REN (renin)

GWB-957056

1:62500

Suggested starting concentrations are provided. Optimal dilutions should be determined by end-user. Differences in calculated versus apparent molecular weight may be due to post-translational modifications or protein hydrophobicity. Renin catalyzes the first step in the activation pathway of angiotensinogen--a cascade that can result in aldosterone release vasoconstriction and increase in blood pressure. Renin an aspartyl protease cleaves angiotensinogen to form angiotensin I which is converted to angiotensin II by angiotensin I converting enzyme an important regulator of blood pressure and electrolyte balance. Mutations in this gene have been shown to cause familial hyperproreninemia. Renin catalyzes the first step in the activation pathway of angiotensinogen--a cascade that can result in aldosterone release vasoconstriction and increase in blood pressure. Renin an aspartyl protease cleaves angiotensinogen to form angiotensin I which is converted to angiotensin II by angiotensin I converting enzyme an important regulator of blood pressure and electrolyte balance. Transcript variants that encode different protein isoforms and that arise from alternative splicing and the use of alternative promoters have been described but their full-length nature has not been determined. Mutations in this gene have been shown to cause familial hyperproreninemia.

Cleavage of Leu-|-Xaa bond in angiotensinogen to generate angiotensin I.

Interacts with ATP6AP2.

Defects in REN are a cause of renal tubular dysgenesis (RTD) [MIM:267430]. RTD is an autosomal recessive severe disorder of renal tubular development characterized by persistent fetal anuria and perinatal death probably due to pulmonary hypoplasia from early-onset oligohydramnios (the Potter phenotype).