人 MYLIP 抗体对
01AB02084
Myosin regulatory light chain interacting protein (MYLIP), also known as Inducible Degrader of the LDL receptor (IDOL), is an E3 ubiquitin-protein ligase that plays a central role in cholesterol homeostasis. It contains a FERM domain and a RING finger domain, which facilitate the ubiquitination of targets such as the LDL receptor (LDLR), VLDLR, and LRP8, directing them toward proteasomal or lysosomal degradation. MYLIP expression is induced by the liver X receptor (LXR) in response to elevated sterol levels, acting as a negative regulator of LDL receptor-mediated cholesterol uptake. Clinically, genetic variations in MYLIP are associated with altered LDLR degradation and increased plasma LDL cholesterol levels, contributing to the risk of dyslipidemia and atherosclerotic cardiovascular disease. Its role in limiting cellular cholesterol uptake makes it a significant therapeutic target for managing familial hypercholesterolemia and related metabolic disorders.
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技术参数
- 靶点基因名
- MYLIP
- 基因别名
- BZF1; IDOL
- 蛋白别名
- myosin regulatory light chain interacting protein; MYLIP
- UniProt
- Q8WY64
- 物种
- Human
产品详情
- 靶点名称
- MYLIP
- 蛋白名称
- myosin regulatory light chain interacting protein
- 蛋白别名
- E3 ubiquitin-protein ligase MYLIP; Inducible degrader of the LDL-receptor; Idol; Myosin regulatory light chain interacting protein; MIR; RING-type E3 ubiquitin transferase MYLIP
- 靶点基因名
- MYLIP
- 基因别名
- BZF1; IDOL
- UniProt
- Q8WY64
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Myosin regulatory light chain interacting protein (MYLIP), also known as Inducible Degrader of the LDL receptor (IDOL), is an E3 ubiquitin-protein ligase that plays a central role in cholesterol homeostasis. It contains a FERM domain and a RING finger domain, which facilitate the ubiquitination of targets such as the LDL receptor (LDLR), VLDLR, and LRP8, directing them toward proteasomal or lysosomal degradation. MYLIP expression is induced by the liver X receptor (LXR) in response to elevated sterol levels, acting as a negative regulator of LDL receptor-mediated cholesterol uptake. Clinically, genetic variations in MYLIP are associated with altered LDLR degradation and increased plasma LDL cholesterol levels, contributing to the risk of dyslipidemia and atherosclerotic cardiovascular disease. Its role in limiting cellular cholesterol uptake makes it a significant therapeutic target for managing familial hypercholesterolemia and related metabolic disorders.