Share This Author
Estrogen receptor (ER)-beta isoforms: a key to understanding ER-beta signaling.
The premise that ER- beta1 is the obligatory partner of an ER-beta dimer, whereas the other isoforms function as variable dimer partners with enhancer activity is supported, and a single functional helix 12 in a dimer is sufficient for gene transactivation is supported.
Androgenic regulation of oxidative stress in the rat prostate: involvement of NAD(P)H oxidases and antioxidant defense machinery during prostatic involution and regrowth.
Dynamic regulation of estrogen receptor-beta expression by DNA methylation during prostate cancer development and metastasis.
Estrogen receptor (ER)-β isoforms: A key to understanding ER-β signaling
- Y. Leung, P. Mak, S. Hassan, S. Ho
- BiologyProceedings of the National Academy of Sciences
- 29 August 2006
The premise that ER-β1 is the obligatory partner of an ER- β dimer, whereas the other isoforms function as variable dimer partners with enhancer activity is supported, and a single functional helix 12 in a dimer is sufficient for gene transactivation is supported.
Estrogen receptor β2 and β5 are associated with poor prognosis in prostate cancer, and promote cancer cell migration and invasion
This is the first study to uncover a metastasis-promoting role of ERβ2 and ERβ5 in PCa, and show that the two isoforms, singularly and conjointly, have prognostic values for PCa progression.
Phosphorylation of human estrogen receptor-beta at serine 105 inhibits breast cancer cell migration and invasion
Sex-specific regulation of collagen I and III expression by 17&bgr;-Estradiol in cardiac fibroblasts: role of estrogen receptors
The mechanism underlying the sex-specific regulation of collagen I and III in the heart appears to involve E2-mediated differential ERα and ERβ signaling in CFs.
Environmental manganese exposure in residents living near a ferromanganese refinery in Southeast Ohio: a pilot study.
Overexpression of cytochrome P450 1A1 and its novel spliced variant in ovarian cancer cells: alternative subcellular enzyme compartmentation may contribute to carcinogenesis.
Data provided the first evidence that CYP1A1 overexpression and alternative splicing could contribute to ovarian cancer initiation and progression.