Looking for online definition of ubiquitin carboxyl-terminal hydrolase 33 in the Medical Dictionary? ubiquitin carboxyl-terminal hydrolase 33 explanation free. What is ubiquitin carboxyl-terminal hydrolase 33? Meaning of ubiquitin carboxyl-terminal hydrolase 33 medical term. What does ubiquitin carboxyl-terminal hydrolase 33 mean?
Looking for online definition of 41-kDa ubiquitin-specific protease in the Medical Dictionary? 41-kDa ubiquitin-specific protease explanation free. What is 41-kDa ubiquitin-specific protease? Meaning of 41-kDa ubiquitin-specific protease medical term. What does 41-kDa ubiquitin-specific protease mean?
Discovery of LSZ102, a Potent, Orally Bioavailable Selective Estrogen Receptor Degrader (SERD) for the Treatment of Estrogen Receptor Positive Breast Cancer. Abstract: The estrogen receptor (ER) is a nuclear hormone receptor that regulates a variety of genes which promote both cell proliferation and cell cycle progression. In the clinical setting ER positive breast cancer accounts for approximately 2/3 of all breast cancer diagnoses. Anti-estrogen therapies, such as selective estrogen receptor modulators (SERMs) and aromatase inhibitors (AI), are the core treatment modalities in patients with ER positive breast cancer. Although a large proportion of patients respond positive to endocrine therapy, resistance to these drug treatments remains an impediment to durable clinical response. Selective estrogen receptor degraders (SERDs) that remove the receptor have been shown to be effective in this setting. We describe the discovery of LSZ102, a potent, orally available SERD found to inhibit ER ...
HERS was a well-designed clinical trial of combined HRT for secondary prevention of CHD in postmenopausal women with a uterus. Most previous studies were observational and suggested that HRT was associated with a ≥ 50% reduction in cardiovascular events (1). However, the protective benefits of HRT may have been overestimated because women who receive HRT may have other healthy behaviors (2). One other major trial of HRT, the Postmenopausal Estrogen/Progestin Interventions (PEPI) trial, examined the surrogate outcome of risk factor changes rather than disease events and found that HRT improved the lipid profile (3). The effects on high-density lipoprotein cholesterol levels differed by treatment regimen. The regimen used in HERS, estrogen plus medroxyprogesterone acetate (E+MPA), elevated HDL cholesterol levels less effectively than did estrogen alone or estrogen plus micronized progesterone. Therefore, less benefit from E+MPA on coronary events might have been expected. HERS found no benefit ...
The classical estrogen receptors, estrogen receptor -α- and estrogen receptor β, are well established in the regulation of body weight and energy homeostasis in both male and female mice, whereas, the role for a G protein-coupled estrogen receptor 1 (GPER) as a modulator of energy homeostasis remains controversial. This study sought to determine whether gene deletion of GPER (GPER KO) alters body weight, body adiposity, food intake, and energy homeostasis in both males and females. Male mice lacking GPER developed moderate obesity and larger adipocyte size beginning at 8 weeks of age, with significant reductions in energy expenditure, but not food intake or adipocyte number. Female GPER KO mice developed increased body weight relative to WT females a full 6 weeks later than the male GPER KO mice. Female GPER KO mice also had reductions in energy expenditure, but not significant increases in body fat content. Consistent with their decrease in energy expenditure, GPER KO males and females showed ...
Endogenous estrogens mediate protective effects in the cardiovascular system in part due to rapid activation of endothelial nitric oxide synthase (eNOS), which involves the classical estrogen receptor (ER) α. Estrogen-dependent increases in NO bioactivity may also be mediated by the G protein-coupled estrogen receptor (GPER/GPR30), although the contribution of GPER to the overall response to estrogen and the mechanisms involved remain unclear. We have investigated GPER-mediated NO signaling in telomerase-immortalized human umbilical vein endothelial (TIVE) cells as well as estrogen-dependent, GPER-mediated relaxation in mouse aortae. Similar to the non-selective ER agonist 17β-estradiol (E2), the GPER-selective agonist G-1 stimulated phosphorylation of eNOS (ser1171) at 100 nM vs. 0.01% DMSO vehicle (53 +/-7 vs. 19+/-4, p=0.035, n=4). Colorimetric detection of nitric oxide demonstrated that Acetylcholine (Ach) (536 +/-18), E2 (425+/- 18) and G-1 (308 +/-18) also increased NO production in ...
Looking for online definition of Conjugated estrogens in the Medical Dictionary? Conjugated estrogens explanation free. What is Conjugated estrogens? Meaning of Conjugated estrogens medical term. What does Conjugated estrogens mean?
