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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]
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).
The protein encoded by this gene is a nuclear receptor that is closely related to the estrogen receptor. Results of both in vitro and in vivo studies suggest that ERRα is required for the activation of mitochondrial genes as well as increased mitochondrial biogenesis.
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
Typically, the antibody used is the anti-Estrogen Receptor (ER) (SP1) Rabbit Monoclonal Antibody. Employing SP1 allows detection of estrogen receptor (ER) antigens in sections of the fixed tissue samples. In conjunction with light microscopy, approximate ER activity can be estimated using the level of staining of the cell's components.
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]
The estrogen receptor, as well as the progesterone receptor, have been detected in the skin, including in keratinocytes and fibroblasts. [ 25 ] [ 26 ] At menopause and thereafter, decreased levels of female sex hormones result in atrophy , thinning, and increased wrinkling of the skin and a reduction in skin elasticity , firmness, and strength.
Membrane estrogen receptors (mERs) are a group of receptors which bind estrogen. [ 1 ] [ 2 ] Unlike nuclear estrogen receptors , which mediate their effects via slower genomic mechanisms, mERs are cell surface receptors that rapidly alter cell signaling via modulation of intracellular signaling cascades .
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