人 G0S2 抗体对
01AB03224
G0/G1 switch 2 (G0S2) is a small, intrinsically disordered protein of approximately 103 to 104 amino acids characterized by a conserved hydrophobic domain that facilitates critical protein-protein interactions. Biophysical analyses indicate that G0S2 adopts a premolten globule-like conformation with a highly disordered C-terminus, allowing for structural versatility and potential oligomerization. Functionally, G0S2 serves as a potent endogenous inhibitor of adipose triglyceride lipase (ATGL), the rate-limiting enzyme in triacylglycerol hydrolysis. By suppressing lipolysis, G0S2 plays a central role in regulating lipid droplet metabolism, insulin sensitivity, and hepatic triglyceride storage. Beyond its metabolic functions, G0S2 interacts with Bcl-2 to promote apoptosis and acts as a tumor suppressor often silenced by promoter methylation in various malignancies. Dysregulation of G0S2 is also implicated in the pathogenesis of non-alcoholic fatty liver disease and certain autoimmune conditions, including rheumatoid arthritis and systemic lupus erythematosus.
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技术参数
- 靶点基因名
- G0S2
- 蛋白别名
- G0/G1 switch 2; G0S2
- UniProt
- P27469
- 物种
- Human
产品详情
- 靶点名称
- G0S2
- 蛋白名称
- G0/G1 switch 2
- 蛋白别名
- G0/G1 switch protein 2; G0/G1 switch regulatory protein 2; Putative lymphocyte G0/G1 switch gene
- 靶点基因名
- G0S2
- UniProt
- P27469
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
G0/G1 switch 2 (G0S2) is a small, intrinsically disordered protein of approximately 103 to 104 amino acids characterized by a conserved hydrophobic domain that facilitates critical protein-protein interactions. Biophysical analyses indicate that G0S2 adopts a premolten globule-like conformation with a highly disordered C-terminus, allowing for structural versatility and potential oligomerization. Functionally, G0S2 serves as a potent endogenous inhibitor of adipose triglyceride lipase (ATGL), the rate-limiting enzyme in triacylglycerol hydrolysis. By suppressing lipolysis, G0S2 plays a central role in regulating lipid droplet metabolism, insulin sensitivity, and hepatic triglyceride storage. Beyond its metabolic functions, G0S2 interacts with Bcl-2 to promote apoptosis and acts as a tumor suppressor often silenced by promoter methylation in various malignancies. Dysregulation of G0S2 is also implicated in the pathogenesis of non-alcoholic fatty liver disease and certain autoimmune conditions, including rheumatoid arthritis and systemic lupus erythematosus.