Ubiquitin carboxyl-terminal hydrolase 6 is an enzyme that in humans is encoded by the USP6 gene. Aneurysmal bone cyst can be associated with a TRE17/USP6 translocation. GRCh38: Ensembl release 89: ENSG00000129204 - Ensembl, May 2017 "Human PubMed Reference:". Puente XS, Sanchez LM, Overall CM, Lopez-Otin C (Jul 2003). "Human and mouse proteases: a comparative genomic approach". Nat Rev Genet. 4 (7): 544-58. doi:10.1038/nrg1111. PMID 12838346. Hoogendijk JE, Hensels GW, Gabreels-Festen AA, Gabreels FJ, Janssen EA, de Jonghe P, Martin JJ, van Broeckhoven C, Valentijn LJ, Baas F, et al. (May 1992). "De-novo mutation in hereditary motor and sensory neuropathy type I". Lancet. 339 (8801): 1081-2. doi:10.1016/0140-6736(92)90668-S. PMID 1349106. "Entrez Gene: USP6 ubiquitin specific peptidase 6 (Tre-2 oncogene)". Ye Y, Pringle LM, Lau AW, et al. (June 2010). "TRE17/USP6 oncogene translocated in aneurysmal bone cyst induces matrix metalloproteinase production via activation of NFκB". Oncogene. 29 (25): ...
TRAF [TNF (tumour necrosis factor)-receptor-associated factor] 2 and 6 are essential adaptor proteins for the NF-κB (nuclear factor κB) signalling pathway, which play important roles in inflammation and immune response. Polyubiquitination of TRAF2 and TRAF6 is critical to their activities and functions in TNFα- and IL (interleukin)-1β-induced NF-κB activation. However, the regulation of TRAF2 and TRAF6 by deubiquitination remains incompletely understood. In the present study, we identified USP (ubiquitin-specific protease) 4 as a novel deubiquitinase targeting TRAF2 and TRAF6 for deubiquitination. We found that USP4 specifically interacts with TRAF2 and TRAF6, but not TRAF3. Moreover, USP4 associates with TRAF6 both in vitro and in vivo, independent of its deubiquitinase activity. The USP domain is responsible for USP4 to interact with TRAF6. Ectopic expression of USP4 inhibits the TRAF2- and TRAF6-stimulated NF-κB reporter gene and negatively regulates the TNFα-induced IκBα (inhibitor ...
PubMed Central Canada (PMC Canada) provides free access to a stable and permanent online digital archive of full-text, peer-reviewed health and life sciences research publications. It builds on PubMed Central (PMC), the U.S. National Institutes of Health (NIH) free digital archive of biomedical and life sciences journal literature and is a member of the broader PMC International (PMCI) network of e-repositories.
The results presented here demonstrate that p53 upregulates estrogen receptor-alpha (ER alpha) expression in the human breast cancer cell line MCF-7. Two approaches were used to alter the activity of p53 in the cells. In the first approach, stable transfectants expressing an antisense p53 were established. In the stable clones, expression of antisense p53 resulted in a decrease in the expression of ER alpha protein. In the second approach, MCF-7 cells were transiently transfected with wild-type p53. Overexpression of p53 increased the amount of ER alpha. To determine whether the effects of p53 on the expression of ER alpha were due to changes in transcription, deletion mutants of the ER alpha promoter were used. This experimental approach demonstrated that p53 up-regulates ER alpha gene expression by increasing transcription of the gene through elements located upstream of promoter A. Transfection assays using p53 mutants further demonstrated that the p53-induced increase in ER alpha gene ...
The ligand binding domain of estrogen receptor and estrogen receptor-related receptors. The ligand binding domain of estrogen receptor (ER) and estrogen receptor-related receptors (ERRs): Estrogen receptors are a group of receptors which are activated by the hormone estrogen. Estrogen regulates many physiological processes including reproduction, bone integrity, cardiovascular health, and behavior. The main mechanism of action of the estrogen receptor is as a transcription factor by binding to the estrogen response element of target genes upon activation by estrogen and then recruiting coactivator proteins which are responsible for the transcription of target genes. Additionally some ERs may associate with other membrane proteins and can be rapidly activated by exposure of cells to estrogen. ERRs are closely related to the estrogen receptor (ER) family. But, it lacks the ability to bind estrogen. ERRs can interfere with the classic ER-mediated estrogen signaling pathway, positively or ...
