人 DELE1 抗体对
01AB01950
DAP3 binding cell death enhancer 1 (DELE1) is a mitochondrial protein that serves as a primary sensor and transducer of mitochondrial stress to the cytosolic integrated stress response (ISR). Under conditions of mitochondrial dysfunction, DELE1 undergoes proteolytic processing to generate a C-terminal fragment that translocates to the cytosol. This fragment oligomerizes and specifically activates the heme-regulated eIF2α kinase (HRI), leading to eIF2α phosphorylation and the induction of a protective transcriptional program. This pathway promotes translational reprogramming, PRKN-independent mitophagy, and adaptation to iron deficiency. Clinically, DELE1 is implicated in mitochondrial cardiomyopathy and various neuromuscular and neurodegenerative disorders. By mitigating mitochondrial stress-driven pathologies and maintaining muscle proteostasis, DELE1 acts as a critical mediator of cellular resilience in the face of organelle-specific damage.
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技术参数
- 靶点基因名
- DELE1
- 基因别名
- DELE; KIAA0141
- 蛋白别名
- DAP3 binding cell death enhancer 1; DELE1
- UniProt
- Q14154
- 物种
- Human
产品详情
- 靶点名称
- DELE1
- 蛋白名称
- DAP3 binding cell death enhancer 1
- 蛋白别名
- DAP3-binding cell death enhancer 1; DAP3-binding cell death enhancer 1; long form; DELE1(L); Death ligand signal enhancer) [Cleaved into: DAP3-binding cell death enhancer 1 short form; DELE1(S); S-DELE1; cDELE1]
- 靶点基因名
- DELE1
- 基因别名
- DELE; KIAA0141
- UniProt
- Q14154
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
DAP3 binding cell death enhancer 1 (DELE1) is a mitochondrial protein that serves as a primary sensor and transducer of mitochondrial stress to the cytosolic integrated stress response (ISR). Under conditions of mitochondrial dysfunction, DELE1 undergoes proteolytic processing to generate a C-terminal fragment that translocates to the cytosol. This fragment oligomerizes and specifically activates the heme-regulated eIF2α kinase (HRI), leading to eIF2α phosphorylation and the induction of a protective transcriptional program. This pathway promotes translational reprogramming, PRKN-independent mitophagy, and adaptation to iron deficiency. Clinically, DELE1 is implicated in mitochondrial cardiomyopathy and various neuromuscular and neurodegenerative disorders. By mitigating mitochondrial stress-driven pathologies and maintaining muscle proteostasis, DELE1 acts as a critical mediator of cellular resilience in the face of organelle-specific damage.