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FRISC: The Faculty Research Interests Science Comparator |
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Assistant Professor of Internal Medicine
Cell Regulation
Office: (214) 648-4793
Building: J, Room: 6.110
Email: stephen.hammes@email.swmed.edu
Home Page: Hammes Lab
A longstanding unanswered question in the field of steroid
physiology is how steroid hormones interact with membranes to mediate presumed
nongenomic , or transcription-independent, effects. The growing list of rapid,
steroid-triggered, nongenomic signaling events includes estrogen-mediated upregulation of
nitric oxide synthase (NOS) in endothelial cells, vitamin D-induced increases in
intracellular calcium in osteosarcoma cells, and progesterone-induced maturation of frog
and fish oocytes. These steroid-induced signaling events may mediate important biological
processes such as blood vessel relaxation, bone metabolism, and fertilization.
Our laboratory uses the phenomenon of progesterone-induced
maturation, or re-entry into meiosis, of frog oocytes as a system to further characterize
the role of membranes and membrane proteins in mediating nongenomic steroid responses. In
contrast to the other processes described above, progesterone-induced oocyte maturation is
reproducible, biologically relevant, and easily measured. In addition, oocytes can be
manipulated with relative ease in vitro to study these nongenomic steroid-mediated events.
We are interested in both identifying novel steroid receptors located at the cell membrane
and further characterizing the signaling events triggered by steroids binding to these
molecules. We hope that our studies will not only give us information about
progesterone-induced processes in oocytes, but will also lead to a better understanding of
the many other fascinating nongenomic effects of steroids.
Selected Publications:
Lutz, L.B., Kim, B.E., Jahani, D., and Hammes, S.R. (2000) G Protein bg
Subunits inhibit Nongenomic Progesterone-Induced Signaling and Maturation in
Xenopus Laevis Oocytes: Evidence for a Release of Inhibition Mechanism for Cell
Cycle Progression, Journal of Biological Chemistry 275, 41512-41520.
Hammes, S.R., Shapiro, M.J., and Coughlin, S.R. (1999)
Shutoff and Agonist Triggered Internalization of Protease-Activated Receptor-1 Are
Separable by Mutation of Putative Phosphorylation Sites in the Cytoplasmic Tail, Biochemistry ,
38, 9508-9516.
Hammes, S.R. and Coughlin, S.R. (1999) Protease-Activated
Receptor-1 can Mediate Responses to SFLLRN in Thrombin-Desensitized Cells --- Evidence for
a novel mechanism for Preventing or Terminating Signaling by PAR1's Tethered Ligand, Biochemistry
38, 2486-2493.
Trejo, J., Hammes, S.R., Coughlin, S.R. (1998) Termination
of Signaling by Protease-Activated Receptor-1 is Linked to Lysosomal Targeting, Proc.
Natl. Acad.Sci. USA. 95, 13698-13702.
Page maintained by Stephanie Robertson
Last updated: 23 Jul 2001
Extraction Method: Expand using Medical Synonyms-
Eliminated words list: MedlinePlus List
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Similarity Method: Weighted keyword count
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Database: Medline abstracts (1967 - Present)
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Publication Type: All
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Score Calculation Method: Cosine Similarity Method
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Results computed on: 6/9/2006