PER1 (Hu), control peptide for AB5424P

For use in blocking the reactivity of AB5424P.

Optimal working dilution must be determined by the end user.

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

FUNCTION: SwissProt: P22966 # Converts angiotensin I to angiotensin II by release of the terminal His-Leu, this results in an increase of the vasoconstrictor activity of angiotensin. Also able to inactivate bradykinin, a potent vasodilator. Has also a glycosidase activity which releases GPI-anchored proteins from the membrane by cleaving the mannose linkage in the GPI moiety.| P12821 # Converts angiotensin I to angiotensin II by release of the terminal His-Leu, this results in an increase of the vasoconstrictor activity of angiotensin. Also able to inactivate bradykinin, a potent vasodilator.
COFACTOR: Binds 1 zinc ion per subunit. & Binds 2 chloride ions per subunit.
SIZE: 732 amino acids; 83330 Da
SUBCELLULAR LOCATION: Angiotensin-converting enzyme, testis- specific isoform, soluble form: Secreted. & Cell membrane; Single-pass type I membrane protein.
TISSUE SPECIFICITY: Spermatocytes, adult testis.
DOMAIN: SwissProt: P22966
PTM: Phosphorylated by CK2 on Ser-725; which allows membrane retention (By similarity).
DISEASE: SwissProt: P12821 # Genetic variations in ACE may be a cause of susceptibility to ischemic stroke [MIM:601367]; also known as cerebrovascular accident or cerebral infarction. A stroke is an acute neurologic event leading to death of neural tissue of the brain and resulting in loss of motor, sensory and/or cognitive function. Ischemic strokes, resulting from vascular occlusion, is considered to be a highly complex disease consisting of a group of heterogeneous disorders with multiple genetic and environmental risk factors. & Defects in ACE 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). & Genetic variations in ACE can influence susceptibility to diabetic nephropathy [MIM:603933]. Diabetic nephropathy is a kidney disease and resultant kidney function impairment due to the long standing effects of diabetes on the microvasculature (glomerulus) of the kidney. Features include increased urine protein and declining kidney function.
SIMILARITY: SwissProt: P22966 ## Belongs to the peptidase M2 family.| P12821 ## Belongs to the peptidase M2 family.
MISCELLANEOUS: The glycosidase activity probably uses different active site residues than the metalloprotease activity. & Inhibitors of ACE are commonly used to treat hypertension and cardiac dysfunction.

Liquid in PBS, pH 7.

Maintain at -20°C in undiluted aliquots for up to 6 months after date of receipt. Avoid repeated freeze/thaw cycles.