Forskolin Stimulates Estrogen Receptor (ER) Transcriptional Activity and Protects ER from Degradation by Distinct Mechanisms.

Estradiol action is mediated by estrogen receptors (ERs), and . Estradiol binding initiates ER-mediated transcription and ER degradation, the latter of which occurs via the ubiquitin-proteasome pathway. Inhibition of proteasome activity prevents estradiol-induced ER degradation and transactivation.

Women at extreme risk for obesity-related carcinogenesis: Baseline endometrial pathology and impact of bariatric surgery on weight, metabolic profiles and quality of life.

Objectives: The study objectives were to determine baseline endometrial histology in morbidly obese women undergoing bariatric surgery and to assess the surgical intervention's impact on serum metabolic parameters, quality of life (QOL), and weight.

Methods: Women undergoing bariatric surgery were enrolled. Demographic and clinicopathologic data, serum, and endometrium (if no prior hysterectomy) were collected preoperatively and serum collected postoperatively.

A new role for wilms tumor protein 1: differential activities of + KTS and -KTS variants to regulate LHβ transcription.

Luteinizing hormone (LH) is synthesized and secreted throughout the reproductive cycle from gonadotrope cells in the anterior pituitary, and is required for steroidogenesis and ovulation. LH contains an α-subunit common with FSH, and a unique LHβ subunit that defines biological activity. Basal LHβ transcription is low and stimulated by hypothalamic GnRH, which induces synthesis of early growth response protein-1 (Egr1), and stimulates binding of transcription factors Egr1 and steroidogenic factor-1 (SF1) on the promoter.

Estrogen modulation of endosome-associated toll-like receptor 8: an IFNα-independent mechanism of sex-bias in systemic lupus erythematosus.

Females of child-bearing age are more resistant to infectious disease and have an increased risk of systemic lupus erythematosus (SLE). We hypothesized that estrogen-induced gene expression could establish an immunoactivated state which would render enhanced defense against infection, but may be deleterious in autoimmune development. Using peripheral blood mononuclear cells (PBMCs), we demonstrate enhanced responses with immunogen stimulation in the presence of 17β-estradiol (E2) and gene array analyses reveal toll-like receptor 8 (TLR8) as an E2-responsive candidate gene.

AMP-activated protein kinase is a key intermediary in GnRH-stimulated LHβ gene transcription.

GnRH regulation of pituitary gonadotropin gene transcription is critical for fertility, and metabolic dysregulation is associated with reproductive disorders and altered hypothalamic-pituitary responses. Here, we examined signaling pathways in gonadotropes through which GnRH modulates gonadotropin levels, and potential common signaling pathways with insulin. Using LβT2 cells, we show that GnRH rapidly (5 minutes) triggers activating phosphorylation of AMP-activated protein kinase (AMPK) up to 5-fold; this stimulation is enhanced by insulin through increased total AMPKα levels and activity.