Difference between revisions of "Part:BBa K364307:Experience"
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In the absence of hormone, estrogen receptors are largely located in the cytosol. Hormone binding to the receptor triggers a number of events starting with migration of the receptor from the cytosol into the nucleus, dimerization of the receptor, and subsequent binding of the receptor dimer to specific sequences of DNA. Some of the effects in humans: Createing proliferative endometrium,breast cell stimulation, increased body fat and weight gain, salt and fluid retention, increased risk of blood clots. | In the absence of hormone, estrogen receptors are largely located in the cytosol. Hormone binding to the receptor triggers a number of events starting with migration of the receptor from the cytosol into the nucleus, dimerization of the receptor, and subsequent binding of the receptor dimer to specific sequences of DNA. Some of the effects in humans: Createing proliferative endometrium,breast cell stimulation, increased body fat and weight gain, salt and fluid retention, increased risk of blood clots. | ||
− | ===Potential pplications of | + | ===Potential pplications of ER DBD=== |
ER-DBD can be fused with various LBDs in order to get heterogenous composite Nuclear Receptors. With addition of the LBD's ligand the receptor can bind to Estrogen Receptor Response element and activate downstream gene expression. | ER-DBD can be fused with various LBDs in order to get heterogenous composite Nuclear Receptors. With addition of the LBD's ligand the receptor can bind to Estrogen Receptor Response element and activate downstream gene expression. | ||
Revision as of 23:15, 24 October 2010
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Physiological effects of ER
In the absence of hormone, estrogen receptors are largely located in the cytosol. Hormone binding to the receptor triggers a number of events starting with migration of the receptor from the cytosol into the nucleus, dimerization of the receptor, and subsequent binding of the receptor dimer to specific sequences of DNA. Some of the effects in humans: Createing proliferative endometrium,breast cell stimulation, increased body fat and weight gain, salt and fluid retention, increased risk of blood clots.
Potential pplications of ER DBD
ER-DBD can be fused with various LBDs in order to get heterogenous composite Nuclear Receptors. With addition of the LBD's ligand the receptor can bind to Estrogen Receptor Response element and activate downstream gene expression.
References
Dahlman-Wright K, Cavailles V, Fuqua SA, Jordan VC, Katzenellenbogen JA, Korach KS, Maggi A, Muramatsu M, Parker MG, Gustafsson JA (2006). "International Union of Pharmacology. LXIV. Estrogen receptors". Pharmacol. Rev. 58 (4): 773–81. doi:10.1124/pr.58.4.8.
Levin ER (2005). "Integration of the extranuclear and nuclear actions of estrogen". Mol. Endocrinol. 19 (8): 1951–9. doi:10.1210/me.2004-0390.
Leung YK, Mak P, Hassan S, Ho SM (August 2006). "Estrogen receptor (ER)-beta isoforms: a key to understanding ER-beta signaling". Proc Natl Acad Sci USA 103 (35): 13162–7.
Deroo BJ, Korach KS (2006). "Estrogen receptors and human disease". J. Clin. Invest. 116 (3): 561–7.
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