|Reactivity||Human, Mouse, Rat|
|Calculated MW||41184 Da|
|Other Names||Type-2 angiotensin II receptor, Angiotensin II type-2 receptor, AT2, AGTR2|
|Target/Specificity||A synthetic peptide corresponding to residues at the C-term of human Type-2 angiotensin II receptor was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Angeiotensin Receptor-Type II Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Receptor for angiotensin II. Cooperates with MTUS1 to inhibit ERK2 activation and cell proliferation.|
|Cellular Location||Cell membrane; Multi-pass membrane protein.|
|Tissue Location||In adult, highly expressed in myometrium with lower levels in adrenal gland and fallopian tube. Expressed in the cerebellum. Very highly expressed in fetal kidney and intestine|
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Provided below are standard protocols that you may find useful for product applications.
The angiotensin II type 2 (AT2) receptor, belonging to the seven transmembrane receptor superfamily, interacts with effector peptide angiotensin II and has demonstrated counterregulatory interactions with angiotensin II type 1 (AT1) receptor in both the cardiovascular and renal systems(1,2). Participation of AT1 and AT2 receptors in regulating blood pressure, cardiovascular growth, fibrosis, and remodeling and renal blood flow, growth, fibrosis, and sodium excretion has been suggested(3). AT2 receptor activation also suppresses renin biosynthesis and release at renal juxtaglomerular cells. (3) Unlike AT1 receptor which is expressed ubiquitously and abundantly in adult tissues, AT2 receptor expression is high in the fetus but low in adult tissues, and its cardiovascular expression increases in response to injury and AT1 receptor blocker therapy(2).
1. Porrello et al. Front Biosci. 14:958-72, 2009. 2. Schulman et al. Curr Hypertens Rep. 10(3): 188-93, 2008. 3. Carey et al. Trends Endocrinol Metab. 19(3):84-7, 2008.
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