人 SETD3 抗体对
01AB02542
SET domain containing 3, actin N3(tau)-histidine methyltransferase (SETD3) is a highly specific S-adenosyl-L-methionine-dependent enzyme that methylates β-actin at the His73 residue. This post-translational modification is critical for promoting F-actin polymerization and maintaining cytoskeletal organization. SETD3 localizes to the cytoplasm and the outer mitochondrial membrane, where it facilitates actin assembly around mitochondria to regulate their morphology, motility, and oxidative phosphorylation. Loss of SETD3 activity results in fragmented mitochondrial networks and a metabolic shift toward glycolysis. Pathophysiologically, SETD3 is required for the efficient replication of enteroviruses and has been implicated in certain hematologic malignancies. Its role in coordinating the cytoskeleton with mitochondrial function suggests it is a key player in cellular mechanotransduction and energy metabolism.
| 规格 | 起售价 |
|---|---|
| 登录后可查看 | |
技术参数
- 靶点基因名
- SETD3
- 基因别名
- C14orf154
- 蛋白别名
- SET domain containing 3, actin N3(tau)-histidine methyltransferase; SETD3
- UniProt
- Q86TU7
- 物种
- Human
产品详情
- 靶点名称
- SETD3
- 蛋白名称
- SET domain containing 3, actin N3(tau)-histidine methyltransferase
- 蛋白别名
- Actin-histidine N-methyltransferase; Protein-L-histidine N-tele-methyltransferase; SET domain-containing protein 3; hSETD3
- 靶点基因名
- SETD3
- 基因别名
- C14orf154
- UniProt
- Q86TU7
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
SET domain containing 3, actin N3(tau)-histidine methyltransferase (SETD3) is a highly specific S-adenosyl-L-methionine-dependent enzyme that methylates β-actin at the His73 residue. This post-translational modification is critical for promoting F-actin polymerization and maintaining cytoskeletal organization. SETD3 localizes to the cytoplasm and the outer mitochondrial membrane, where it facilitates actin assembly around mitochondria to regulate their morphology, motility, and oxidative phosphorylation. Loss of SETD3 activity results in fragmented mitochondrial networks and a metabolic shift toward glycolysis. Pathophysiologically, SETD3 is required for the efficient replication of enteroviruses and has been implicated in certain hematologic malignancies. Its role in coordinating the cytoskeleton with mitochondrial function suggests it is a key player in cellular mechanotransduction and energy metabolism.