NR3C2 Antibody (Center) Blocking Peptide
Synthetic peptide
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Primary Accession | P08235 |
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Clone Names | 100507204 |
Gene ID | 4306 |
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Other Names | Mineralocorticoid receptor, MR, Nuclear receptor subfamily 3 group C member 2, NR3C2, MCR, MLR |
Format | Peptides are lyophilized in a solid powder format. Peptides can be reconstituted in solution using the appropriate buffer as needed. |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. |
Precautions | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
Name | NR3C2 |
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Synonyms | MCR, MLR |
Function | 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. |
Cellular Location | Cytoplasm. Nucleus. Endoplasmic reticulum membrane; Peripheral membrane protein. Note=Cytoplasmic and nuclear in the absence of ligand; nuclear after ligand-binding. When bound to HSD11B2, it is found associated with the endoplasmic reticulum membrane |
Tissue Location | Ubiquitous. Highly expressed in distal tubules, convoluted tubules and cortical collecting duct in kidney, and in sweat glands. Detected at lower levels in cardiomyocytes, in epidermis and in colon enterocytes. |
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Provided below are standard protocols that you may find useful for product applications.
Background
This gene encodes the mineralocorticoid receptor, whichmediates aldosterone actions on salt and water balance withinrestricted target cells. The protein functions as aligand-dependent transcription factor that binds tomineralocorticoid response elements in order to transactivatetarget genes. Mutations in this gene cause autosomal dominantpseudohypoaldosteronism type I, a disorder characterized by urinarysalt wasting. Defects in this gene are also associated with earlyonset hypertension with severe exacerbation in pregnancy.Alternative splicing results in multiple transcript variants.
References
van Leeuwen, N., et al. Hypertension 56(5):995-1002(2010)Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)Bouma, E.M., et al. Behav. Genet. (2010) In press :Bogdan, R., et al. Genes Brain Behav. 9(6):658-667(2010)Gu, D., et al. J. Hypertens. 28(6):1210-1220(2010)
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