2024年12月24日 · CD2AP (CD2 Associated Protein) is a Protein Coding gene. Diseases associated with CD2AP include Focal Segmental Glomerulosclerosis 3 and Genetic Steroid-Resistant Nephrotic Syndrome. Among its related pathways are Cell junction organization and Nephrin/Neph1 signaling in the kidney podocyte.

CD2相關蛋白質(CD2-associated protein)是在人類中由CD2AP基因所編碼的蛋白質。 [1] [2] 該基因編碼一種調節肌動蛋白細胞骨架的"支架分子"(在神經元通路中的廣大連結區域聚積的蛋白分子)。

CD2-associated protein is a protein that in humans is encoded by the CD2AP gene. [5][6] This gene encodes a scaffolding molecule that regulates the actin cytoskeleton.

CD2AP (CD2-associated protein)是在人类中由CD2AP 基因 所编码的 蛋白质。 该基因编码一种调节肌动蛋白细胞骨架的"支架分子" (在神经元通路中的广大连结区域聚积的蛋白分子)。 该蛋白质直接与丝状肌动蛋白、及通过多种肌动蛋白结合位点的各种细胞膜的蛋白质、SH3结构域(SH3 domain)，以及含有SH3结构域结合位点之"富含 脯氨酸 区域" (proline-rich region)等交互作用。 胞质蛋白定位于 膜皱褶 (Membrane ruffling)， 脂筏 (Lipid raft)和细胞的前缘。

CD2相关蛋白质(CD2-associated protein)是在人类中由CD2AP基因所编码的蛋白质。 [1] [2] 该基因编码一种调节肌动蛋白细胞骨架的"支架分子"(在神经元通路中的广大连结区域聚积的蛋白分子)。

CD2AP（CD2-associated protein）作为一种适配器蛋白,与细胞内蛋白转运以及细胞骨架重塑密切相关。CD2AP被发现是AD的一个风险因子。目前的研究显示CD2AP能够影响Aβ的生成和沉积以及参与介导Tau蛋白的神经毒性。

2024年12月18日 · We demonstrate that CD2AP haploinsufficiency in microglia significantly attenuates cognitive and synaptic deficits, weakens the response of microglia to Aβ and the formation of disease-associated microglia (DAM), and alleviates synapse loss in 5xFAD mice. We show that CD2AP-deficient microglia exhibit compromised uptake ability.

2024年12月19日 · Our study presents the first in vivo evidence that CD2AP deficiency exacerbates the phenotypes and pathology of AD through the p38 MAPK pathway, identifying CD2AP/p38 MAPK as promising therapeutic targets for AD.

CD2AP（CD2-associated protein）是一种新发现的蛋白，在肾脏特异地表达于足细胞。 CD2AP单基因缺失小鼠发生大量蛋白尿，病理表现为足细胞足突广泛融合，提示CD2AP是调节足细胞功能并参与蛋白尿发生的关键分子，然而其功能机制未明。

Although the association between CD2AP and higher risk of AD has been well addressed, the mechanisms of CD2AP implicated in AD pathogenesis still unclear. More and more evidence reveals that CD2AP loss of function results to enhanced Aβ metabolism, Tau-induced neurotoxicity, synapse dysfunction and abnormal neurite structure.