BACKGROUND: The causes of prostate cancer are poorly understood, but genetic factors may be more important than for many other malignancies, and dietary phytoestrogens may be protective. Because phytoestrogens bind tightly to the estrogen receptor-beta, we conducted an epidemiologic investigation of synergistic effects between phytoestrogen intake and estrogen receptor-beta gene polymorphisms. METHODS: We performed a population-based case-control study in Sweden. All participants reported their phytoestrogen intake and donated a blood sample. We identified four haplotype-tagging single nucleotide polymorphisms (htSNPs) and genotyped these htSNPs in 1314 prostate cancer patients and 782 controls. Odds ratios were estimated by multivariate logistic regression. Interactions between phytoestrogen intake and estrogen receptor-beta SNPs on prostate cancer risk were evaluated considering both multiplicative and additive effect scales. RESULTS: We found a significant multiplicative interaction (P = ...
Sales, means the sales volume of Selective Estrogen Receptor Modulator Revenue, means the sales value of Selective Estrogen Receptor Modulator This report studies sales (consumption) of Selective Estrogen Receptor Modulator in United States market, focuses on the top players, with sales, price, revenue and market share for each player, covering Pfizer Inc. (USA) Abbott Laboratories (USA)
NEW YORK & SAN DIEGO-- Pfizer Inc. (NYSE: PFE) and Ligand Pharmaceuticals Incorporated (NASDAQ: LGND) today announced that the United States Food and Drug Administration (FDA) accepted for review a New Drug Application (NDA) for bazedoxifene/conjugated estrogens (BZA/CE), a potential new medicine for non-hysterectomized women for the treatment of moderate-to-severe vasomotor symptoms (VMS) and vulvar and vaginal atrophy (VVA) associated with menopause, as well as the prevention of postmenopausal osteoporosis. The FDA Prescription Drug User Fee Act (PDUFA) date is October 3, 2013. BZA/CE pairs the selective estrogen receptor modulator (SERM) bazedoxifene with conjugated estrogens. BZA/CE has been studied in a Phase III clinical development program (Selective estrogens, Menopause And Response to Therapy [SMART] trials), which included approximately 7,500 postmenopausal women and assessed the safety and efficacy of BZA/CE for the treatment of moderate-to-severe VMS and VVA associated with ...
Summary Two polymorphisms of the aromatase and estrogen receptor genes appeared to interact to influence the risk of hip fractures in women. Introduction Allelic variants of the aromatase gene have been associated with bone mineral density and vertebral fractures. Our objective was to analyze the relationship between two polymorphisms of the aromatase and estrogen receptor genes and hip ...
Adult Solid Tumor Adenocarcinoma of the Colon Adenocarcinoma of the Rectum Adult Central Nervous System Germ Cell Tumor Adult Teratoma Benign Teratoma Estrogen Receptor-negative Breast Cancer Estrogen Receptor-positive Breast Cancer Familial Testicular Germ Cell Tumor HER2-negative Breast Cancer HER2-positive Breast Cancer Male Breast Cancer Ovarian Immature Teratoma Ovarian Mature Teratoma Ovarian Monodermal and Highly Specialized Teratoma Progesterone Receptor-negative Breast Cancer Progesterone Receptor-positive Breast Cancer Recurrent Breast Cancer Recurrent Colon Cancer Recurrent Extragonadal Germ Cell Tumor Recurrent Extragonadal Non-seminomatous Germ Cell Tumor Recurrent Extragonadal Seminoma Recurrent Malignant Testicular Germ Cell Tumor Recurrent Melanoma Recurrent Ovarian Germ Cell Tumor Recurrent Rectal Cancer Stage III Extragonadal Non-seminomatous Germ Cell Tumor Stage III Extragonadal Seminoma Stage III Malignant Testicular Germ Cell Tumor Stage III Ovarian Germ Cell Tumor Stage IV ...
