抗人 ATAT1 抗体对
01AB01020
Alpha tubulin acetyltransferase 1 (ATAT1) is a key enzyme responsible for the acetylation of α-tubulin at lysine 40, a post-translational modification that stabilizes microtubules and enhances their resistance to mechanical stress. Structurally, ATAT1 shares similarities with Gcn5 histone acetyltransferases but features a unique substrate-binding groove that confers specificity for α-tubulin. It plays crucial roles in cellular processes such as cytoskeletal organization, intracellular trafficking, mitosis, and cell motility. ATAT1 activity is tightly regulated, and mutations affecting its catalytic residues significantly alter tubulin acetylation levels in vivo. Dysregulation of ATAT1-mediated tubulin acetylation is implicated in various diseases, including neurological disorders like Charcot-Marie-Tooth disease, Parkinson’s, and Alzheimer’s disease, as well as cancers such as breast, pancreatic, and head and neck squamous cell carcinoma. In the nervous system, ATAT1 influences axonal growth and regeneration, with reduced ATAT1 linked to impaired neurite outgrowth and axon injury.
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技术参数
- 靶点基因名
- ATAT1
- 基因别名
- C6orf134; MEC17
- 蛋白别名
- alpha tubulin acetyltransferase 1; ATAT1
- UniProt
- Q5SQI0
- 物种
- Human
产品详情
- 靶点名称
- ATAT1
- 蛋白名称
- alpha tubulin acetyltransferase 1
- 蛋白别名
- Alpha-tubulin N-acetyltransferase 1; Alpha-TAT; Alpha-TAT1; TAT; Acetyltransferase mec-17 homolog
- 靶点基因名
- ATAT1
- 基因别名
- C6orf134; MEC17
- UniProt
- Q5SQI0
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Alpha tubulin acetyltransferase 1 (ATAT1) is a key enzyme responsible for the acetylation of α-tubulin at lysine 40, a post-translational modification that stabilizes microtubules and enhances their resistance to mechanical stress. Structurally, ATAT1 shares similarities with Gcn5 histone acetyltransferases but features a unique substrate-binding groove that confers specificity for α-tubulin. It plays crucial roles in cellular processes such as cytoskeletal organization, intracellular trafficking, mitosis, and cell motility. ATAT1 activity is tightly regulated, and mutations affecting its catalytic residues significantly alter tubulin acetylation levels in vivo. Dysregulation of ATAT1-mediated tubulin acetylation is implicated in various diseases, including neurological disorders like Charcot-Marie-Tooth disease, Parkinson’s, and Alzheimer’s disease, as well as cancers such as breast, pancreatic, and head and neck squamous cell carcinoma. In the nervous system, ATAT1 influences axonal growth and regeneration, with reduced ATAT1 linked to impaired neurite outgrowth and axon injury.