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人 TNFSF10 抗体对
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人 TNFSF10 抗体对

01AB00435

TNF superfamily member 10 (TNFSF10), also known as TRAIL, is a cytokine that belongs to the tumor necrosis factor ligand family. It is a type II transmembrane protein with a carboxy-terminal extracellular domain that exhibits homology to other TNF superfamily members. TNFSF10 preferentially induces apoptosis in transformed and tumor cells by binding to several TNF receptor superfamily members, including TNFRSF10A/TRAILR1 and TNFRSF10B/TRAILR2. Its activity can be modulated by binding to decoy receptors TNFRSF10C/TRAILR3 and TNFRSF10D/TRAILR4. TNFSF10 triggers the activation of MAPK8/JNK, caspase 8, and caspase 3, leading to apoptosis. In terms of disease associations, TNFSF10 has been implicated in various cancers, including colorectal and pancreatic cancer, due to its role in tumor cell apoptosis.

Human
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技术参数

靶点基因名
TNFSF10
基因别名
APO2L; TRAIL
蛋白别名
TNF superfamily member 10; TNFSF10
UniProt
P50591
物种
Human

产品详情

靶点名称
TNFSF10
蛋白名称
TNF superfamily member 10
蛋白别名
Tumor necrosis factor ligand superfamily member 10; Apo-2 ligand; Apo-2L; TNF-related apoptosis-inducing ligand; Protein TRAIL; CD antigen CD253
靶点基因名
TNFSF10
基因别名
APO2L; TRAIL
UniProt
P50591
来源物种
Homo sapiens (Human)
物种反应性
Human

背景介绍

TNF superfamily member 10 (TNFSF10), also known as TRAIL, is a cytokine that belongs to the tumor necrosis factor ligand family. It is a type II transmembrane protein with a carboxy-terminal extracellular domain that exhibits homology to other TNF superfamily members. TNFSF10 preferentially induces apoptosis in transformed and tumor cells by binding to several TNF receptor superfamily members, including TNFRSF10A/TRAILR1 and TNFRSF10B/TRAILR2. Its activity can be modulated by binding to decoy receptors TNFRSF10C/TRAILR3 and TNFRSF10D/TRAILR4. TNFSF10 triggers the activation of MAPK8/JNK, caspase 8, and caspase 3, leading to apoptosis. In terms of disease associations, TNFSF10 has been implicated in various cancers, including colorectal and pancreatic cancer, due to its role in tumor cell apoptosis.