Description of disease ERT (estrogen replacement therapy). Treatment ERT (estrogen replacement therapy). Symptoms and causes ERT (estrogen replacement therapy) Prophylaxis ERT (estrogen replacement therapy)
Status: Recruiting. Condition Summary: Adult Solid Tumor; Adenocarcinoma of the Colon; Adenocarcinoma of the Rectum; Adult Central Nervous System Germ Cell Tumor; Adult Teratoma; Benign Teratoma; Estrogen Receptor-negative Breast Cancer; Estrogen Receptor-positive Breast Cancer; Familial Testicular Germ Cell Tumor; HER2-negative Breast Cancer; HER2-positive Breast Cancer; Male Breast Cancer; Ovarian Immature Teratoma; Ovarian Mature Teratoma; Ovarian Monodermal and Highly Specialized Teratoma; Progesterone Receptor-negative Breast Cancer; Progesterone Receptor-positive Breast Cancer; Recurrent Breast Cancer; Recurrent Colon Cancer; Recurrent Extragonadal Germ Cell Tumor; Recurrent Extragonadal Non-seminomatous Germ Cell Tumor; Recurrent Extragonadal Seminoma; Recurrent Malignant Testicular Germ Cell Tumor; Recurrent Melanoma; Recurrent Ovarian Germ Cell Tumor; Recurrent Rectal Cancer; Stage III Extragonadal Non-seminomatous Germ Cell Tumor; Stage III Extragonadal Seminoma; Stage III Malignant ...
Looking for online definition of Deubiquitinating enzyme 46 in the Medical Dictionary? Deubiquitinating enzyme 46 explanation free. What is Deubiquitinating enzyme 46? Meaning of Deubiquitinating enzyme 46 medical term. What does Deubiquitinating enzyme 46 mean?
What are Esterified Estrogens and Methyltestosterone Tablets and Esterified Estrogens and Methyltestosterone Tablets H.S.? Esterified Estrogens and Methyltestosterone Tablets and Esterified Estrogens and Methyltestosterone Tablets H.S. are medicines that contain estrogen and androgen hormones.. What are Esterified Estrogens and Methyltestosterone Tablets and Esterified Estrogens and Methyltestosterone Tablets H.S. used for? Esterified Estrogens and Methyltestosterone Tablets and Esterified Estrogens and Methyltestosterone Tablets H.S. are used after menopause to:. • reduce moderate to severe hot flashes. Estrogens are hormones made by a womans ovaries. The ovaries normally stop making estrogens when a woman is between 45 to 55 years old. This drop in body estrogen levels causes the "change of life" or menopause (the end of monthly menstrual periods). Sometimes, both ovaries are removed during an operation before natural menopause takes place.. The sudden drop in estrogen levels causes ...
EstroVoid XT is an Estrogen Blocker & Anti Estrogen Supplement. EstroVoid XT is an aromatase inhibitor that blocks estrogen production while providing testosterone boosting support. Blocking estrogen is a common desire for many different purposes. The need to block estrogen production has never been higher which is why VH Nutrition developed a proprietary ingredient matrix to block estrogen and improve natural testosterone production. Our formula uses, Cordyceps, Eurycoma, Eleuthero Senticosus, Rhodiola Rosea Extract, Panax Ginseng, and Ashwagandha which uses ingredients that have been shown to be effective in preventing estrogen production and absorption. We are so confident in our product that we offer our customers a satisfaction guarantee or your money back for 30 days.. ...
G protein-coupled Estrogen Receptor 1 is a member of the GPCR family and is encoded in Humans by the GPER gene. Alternate transcriptional splice variants that encode the same protein have been characterized. It is a member of the rhodopsin-like family and is localized to the endoplasmic reticulum membrane. GPER binds estrogen with high affinity, resulting in intracellular calcium mobilization and synthesis of phosphatidylinositol 3,4,5-trisphosphate in the nucleus.
Women between the ages of 25 to 50 who are estrogen deficient are generally prescribed a high dose of estrogen. This can reduce the risk of bone loss, cardiovascular disease, and other hormonal imbalances.. In some cases, long-term treatment may be needed even after your estrogen levels return to normal. This may require lower doses of administered estrogen over time in order to sustain your current level.. Estrogen therapy may also ease the severity of menopausal symptoms and reduce your risk of fractures.. Long-term estrogen therapy is primarily recommended for women who are approaching menopause and have also had a hysterectomy and all transgender. In all other cases, estrogen therapy is only recommended for one to two years. This is because estrogen therapy may increase your risk of cancer.. ...
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TY - CHAP. T1 - Detection of endogenous selective estrogen receptor modulators such as 27-hydroxycholesterol. AU - Nelson, Erik R.. PY - 2016/1/1. Y1 - 2016/1/1. N2 - The estrogen receptors (ERs) belong to the nuclear receptor superfamily, and as such act as ligand inducible transcription factors, mediating the effects of estrogens. However, their pharmacology is complex, having the ability to be differentially activated by ligands. Such ligands possess the ability to behave as either ER-agonists or ER-antagonists, depending on the cellular and tissue context, and have been termed Selective Estrogen Receptor Modulators (SERMs). Several SERMs have been identified with clinical relevance such as tamoxifen and raloxifene. Recently, 27-hydroxycholesterol has been characterized as the first identified endogenous SERM leading to the notion that other endogenous SERMs may exist, each having potential pathophysiological functions. This, coupled with the historic pharmaceutical interest as well as ...
