Human Apolipoprotein AI

GWB-90B18F

Purified Lipoproteins

3M Guanidine hydrochloride 10mM Tris 5mM DTT pH 8. 0Applications Notes : Apo AI can be re-natured into PBS TBS and other common buffers by dialysis using a membrane with a nominal molecular weight cut-off of 14 000 or less. This should be performed in a cold room. Each laboratory should determine an optimum working titer for use in its particular application. Other applications have not been tested but use in such assays should not necessarily be excluded. Warnings: All human source materials have tested negative for NHCV/NHIV nucleic acid test. HCV antigen; HBsAg. HBcAg. HIV1 Ag; and syplilis. No test guarantees a product to be non-infectious. Therefore. all material derived from human fluids or tissues should be considered as potentially infectious.

Participates in the reverse transport of cholesterol from tissues to the liver for excretion by promoting cholesterol efflux from tissues and by acting as a cofactor for the lecithin cholesterol acyltransferase (LCAT).

Secreted.

Palmitoylated.

Defects in APOA1 are a cause of the low HDL levels observed in high density lipoprotein deficiency type 1 (HDLD1) [MIM:205400]; also known as analphalipoproteinemia or Tangier disease (TGD). HDLD1 is a recessive disorder characterized by the absence of plasma HDL accumulation of cholesteryl esters premature coronary artery disease hepatosplenomegaly recurrent peripheral neuropathy and progressive muscle wasting and weakness. In HDLD1 patients ApoA-I fails to associate with HDL probably because of the faulty conversion of pro-ApoA-I molecules into mature chains either due to a defect in the converting enzyme activity or a specific structural defect in Tangier ApoA-I.

Defects in APOA1 are a cause of amyloidosis type 8 (AMYL8) [MIM:105200]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1 fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome arterial hypertension hepatosplenomegaly cholestasis petechial skin rash.