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Estrogen receptor alpha (ERα), also known as NR3A1 (nuclear receptor subfamily 3, group A, member 1), is one of two main types of estrogen receptor, a nuclear receptor (mainly found as a chromatin-binding protein [5]) that is activated by the sex hormone estrogen. In humans, ERα is encoded by the gene ESR1 (EStrogen Receptor 1). [6] [7] [8]
2101 26379 Ensembl ENSG00000173153 ENSMUSG00000024955 UniProt P11474 O08580 RefSeq (mRNA) NM_001282450 NM_001282451 NM_004451 NM_007953 RefSeq (protein) NP_001269379 NP_001269380 NP_004442 NP_031979 Location (UCSC) Chr 11: 64.31 – 64.32 Mb Chr 19: 6.89 – 6.9 Mb PubMed search Wikidata View/Edit Human View/Edit Mouse Estrogen-related receptor alpha (ERRα), also known as NR3B1 (nuclear ...
The activation of the two different estrogen receptors has different effects on human. ERα and ERβ also mediate Selective estrogen-receptor modulators ' (SERMs') function, [ 17 ] but the selective ERα agitator can always cause some side effects such as breast cancer or endometrial hyperplasia, while the selective ERβ agitator may play an ...
The ERRs are orphan nuclear receptors, meaning the identity of their endogenous ligand has yet to be unambiguously determined. They are named because of sequence homology with estrogen receptors, but do not appear to bind estrogens or other tested steroid hormones. There are three human estrogen related receptors: ERRα ; ERRβ ; ERRγ
The first includes the intracellular estrogen receptors, namely ERα and ERβ, which belong to the nuclear receptor family. The second class consists of membrane estrogen receptors (mERs), such as GPER (GPR30), ER-X, and G q-mER, which are primarily G protein-coupled receptors. This article focuses on the nuclear estrogen receptors (ERα and ERβ).
Estrogen insensitivity syndrome (EIS), or estrogen resistance, is a form of congenital estrogen deficiency or hypoestrogenism [2] which is caused by a defective estrogen receptor (ER) – specifically, the estrogen receptor alpha (ERα) – that results in an inability of estrogen to mediate its biological effects in the body. [3]
Katzenellenbogen's work has delineated structure-function relationships and mechanisms of action of estrogen receptors alpha and beta. She has clarified the molecular basis of action of SERMs such as tamoxifen and raloxifene in treatment and prevention of breast cancer, and she has identified critical aggressiveness factors in breast tumors that promote metastasis and resistance to cancer ...
Estradiol is a naturally occurring and bioidentical estrogen, or an agonist of the estrogen receptor, the biological target of estrogens like endogenous estradiol. [11] Due to its estrogenic activity, estradiol has antigonadotropic effects and can inhibit fertility and suppress sex hormone production in both women and men.