OBJECTIVE: To examine whether binding of [3H]paroxetine to the platelet serotonin transporter or binding of [3H]lysergic acid diethylamide (LSD) to the platelet 5-HT(2A) receptor are influenced by postmenopausal estrogen/progestogen treatment. METHODS: Twenty-three postmenopausal women with climacteric symptoms completed this double-blind, randomized, crossover study. The women received 2 mg of estradiol continuously during four 28-day cycles. In the last 14 days of each cycle, 10 mg of medroxyprogesterone acetate, 1 mg of norethindrone acetate, or placebo was given. Before treatment, as well as once during the last week of each treatment, blood samples were collected for analysis of [3H]LSD and [3H]paroxetine binding. The power of the study setup was 81%. The study had an effect size of 0.36, corresponding to the ability to detect a 15% difference in [3H]paroxetine and [3H]LSD binding between treatments with alpha =.05 and beta =.20, based on a previously reported standard deviation within ...
Advanced Adult Primary Liver Cancer Carcinoma of the Appendix Estrogen Receptor-negative Breast Cancer Extensive Stage Small Cell Lung Cancer Gastrointestinal Stromal Tumor HER2-negative Breast Cancer Metastatic Gastrointestinal Carcinoid Tumor Ovarian Sarcoma Ovarian Stromal Cancer Progesterone Receptor-negative Breast Cancer Recurrent Adenoid Cystic Carcinoma of the Oral Cavity Recurrent Adult Primary Liver Cancer Recurrent Anal Cancer Recurrent Basal Cell Carcinoma of the Lip Recurrent Borderline Ovarian Surface Epithelial-stromal Tumor Recurrent Breast Cancer Recurrent Cervical Cancer Recurrent Colon Cancer Recurrent Endometrial Carcinoma Recurrent Esophageal Cancer Recurrent Esthesioneuroblastoma of the Paranasal Sinus and Nasal Cavity Recurrent Extrahepatic Bile Duct Cancer Recurrent Gallbladder Cancer Recurrent Gastric Cancer Recurrent Gastrointestinal Carcinoid Tumor Recurrent Inverted Papilloma of the Paranasal Sinus and Nasal Cavity Recurrent Lymphoepithelioma of the Nasopharynx ...
Effects of 26 weeks plyometric and dynamic strength training and estrogen replacement therapy on isometric muscle strength of postmenopausal ...
TY - JOUR. T1 - Body mass index, mammographic density, and breast cancer risk by estrogen receptor subtype. AU - Shieh, Yiwey. AU - Scott, Christopher G.. AU - Jensen, Matthew R.. AU - Norman, Aaron D.. AU - Bertrand, Kimberly A.. AU - Pankratz, V. Shane. AU - Brandt, Kathleen R. AU - Visscher, Daniel W. AU - Shepherd, John A.. AU - Tamimi, Rulla M.. AU - Vachon, Celine M. AU - Kerlikowske, Karla. PY - 2019/4/3. Y1 - 2019/4/3. N2 - Background: Obesity and elevated breast density are common risk factors for breast cancer, and their effects may vary by estrogen receptor (ER) subtype. However, their joint effects on ER subtype-specific risk are unknown. Understanding this relationship could enhance risk stratification for screening and prevention. Thus, we assessed the association between breast density and ER subtype according to body mass index (BMI) and menopausal status. Methods: We conducted a case-control study nested within two mammography screening cohorts, the Mayo Mammography Health Study ...
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Venous thrombosis occurred in 167 women taking estrogen plus progestin and in 76 taking placebo (twice the risk for venous thrombosis for women taking hormone therapy). Compared with women between the ages of 50 and 59 years who were taking placebo, the risk associated with hormone therapy was higher with age: 4.3 times the risk for women aged 60 to 69 years and 7.5 times the risk for women aged 70 to 79 years. Compared with women who were of normal weight and taking placebo, the risk associated with taking estrogen plus progestin was increased among overweight (3.8 times the risk) and obese women (5.6 times the risk). Participants with the hereditary blood coagulation disorder Factor V Leiden had a 6.7 times increased risk of thrombosis compared with women in the placebo group without the genetic mutation ...
