抗人 MAP3K5 抗体对
01AB00897
Mitogen-activated protein kinase kinase kinase 5 (MAP3K5), also termed apoptosis signal-regulating kinase 1 (ASK1), is a serine/threonine kinase that activates the JNK and p38 MAPK pathways, mediating cellular responses to oxidative stress, cytokines, and endoplasmic reticulum stress. Structurally, MAP3K5 contains an N-terminal thioredoxin-binding domain, a central kinase domain, and a C-terminal coiled-coil domain, enabling interactions with regulators like thioredoxin (inhibiting its activity under redox balance) and TRAF proteins. Post-translational modifications, such as phosphorylation (e.g., at Thr845) and ubiquitination, tightly regulate its function in apoptosis, inflammation, and differentiation. Dysregulation of MAP3K5 is linked to multiple diseases. Overactivation due to mutations or oxidative stress is associated with cardiovascular disorders, including dilated cardiomyopathy, and diabetic nephropathy via excessive apoptosis. Conversely, impaired MAP3K5 activity may promote cancer by reducing stress-induced cell death. Its role in neuroinflammation also implicates it in neurodegenerative diseases like Alzheimer’s.
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技术参数
- 靶点基因名
- MAP3K5
- 基因别名
- ASK1; MAPKKK5; MEKK5
- 蛋白别名
- mitogen-activated protein kinase kinase kinase 5; MAP3K5
- UniProt
- Q99683
- 物种
- Human
产品详情
- 靶点名称
- MAP3K5
- 蛋白名称
- mitogen-activated protein kinase kinase kinase 5
- 蛋白别名
- Mitogen-activated protein kinase kinase kinase 5; Apoptosis signal-regulating kinase 1; ASK-1; MAPK/ERK kinase kinase 5; MEK kinase 5; MEKK 5
- 靶点基因名
- MAP3K5
- 基因别名
- ASK1; MAPKKK5; MEKK5
- UniProt
- Q99683
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Mitogen-activated protein kinase kinase kinase 5 (MAP3K5), also termed apoptosis signal-regulating kinase 1 (ASK1), is a serine/threonine kinase that activates the JNK and p38 MAPK pathways, mediating cellular responses to oxidative stress, cytokines, and endoplasmic reticulum stress. Structurally, MAP3K5 contains an N-terminal thioredoxin-binding domain, a central kinase domain, and a C-terminal coiled-coil domain, enabling interactions with regulators like thioredoxin (inhibiting its activity under redox balance) and TRAF proteins. Post-translational modifications, such as phosphorylation (e.g., at Thr845) and ubiquitination, tightly regulate its function in apoptosis, inflammation, and differentiation. Dysregulation of MAP3K5 is linked to multiple diseases. Overactivation due to mutations or oxidative stress is associated with cardiovascular disorders, including dilated cardiomyopathy, and diabetic nephropathy via excessive apoptosis. Conversely, impaired MAP3K5 activity may promote cancer by reducing stress-induced cell death. Its role in neuroinflammation also implicates it in neurodegenerative diseases like Alzheimer’s.