Mouse Mineralocorticoid Receptor Monoclonal Antibody | anti-NR3C2 antibody

Mineralocorticoid Receptor (MR)

Cat. Num. AAA604255

• Gene Names: NR3C2; MR; MCR; MLR; FLJ41052; NR3C2VIT; MGC133092
• Reactivity: Chicken, Human, Rabbit, Rat
• Applications: Western Blot, Immunohistochemistry, Immunocytochemistry
• Purity: Affinity Purified; Purified by Protein A affinity chromatography.
• Synonyms: Mineralocorticoid Receptor; Monoclonal Antibody; Mineralocorticoid Receptor (MR); Anti -Mineralocorticoid Receptor (MR); anti-NR3C2 antibody

• Host: Mouse
• Reactivity: Chicken, Human, Rabbit, Rat
• Clonality: Monoclonal
• Isotype: IgG1
• Clone Number: 6D587
• Specificity: Recognizes human Mineralocorticoid Receptor (MR) at ~116kD. Species Crossreactivity: rat, rabbit and chicken
• Purity/Purification: Affinity Purified; Purified by Protein A affinity chromatography.
• Form/Format: Supplied as a liquid in PBS, pH 7.2, 0.05% sodium azide.

• Applicable Applications for anti-NR3C2 antibody: Western Blot (WB), Immunohistochemistry (IHC), Immunocytochemistry (ICC)
• Application Notes: Suitable for use in Western Blot, Immunocytochemistry, Immunohistochemistry and Functional Assays. Not suitable for use in Immunoprecipitation.; Dilution: Western Blot: 1:1000 using ECL.; Immunohistochemistry (Paraffin): 1:100. Staining is blocked by pre-incubating the sample with aldosterone.; Functional Assays: Blocks the binding of aldosterone to the MR.
• Immunogen: Aldosterone
• Preparation and Storage: May be stored at 4 degree C for short-term only. Aliquot to avoid repeated freezing and thawing. Store at -20 degree C. Aliquots are stable for at least 12 months. For maximum recovery of product, centrifuge the original vial after thawing and prior to removing the cap.

Related Product Information for anti-NR3C2 antibody

Steroid receptors are ligand dependent, intracellular proteins that stimulate transcription of specific genes by binding to specific DNA sequences following activation by the appropriate hormone. Mineralocorticoids are a family of steroids, secreted by the adrenal cortex, necessary for the regulation of a number of metabolic processes including electrolyte regulation. These compounds exert their effect through their interaction with the mineralocorticoid receptor and that complex's subsequent association with DNA. Given the function of mineralocorticoids, it is not surprising to find that the kidney is a primary target organ for mineralocorticoids and that this organ has been shown to contain MR.

Product Categories/Family for anti-NR3C2 antibody

Antibodies; Abs to Receptors

NCBI and Uniprot Product Information

• NCBI GI #: 307166
• NCBI GeneID: 4306
• UniProt Accession #: P08235; Q96KQ8; Q96KQ9; Q2NKL1; Q4W5E8; Q59GQ3
• Molecular Weight: 107,067 Da
• NCBI Official Full Name: mineralocorticoid receptor
• NCBI Official Synonym Full Names: nuclear receptor subfamily 3, group C, member 2
• NCBI Official Symbol: NR3C2
• NCBI Official Synonym Symbols: MR; MCR; MLR; FLJ41052; NR3C2VIT; MGC133092
• NCBI Protein Information: mineralocorticoid receptor; OTTHUMP00000220257; OTTHUMP00000220259; OTTHUMP00000220260; OTTHUMP00000220261; aldosterone receptor; mineralocorticoid receptor 1; mineralocorticoid receptor delta
• UniProt Protein Name: Mineralocorticoid receptor
• Protein Family: Mineralocorticoid receptor
• UniProt Gene Name: NR3C2
• UniProt Synonym Gene Names: MCR; MLR
• UniProt Entry Name: MCR_HUMAN

NCBI Description

This gene encodes the mineralocorticoid receptor, which mediates aldosterone actions on salt and water balance within restricted target cells. The protein functions as a ligand-dependent transcription factor that binds to mineralocorticoid response elements in order to transactivate target genes. Mutations in this gene cause autosomal dominant pseudohypoaldosteronism type I, a disorder characterized by urinary salt wasting. Defects in this gene are also associated with early onset hypertension with severe exacerbation in pregnancy. Alternative splicing results in multiple transcript variants. [provided by RefSeq]

Uniprot Description

MCR: Receptor for both mineralocorticoids (MC) such as aldosterone and glucocorticoids (GC) such as corticosterone or cortisol. Binds to mineralocorticoid response elements (MRE) and transactivates target genes. The effect of MC is to increase ion and water transport and thus raise extracellular fluid volume and blood pressure and lower potassium levels. Defects in NR3C2 are a cause of autosomal dominant pseudohypoaldosteronism type I (AD-PHA1). PHA1 is characterized by urinary salt wasting, resulting from target organ unresponsiveness to mineralocorticoids. There are 2 forms of PHA1: the autosomal dominant form that is mild, and the recessive form which is more severe and due to defects in any of the epithelial sodium channel subunits. In AD-PHA1 the target organ defect is confined to kidney. Clinical expression can vary from asymptomatic to moderate. It may be severe at birth, but symptoms remit with age. Familial and sporadic cases have been reported. Defects in NR3C2 are a cause of early-onset hypertension with severe exacerbation in pregnancy (EOHSEP). Inheritance is autosomal dominant. The disease is characterized by the onset of severe hypertension before the age of 20, and by suppression of aldosterone secretion. Belongs to the nuclear hormone receptor family. NR3 subfamily. 4 isoforms of the human protein are produced by alternative splicing.

Protein type: Nuclear receptor; DNA-binding

Chromosomal Location of Human Ortholog: 4q31.1

Cellular Component: nucleoplasm; endoplasmic reticulum membrane; receptor complex

Molecular Function: protein binding; zinc ion binding; sequence-specific DNA binding; steroid hormone receptor activity; transcription factor activity; steroid binding

Biological Process: transcription initiation from RNA polymerase II promoter; regulation of transcription, DNA-dependent; steroid hormone mediated signaling; gene expression; signal transduction

Disease: Hypertension, Early-onset, Autosomal Dominant, With Severe Exacerbation In Pregnancy; Pseudohypoaldosteronism, Type I, Autosomal Dominant