人 AGBL2 抗体对
01AB02465
AGBL carboxypeptidase 2 (AGBL2), also known as cytosolic carboxypeptidase 2, is a metallocarboxypeptidase that mediates the deglutamylation of tubulin and other intracellular substrates. It specifically removes polyglutamate side chains from the C-terminal glutamate residues of proteins, thereby regulating microtubule post-translational modifications and dynamics. AGBL2 localizes to centrioles and ciliary basal bodies, suggesting a specialized role in the maintenance of ciliary structure and cytoskeletal organization. By trimming long polyglutamate chains, it modulates the recruitment of microtubule-associated proteins and motor proteins. Clinically, AGBL2 has been associated with palindromic rheumatism and cardiofaciocutaneous syndrome 2, reflecting its importance in systemic physiological processes and developmental regulation.
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技术参数
- 靶点基因名
- AGBL2
- 基因别名
- CCP2
- 蛋白别名
- AGBL carboxypeptidase 2; AGBL2
- UniProt
- Q5U5Z8
- 物种
- Human
产品详情
- 靶点名称
- AGBL2
- 蛋白名称
- AGBL carboxypeptidase 2
- 蛋白别名
- Cytosolic carboxypeptidase 2; ATP/GTP-binding protein-like 2; Protein deglutamylase CCP2
- 靶点基因名
- AGBL2
- 基因别名
- CCP2
- UniProt
- Q5U5Z8
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
AGBL carboxypeptidase 2 (AGBL2), also known as cytosolic carboxypeptidase 2, is a metallocarboxypeptidase that mediates the deglutamylation of tubulin and other intracellular substrates. It specifically removes polyglutamate side chains from the C-terminal glutamate residues of proteins, thereby regulating microtubule post-translational modifications and dynamics. AGBL2 localizes to centrioles and ciliary basal bodies, suggesting a specialized role in the maintenance of ciliary structure and cytoskeletal organization. By trimming long polyglutamate chains, it modulates the recruitment of microtubule-associated proteins and motor proteins. Clinically, AGBL2 has been associated with palindromic rheumatism and cardiofaciocutaneous syndrome 2, reflecting its importance in systemic physiological processes and developmental regulation.