人 PICALM 抗体对
01AB02257
Phosphatidylinositol binding clathrin assembly protein (PICALM) is a cytosolic adaptor essential for clathrin-mediated endocytosis. It binds phosphatidylinositol lipids and recruits AP-2 and clathrin to the plasma membrane to drive the assembly of clathrin-coated vesicles. PICALM also mediates the endocytosis of R-SNAREs, coupling vesicle trafficking to synaptic transmission and receptor internalization. Additionally, it regulates autophagy-mediated turnover of proteins such as TAU and APP. Clinically, PICALM is involved in chromosomal translocations that create MLLT10-PICALM fusions in acute myeloid and T-cell lymphoblastic leukemias. Furthermore, PICALM variants are established risk factors for late-onset Alzheimer’s disease, where they influence amyloid-beta trafficking and clearance across the blood-brain barrier.
| 规格 | 起售价 |
|---|---|
| 登录后可查看 | |
技术参数
- 靶点基因名
- PICALM
- 基因别名
- CALM
- 蛋白别名
- phosphatidylinositol binding clathrin assembly protein; PICALM
- UniProt
- Q13492
- 物种
- Human
产品详情
- 靶点名称
- PICALM
- 蛋白名称
- phosphatidylinositol binding clathrin assembly protein
- 蛋白别名
- Phosphatidylinositol-binding clathrin assembly protein; Clathrin assembly lymphoid myeloid leukemia protein
- 靶点基因名
- PICALM
- 基因别名
- CALM
- UniProt
- Q13492
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
Phosphatidylinositol binding clathrin assembly protein (PICALM) is a cytosolic adaptor essential for clathrin-mediated endocytosis. It binds phosphatidylinositol lipids and recruits AP-2 and clathrin to the plasma membrane to drive the assembly of clathrin-coated vesicles. PICALM also mediates the endocytosis of R-SNAREs, coupling vesicle trafficking to synaptic transmission and receptor internalization. Additionally, it regulates autophagy-mediated turnover of proteins such as TAU and APP. Clinically, PICALM is involved in chromosomal translocations that create MLLT10-PICALM fusions in acute myeloid and T-cell lymphoblastic leukemias. Furthermore, PICALM variants are established risk factors for late-onset Alzheimer’s disease, where they influence amyloid-beta trafficking and clearance across the blood-brain barrier.