and Pharmacology, University of Minnesota, Minneapolis, United States
C Hagan, Medicine and Pharmacology, University of Minnesota, Minneapolis, United States
T Knutson, Medicine and Pharmacology, University of Minnesota, Minneapolis, United States
A Daniel, Medicine and Pharmacology, University of Minnesota, Minneapolis, United States
C Lange, Medicine and Pharmacology, University of Minnesota, Minneapolis, United States
Correspondence: Gwen Dressing, Email: dress088{at}umn.edu
Abstract
Progesterone receptors (PR), members of the nuclear receptor superfamily, function as ligand-activated transcription factors and initiators of c-Src and mitogen activated protein kinase (MAPK) signaling. Bi-directional 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.
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