Objective Transient receptor potential vanilloid type 1 (TRPV1) has been shown to play an important role in visceral hypersensitivity. A significant proportion of patients with inflammatory bowel disease (IBD) continue to complain of abdominal pain despite their disease being otherwise quiescent. We investigated TRPV1-immunoreactive fibres in rectosigmoid biopsies taken from such patients with correlation to abdominal pain severity.. Methods Rectosigmoid biopsies were collected from 20 patients with quiescent IBD fulfilling Rome II criteria for irritable bowel syndrome (IBS), from 20 asymptomatic patients with quiescent IBD and from 28 controls. Abdominal pain scores were recorded using a validated questionnaire. TRPV1- and neuronal marker protein gene product 9.5 (PGP 9.5)-expressing nerve fibres, and lymphocytes (CD3 and CD4) were quantified, following immunohistochemistry with specific antibodies. The biopsy findings were related to abdominal pain scores.. Results A significant 3.9-fold ...
OBJECTIVE: To examine the effects of hormone replacement therapy (HRT) on lipid metabolism, glycemic control, total body and central abdominal fat, blood pressure (BP), and arterial pulse wave velocity (APWV) in overweight postmenopausal females with type 2 diabetes. RESEARCH DESIGN AND METHODS: This was a 12-month prospective study of 14 subjects (mean +/- SD age 57.5+/-5.6 years, BMI 29.5+/-4.8 kg/m2) randomized to 6 months of observation or HRT before crossover. HRT consisted of 2 months of conjugated equine estrogen (CEE) 0.625 mg daily, followed by 4 months CEE and medroxyprogesterone 5 mg daily. Measures included anthropometry, fasting glucose, insulin, HbA1c, total and HDL cholesterol, triglycerides, apolipoprotein B, LDL particle size, nonesterified fatty acids (NEFA), sex hormone-binding globulin, resting energy expenditure (REE), total and central abdominal fat (by dual-energy X-ray absorptiometry), resting BP, APWV (by applanation tonometry), physical activity, well-being, and sexual function
Title: GPER and ER: Estrogen Receptors with Distinct Biological Roles in Breast Cancer. VOLUME: 11 ISSUE: 4. Author(s):Edward J. Filardo. Affiliation:Rhode Island Hospital, Department of Medicine, 593 Eddy Street, Aldrich Building Rm 708, Providence, RI 02903, USA.. Keywords:Estrogen, G-protein-coupled estrogen receptor (GPER), seven transmembrane receptors, estrogen receptors (ERs), nuclear steroid hormone receptors, tamoxifen, faslodex, epidermal growth factor receptors (EGFRs), aromatase inhibitors, breast cancer. Abstract: Comparative clinical studies indicate that blockade of estrogen biosynthesis by the use of aromatase inhibitors may have benefit over estrogen receptor (ER) antagonism as a strategy for treating breast cancer. One plausible explanation for this idea is that more than one type of estrogen receptor may promote the biological effects of estrogen. Recent findings that G-protein-coupled receptor-30, (GPR30/GPER) promotes specific estrogen binding and manifests plasma ...
Premenopausal women are at highest risk for papillary and follicular thyroid carcinoma, implicating a role for estrogens in thyroid cancer. The expression of estrogen receptors α and β (ER), the effects of estradiol (E2), selective estrogen receptor modulators (SERMs) 4-hydroxytamoxifen and raloxifene, and ER subtype selective agonists were examined in NPA87 and KAT5 papillary and WRO follicular thyroid carcinoma cell lines. All three thyroid cancer cell lines expressed full-length ERα and ERβ proteins with cytoplasmic localization that was unaffected by E2. ICI 182,780 (Fulvestrant, an ER antagonist), and inhibitors of non-genomic E2-activated MAPK and PI3K signaling blocked E2-induced cell proliferation. SERMs acted in a cell line-specific manner. No E2-induced estrogen response element (ERE)-driven reporter activity was observed in transiently transfected thyroid cancer cells. However, E2 increased transcription of established endogenous E2-target genes, i.e., cathepsin D in WRO and ...
CONTEXT: Cushing disease (CD) is a rare disorder with severe sequels and incompletely understood pathogenesis. The underlying corticotroph adenomas harbor frequently somatic mutations in the ubiquitin-specific peptidase 8 (USP8) gene. These mutations render USP8 hyperactive and prevent client proteins from degradation.. OBJECTIVE: To investigate the impact of USP8 mutations on proteins deregulated in CD.. DESIGN: One hundred eight pituitary adenomas (75 corticotroph [58 USP8 wild type (WT) and 17 USP8 mutated], 14 somatotroph, and 19 nonfunctioning) were investigated by immunohistochemistry. All evaluated proteins [USP8, arginine vasopressin receptor 1b and 2, corticotropin-releasing hormone receptor, cAMP response element-binding protein (CREB), p27/kip1, cyclin E, heat shock protein 90 (HSP90), orphan nuclear receptor 4, epidermal growth factor receptor, histone deacetylase 2, glucocorticoid receptor, cyclin-dependent kinase 5 and Abelson murine leukemia viral oncogene homolog 1 enzyme ...
