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Human Apolipoprotein AI



0.5 mg
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Specificity: Apolipoprotein AI (Apo AI), Human

Preservative: None Inactivation: Not applicable

Buffer: 10mM NH4HCO3, pH 7.4

Applications Notes : Specific methodologies have not been tested using this product. Concentration: Concentration is lot specific Human Apolipoprotein AI. Human Apolipoprotein AI (Apo AI)

Function: 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).

Subunit: Interacts with APOA1BP.

Subcellular Location: Secreted.

Tissue Specificity: Major protein of plasma HDL, also found in chylomicrons. Synthesized in the liver and small intestine.

Ptm: Palmitoylated.

Disease: Defects in APOA1 are a cause of high density lipoprotein deficiency type 2 (HDLD2) [MIM:604091]; also known as familial hypoalphalipoproteinemia (FHA). Inheritance is autosomal dominant.

Disease: 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.

Disease: Defects in APOA1 are the cause of amyloid polyneuropathy-nephropathy Iowa type (AMYLIOWA) [MIM:107680]; also known as amyloidosis van Allen type or familial amyloid polyneuropathy type III. AMYLIOWA is a hereditary generalized amyloidosis due to deposition of amyloid mainly constituted by apolipoprotein A1. The clinical picture is dominated by neuropathy in the early stages of the disease and nephropathy late in the course. Death is due in most cases to renal amyloidosis. Severe peptic ulcer disease can occurr in some and hearing loss is frequent. Cataracts is present in several, but vitreous opacities are not observed.

Disease: 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.

Similarity: Belongs to the apolipoprotein A1/A4/E family.

Additional Information

Name Human Apolipoprotein AI
Related Product Names Human Apolipoprotein AI; Apo-AI; ApoA-I Human Apolipoprotein AIAPOA1
NCBI Acc Number NP_000030.1
Molecular Weight 30778
Datasheets / Downloads GWB-108328 Datasheet
Swiss Prot Number P02647
Purity >95% pure (SDS-PAGE). Column chromatography
Source Human Plasma HDL
Format Purified, Liquid
Storage Upon receipt, store at -70 C. Keep concentration >1mg/ml as precipitation may occur below 1mg/ml. Avoid multiple freeze/thaw cycles.
Intended Use Research Use Only