Zobrazeno 1 - 10
of 69
pro vyhledávání: '"Mahnaz Razandi"'
Publikováno v:
Molecular and Cellular Endocrinology. 434:57-68
Cardiac fibrosis evolves from the cardiac hypertrophic state. In this respect, estrogen and estrogen receptor beta (ERβ) inhibit the effects of cardiac hypertrophic peptides that also stimulate fibrosis. Here we determine details of the anti-fibroti
Publikováno v:
Pedram, A; Razandi, M; Blumberg, B; & Levin, ER. (2016). Membrane and nuclear estrogen receptor a collaborate to suppress adipogenesis but not triglyceride content. FASEB JOURNAL, 30(1), 230-240. doi: 10.1096/fj.15-274878. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/1jb8h097
Estrogen and estrogen receptor (ER)-α suppress visceral fat development through actions in several organs via unclear mechanisms that we sought to identify. Using mice that express only nuclear ER-α [nuclear-only ER-α (NOER) mice] or plasma membra
Autor:
Kenneth S. Korach, James T. Dalton, Mahnaz Razandi, Ali Pedram, Ramesh Narayanan, Ellis R. Levin
Publikováno v:
Endocrinology. 154:4352-4364
Cardiac hypertrophy in humans can progress to cardiac failure if the underlying impetus is poorly controlled. An important direct stimulator of hypertrophy and its progression is the angiotensin II (AngII) peptide. AngII also causes hypertension that
Publikováno v:
Molecular Endocrinology. 26:2058-2070
Most cancers use glucose as substrate for aerobic glycolysis in preference to oxidative phosphorylation. However, variable glucose concentrations within the in-vivo tumor microenvironment may necessitate metabolic plasticity. Furthermore, little info
Publikováno v:
Molecular Endocrinology. 24:2152-2165
Development of cardiac fibrosis portends the transition and deterioration from hypertrophy to dilation and heart failure. Here we examined how estrogen blocks this important development. Angiotensin II (AngII) and endothelin-1 induce cardiac hypertro
Autor:
Richard C.A. Sainson, Ellis R. Levin, Jin Kyung Kim, Ali Pedram, Christopher C.W. Hughes, Mahnaz Razandi
Publikováno v:
Journal of Biological Chemistry. 282:22278-22288
Multiple steroid receptors (SR) have been proposed to localize to the plasma membrane. Some structural elements for membrane translocation of the estrogen receptor alpha (ER alpha) have been described, but the mechanisms relevant to other steroid rec
Publikováno v:
Molecular Endocrinology. 20:1996-2009
Although rapid signaling by estrogen at the plasma membrane is established, it is controversial as to the nature of the receptor protein. Estrogen may bind membrane proteins comparable to classical nuclear estrogen receptors (ERs), but some studies i
Publikováno v:
Molecular Biology of the Cell. 17:2125-2137
Steroid hormones have been reported to indirectly impact mitochondrial functions, attributed to nuclear receptor-induced production of proteins that localize in this cytoplasmic organelle. Here we show high-affinity estrogen receptors in the mitochon
Publikováno v:
Journal of Biological Chemistry. 280:26339-26348
Evidence from in vivo studies suggests that some inputs to cardiac hypertrophy are opposed by the actions of estrogen. However, the mechanisms of E2 action in this respect are mainly unknown. An important pathway that is utilized by multiple hypertro
Publikováno v:
Journal of Biological Chemistry. 280:19704-19710
Estrogen has been shown to affect vascular cell and arterial function in vitro and in vivo. Here we examined the ability of estradiol (E2) to cause rapid arterial dilation of elastic and muscular arteries in vivo and the mechanisms involved. E2 admin