| | | |
| | |
| |
Speaker
| | Carol Lange, Professor of Medicine and Pharmacology, University of Minnesota Masonic Cancer Center |
| | | | |
| | Date | | Oct 19, 2009 |
| | | | |
| | Time | | 12:00 pm
|
| | | | |
| | Location | | Room 1000 Micro and Nano Laboratory, 208 N. Wright St., Urbana, IL |
| | | | |
| | Sponsor | | College of Veterinary Medicine and Division of Biomedical Sciences |
| | | | |
| | Contact | | Nikki Hausmann |
| | | | |
| | E-Mail | | nhausman@illinois.edu |
| | | | |
| | Phone | | (217) 333-4291 |
| | | | |
| | Event type | | Seminar |
| | | | |
| | Views | | 771 |
| | | | |
|
|
| |
| |
| Recent discoveries suggest that protein kinases are rapidly activated in response to ligand binding to cytoplasmic steroid hormone receptors (SRs), including progesterone receptors (PRs). Thus, PRs act as ligand-activated transcription factor sensors for growth factor-initiated signaling pathways in hormonally regulated tissues, such as the breast. Induction of rapid signaling upon progestin binding to PR-B provides a means to ensure that receptors and co-regulators are appropriately phosphorylated as part of optimal transcription complexes at selected gene promoters. For example, an important consequence of direct phosphorylation of PR Ser345 includes PR tethering to SP1, a transcription factor mediator of progestin action at SP1-regulated genes. Additionally, Ser294 phosphorylated receptors are under-sumoylated and de-repressed at selected SUMO-sensitive promoters, thereby able to regulate PR target genes independently of steroid hormones. Ligand-independent regulation of growth regulatory genes by phosphorylated PRs explains why breast cancer models often remain relatively insensitive to PR agonists, but are growth-inhibited by anti-progestins. Kinases are emerging as key mediators of PR action. Cross-talk between SR and membrane-initiated signaling events suggests a mechanism for coordinate regulation of gene subsets by mitogenic stimuli in hormonally responsive normal tissues, and is suspected to contribute to cancer biology. |
| |
| |
|
|
