抗人胰岛素受体抗体对
01AB01178
Insulin receptor (INSR) is a transmembrane receptor tyrosine kinase that plays a central role in mediating the effects of insulin on glucose homeostasis and metabolism. Structurally, the mature receptor is a tetramer composed of two extracellular α-subunits, responsible for insulin binding, and two transmembrane β-subunits, which possess intrinsic tyrosine kinase activity and mediate intracellular signaling upon insulin binding. The INSR gene undergoes alternative splicing to produce two main isoforms, IR-A and IR-B, which differ in their tissue distribution and functional properties. Upon insulin binding, the receptor undergoes autophosphorylation and activates downstream signaling pathways that regulate glucose uptake, lipid metabolism, cell growth, and survival. Dysfunction or mutations in INSR can impair insulin signaling, leading to insulin resistance and contributing to metabolic disorders such as type 2 diabetes and, less commonly, rare syndromes of severe insulin resistance; aberrant signaling is also implicated in certain cancers due to its role in cell proliferation and apoptosis.
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技术参数
- 靶点基因名
- INSR
- 蛋白别名
- insulin receptor; Insulin Receptor
- UniProt
- P06213
- 物种
- Human
产品详情
- 靶点名称
- Insulin Receptor
- 蛋白名称
- insulin receptor
- 蛋白别名
- Insulin receptor; IR; CD antigen CD220) [Cleaved into: Insulin receptor subunit alpha; Insulin receptor subunit beta]
- 靶点基因名
- INSR
- UniProt
- P06213
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Insulin receptor (INSR) is a transmembrane receptor tyrosine kinase that plays a central role in mediating the effects of insulin on glucose homeostasis and metabolism. Structurally, the mature receptor is a tetramer composed of two extracellular α-subunits, responsible for insulin binding, and two transmembrane β-subunits, which possess intrinsic tyrosine kinase activity and mediate intracellular signaling upon insulin binding. The INSR gene undergoes alternative splicing to produce two main isoforms, IR-A and IR-B, which differ in their tissue distribution and functional properties. Upon insulin binding, the receptor undergoes autophosphorylation and activates downstream signaling pathways that regulate glucose uptake, lipid metabolism, cell growth, and survival. Dysfunction or mutations in INSR can impair insulin signaling, leading to insulin resistance and contributing to metabolic disorders such as type 2 diabetes and, less commonly, rare syndromes of severe insulin resistance; aberrant signaling is also implicated in certain cancers due to its role in cell proliferation and apoptosis.