Manufacturer GENWAY
Type Antibody
Specific against other
Clone i2H5
Applications FC
Amount 0.025 mg
ArtNr 20-783-310226
Genway ID:
Human lung CD143 (Angiotensin converting enzyme)
Fusion Partner:
Spleen cells from immunised Balb/c mice were fused with cells of the mouse X36 - Ag8 - 653 myeloma cell line.
Preservative Stabilisers:
0. 09%Sodium Azide1. 0%Bovine Serum AlbuminSuggested
Flow Cytometry:
Use 10ul of the suggested working dilution to label 106 cells in 100ul. Suggested
Flow Cytometry - Neat - 1/10
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.
Catalytic Activity:
Release of a C-terminal dipeptide oligopeptide-|-Xaa-Yaa when Xaa is not Pro and Yaa is neither Asp nor Glu. Thus conversion of angiotensin I to angiotensin II with increase in vasoconstrictor activity but no action on angiotensin II. Cofactor: Binds 2 zinc ions per subunit. The Testis-specific isoform only binds 1 zinc ion per subunit. Cofactor: Binds 3 chloride ions per subunit.
Enzyme Regulation:
Strongly activated by chloride. Specifically inhibited by lisinopril captopril and enalaprilat. Biophysicochemical Properties:
Subcellular Location:
Angiotensin-converting enzyme soluble form: Secreted.
Subcellular Location:
Cell membrane; Single-pass type I membrane protein.
Tissue Specificity:
Ubiquitously expressed with highest levels in lung kidney heart gastrointestinal system and prostate. The testis-specific isoforn is expressed in spermatocytes adult testis.
Up-regulated in failing heart.
Phosphorylated by CK2 on Ser-1299; which allows membrane retention.
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.
Inhibitors of ACE are commonly used to treat hypertension and some types of renal and cardiac dysfunction.
The glycosidase activity probably uses different active site residues than the metalloprotease activity.
Belongs to the peptidase M2 family [view classification]. 1. Danilov. S. M. et al. (1994) Structure-function analysis of angiotensin I-converting enzyme using monoclonal antibodies. Selective inhibition of amino-terminal active site. 2. Metzger. R. et al. (2000) CD143 in the development of atherosclerosis.
Amount: 0.025 mg
Available: In stock
Listprice: €258.32
Discount: -10.0%
Price: €232.49
You save: €25.83

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