TY - JOUR. T1 - Repression of translation of human estrogen receptor α by G-quadruplex formation. AU - Balkwill, Graham D.. AU - Derecka, Kamila. AU - Garner, Thomas P.. AU - Hodgman, Charlie. AU - Flint, A. P F. AU - Searle, Mark S.. PY - 2009/12/8. Y1 - 2009/12/8. N2 - Tissue-specific expression of the human estrogen receptor α gene (ESR1) is achieved through multiple promoter sequences resulting in various mRNA transcripts encoding a common protein but differing in their 5′-untranslated region (5′-UTR). Many cancers are estrogen-sensitive with neoplastic growth stimulated through the estrogen receptor, a transcription factor that regulates developmental genes. We demonstrate that the human ESR1 gene is rich in potential quadruplex-forming sequences with 3 of 20 identified within exonic regions. In particular,we show using CD, UV, and NMR spectroscopy that a stable DNAG-quadruplex motif is formed within the exon C gene sequence. This motif, which PCR shows is transcribed in normal and ...
TY - JOUR. T1 - Estrogen response elements function as allosteric modulators of estrogen receptor conformation. AU - Wood, Jennifer R.. AU - Greene, Geoffrey L.. AU - Nardulli, Ann M.. PY - 1998/4. Y1 - 1998/4. N2 - The estrogen receptor (ER) is a ligand-dependent transcription factor that regulates the expression of estrogen-responsive genes. ER-mediated transcriptional changes are brought about by interaction of the ER with the estrogen response element (ERE). In this study, we examined the interaction of the Xenopus laevis ER DNA binding domain (DBD) and the intact ER with the X. laevis vitellogenin A2 ERE and the human pS2 ERE. Using gel mobility shift, DNase I footprinting, and methylation interference assays, we demonstrated that the DBD bound only as a dimer to the A2 ERE. However, the DBD bound as a monomer to the consensus pS2 ERE half site at lower DBD concentrations and then as a homodimer to the consensus and imperfect pS2 ERE half site at higher DBD concentrations. Antibody ...
Epidemiologic evidence supports an inverse association between physical activity and postmenopausal breast cancer. Whether associations exist for moderate activities, such as walking, and whether associations differ by estrogen receptor (ER) status, body mass index (BMI, kg/m2), adult weight gain, or use of postmenopausal hormones (PMH) is unclear. The relation between time spent sitting and breast cancer also is unclear. Among 73,615 postmenopausal women in the American Cancer Society Cancer Prevention Study II Nutrition Cohort, 4,760 women were diagnosed with breast cancer between 1992 and 2009. Extended Cox regression was used to estimate multivariable-adjusted relative risks (RR) of breast cancer in relation to total recreational physical activity, walking, and leisure-time sitting. Differences in associations by ER status, BMI, weight gain, and PMH use were also evaluated. The most active women (those reporting ,42 MET-hours/week physical activity) experienced 25% lower risk of breast ...
Substantial evidence suggests that the estrogen status has significant impact on cardiovascular morbidity and mortality.23 24 In particular, ERT lowers cardiovascular mortality and improves vascular reactivity in postmenopausal women.23 24 25 26 The underlying mechanisms are incompletely understood.27 Activation of the renin-angiotensin system, or high renin levels, on the other hand, has been implicated to be an adverse factor in vascular and cardiac pathophysiology.14 In the present study, several lines of evidence suggest that the estrogen status affects the level of renin in the circulation. First, women replacing estrogen during menopause presented with significantly lower renin levels than those not using such therapy; second, women with premenopausal circulating estradiol levels displayed renin levels that were lower than found in women with postmenopausal estradiol levels; third, these differences were evident also in women using ACE inhibitors (despite feedback activation of renin by ...
