This antibody is purified through a protein G column, followed by dialysis against PBS.
Immunogen
This AGT antibody is generated from mice immunized with a KLH conjugated synthetic peptide between 37-65 amino acids from the N-terminal region of human AGT.
Purified monoclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.
Preservative
Sodium azide
Precaution of Use
This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.
Storage
4 °C,-20 °C
Expiry Date
6 months
Desong Liu, Fang Lu, Songhui Zhai, Liu Wei, Shi Ma, Xiuying Chen, Liqun Dong, Yannan Guo, Jin Wu, Zheng Wang: "Renin-angiotensin system gene polymorphisms in children with Henoch-Schönlein purpura in West China." in: Journal of the renin-angiotensin-aldosterone system : JRAAS, Vol. 11, Issue 4, pp. 248-55, (2010) (PubMed).
Kieć-Wilk, Olszanecka, Mikołajczyk, Kawecka-Jaszcz et al.: "[Role of the M235T (c.704c>T) polymorphism of angiotensynogen gene as well as A724A (c.2171G>A) polymorphism of SERCA2a gene in ethiopathogenesis of left ventricular hypertrophy in essential..." in: Przegla̧d lekarski, Vol. 67, Issue 3, pp. 151-6, (2010) (PubMed).
Procopciuc, Sitar-Tăut, Pop, Sitar-Tăut, Olteanu, Zdrenghea: "Renin angiotensin system polymorphisms in patients with metabolic syndrome (MetS)." in: European journal of internal medicine, Vol. 21, Issue 5, pp. 414-8, (2010) (PubMed).
Target
AGT
(Angiotensinogen (serpin Peptidase Inhibitor, Clade A, Member 8) (AGT))
The protein encoded by this gene, pre-angiotensinogen or angiotensinogen precursor, is expressed in the liver and is cleaved by the enzyme renin in response to lowered blood pressure. The resulting product, angiotensin I, is then cleaved by angiotensin converting enzyme (ACE) to generate the physiologically active enzyme angiotensin II. The protein is involved in maintaining blood pressure and in the pathogenesis of essential hypertension and preeclampsia. Mutations in this gene are associated with susceptibility to essential hypertension, and can cause renal tubular dysgenesis, a severe disorder of renal tubular development. Defects in this gene have also been associated with non-familial structural atrial fibrillation, and inflammatory bowel disease.