抗人 ApoA1 抗体对
01AB03942
Apolipoprotein A-I (ApoA-I) is a major protein component of high-density lipoprotein (HDL), encoded by the APOA1 gene located on chromosome 11. This 28 kDa protein, composed of 243 amino acids, plays a crucial role in lipid metabolism, particularly in reverse cholesterol transport, where it facilitates the efflux of cholesterol from peripheral tissues to the liver for excretion. ApoA-I is essential for the formation and stability of HDL particles and activates lecithin-cholesterol acyltransferase (LCAT), which converts free cholesterol to cholesteryl esters for incorporation into HDL. Dysregulation or mutations in the APOA1 gene can lead to conditions such as familial HDL deficiency, characterized by low HDL levels and increased risk of premature cardiovascular disease. Additionally, mutations may result in familial visceral amyloidosis, where abnormal ApoA-I proteins aggregate to form amyloid deposits that impair organ function.
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技术参数
- 靶点基因名
- APOA1
- 蛋白别名
- apolipoprotein A1; ApoA1
- UniProt
- P02647
- 物种
- Human
产品详情
- 靶点名称
- ApoA1
- 蛋白名称
- apolipoprotein A1
- 蛋白别名
- Apolipoprotein A-I; Apo-AI; ApoA-I; Apolipoprotein A1) [Cleaved into: Proapolipoprotein A-I; ProapoA-I; Truncated apolipoprotein A-I; Apolipoprotein A-I(1-242)]
- 靶点基因名
- APOA1
- UniProt
- P02647
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Apolipoprotein A-I (ApoA-I) is a major protein component of high-density lipoprotein (HDL), encoded by the APOA1 gene located on chromosome 11. This 28 kDa protein, composed of 243 amino acids, plays a crucial role in lipid metabolism, particularly in reverse cholesterol transport, where it facilitates the efflux of cholesterol from peripheral tissues to the liver for excretion. ApoA-I is essential for the formation and stability of HDL particles and activates lecithin-cholesterol acyltransferase (LCAT), which converts free cholesterol to cholesteryl esters for incorporation into HDL. Dysregulation or mutations in the APOA1 gene can lead to conditions such as familial HDL deficiency, characterized by low HDL levels and increased risk of premature cardiovascular disease. Additionally, mutations may result in familial visceral amyloidosis, where abnormal ApoA-I proteins aggregate to form amyloid deposits that impair organ function.