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Summary Safety Review - Hormone Replacement Therapy (Estrogenic and Progestogenic Agents) and Selective Estrogen Receptor Modulators (SERMs) - Assessing the Potential Risk of Ovarian Cancer
Recently in the pig hypothalamus a vasopressin- and oxytocin-containing nucleus was identified which, like the supraoptic nucleus, becomes sexually dimorphic after puberty. Following the increase in circulating steroids at puberty, the vasopressin- and oxytocin-containing nucleus becomes twice as large in both males and females. In adulthood, the vasopressin- and oxytocin-containing nucleus of females is approximately twice as large as that in males. Because these alterations are possibly due to an influence of gonadal steroids, i.e. estrogens, the vasopressin- and oxytocin-containing the presence of estrogen receptors. In addition to the area of the vasopressin- and oxytocin-containing nucleus, the present study documented the distribution of estrogen receptors in the septal area and other parts of the hypothalamus of intact post-pubertal male and female pigs, by utilizing immunocytochemical methodology. Intense nuclear estrogen receptor staining was found in a number of areas, i.e. the medial preoptic
I read with interest the recent report by Snyder et al[1] describing melasma associated with the application of a topical estrogen cream. The development of melasma is multifactorial and female sex hormones have been implicated in the pathogenesis of this condition.[2] Estrogen receptor expression is increased in melasma lesions.[3] Also, melanogenesis of cultured human melanocytes can be stimulated by estrogens and inhibited by estrogen antagonists.[4]. The induction of melasma with a topical estrogen raises the possibility that the treatment of this condition could be facilitated by the use of a topical anti-estrogen. I recently proposed a novel topical approach for the treatment of melasma that utilized an anti-estrogen, such as a selective estrogen receptor modulator (tamoxifen or raloxifene) or an aromatase inhibitor (anastrozole or tetrozole or exemestane).[5] The topical agent would also include a vascular endothelial growth factor inhibitor (bevacizumab) that would be directed toward ...
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Addition of ammonium ions to yeast cells growing on proline as the sole nitrogen source induces internalization of the general amino acid permease Gap1p and its subsequent degradation in the vacuole. An essential step in this down-regulation is Gap1p ubiquitination through a process requiring the Npi1p/Rsp5p ubiquitin ligase. We show in this report that NPI2, a second gene required for NH4+-induced down-regulation of Gap1p, codes for the ubiquitin hydrolase Doa4p/Ubp4p/Ssv7p and that NH4+-induced Gap1p ubiquitination is strongly reduced in npi2 cells. The npi2 mutation results in substitution of an aromatic amino acid located in a 33-residue sequence shared by some ubiquitin hydrolases of the Ubp family. In this mutant, as in doa4(delta) cells, the amount of free monomeric ubiquitin is at least four times lower than in wild-type cells. Both ubiquitination and down-regulation of the permease can be restored in npi2 cells by over-expression of ubiquitin. In proline-grown wild-type and npi2/doa4 ...
Histone deacetylases are important targets for cancer therapeutics, but their regulation is poorly understood. Our data show coordinated transcription of HDAC1 and HDAC2 in lung cancer cell lines, but suggest HDAC2 protein expression is cell-context specific. Through an unbiased siRNA screen we found that BRCA1-associated protein 1 (BAP1) regulates their expression, with HDAC2 reduced and HDAC1 increased in BAP1 depleted cells. BAP1 loss-of-function is increasingly reported in cancers including thoracic malignancies, with frequent mutation in malignant pleural mesothelioma. Endogenous HDAC2 directly correlates with BAP1 across a panel of lung cancer cell lines, and is downregulated in mesothelioma cell lines with genetic BAP1 inactivation. We find that BAP1 regulates HDAC2 by increasing transcript abundance, rather than opposing its ubiquitylation. Importantly, although total cellular HDAC activity is unaffected by transient depletion of HDAC2 or of BAP1 due to HDAC1 compensation, this isoenzyme ...
Tissue-specific gene deletion has proved informative in the analysis of pain pathways. Advillin has been shown to be a pan-neuronal marker of spinal and cranial sensory ganglia. We generated BAC transgenic mice using the Advillin promoter to drive a tamoxifen-inducible CreERT2 recombinase construct in order to be able to delete genes in adult animals. We used a floxed stop ROSA26LacZ reporter mouse to examine functional Cre expression, and analysed the behaviour of mice expressing Cre recombinase. We used recombineering to introduce a CreERT2 cassette in place of exon 2 of the Advillin gene into a BAC clone (RPCI23-424F19) containing the 5 region of the Advillin gene. Transgenic mice were generated using pronuclear injection. The resulting AvCreERT2 transgenic mice showed a highly specific expression pattern of Cre activity after tamoxifen induction. Recombinase activity was confined to sensory neurons and no expression was found in other organs. Less than 1% of neurons showed Cre expression in the