组装过程受到衔接蛋白(如AP2复合物)的动态调控。 功能多样性 内吞与物质运输:Clathrin介导受体-配体内吞,例如低密度脂蛋白(LDL)的摄取。囊泡形成后脱去包被,与早期内体融合完成物质分选。 细胞分裂调控:在有丝分裂中,Clathrin通过调控细胞膜重塑参与胞质分裂。 信号转导辅助:通过内化膜受体(如G蛋...
It is now apparent that AP2 serves as a pivotal hub for protein interactions to mediate clathrin coated pit maturation, and couples lattice formation to membrane deformation. As a key driver for clathrin assembly, AP2 complements the attenuating role of clathrin light chain subunits, which enable...
AP2 clathrin adaptor: target recognition unveiled
clathrin adaptor complex AP2, mu subunit clathrin adaptor complex AP3 mu-3A subunit clathrin adaptor protein AP47 Clathrin assembly protein 2 small chain Clathrin assembly protein complex 1 beta large chain clathrin assembly protein complex 1 gamma large chain ...
Here we use atomic force microscopy to assess the contributions of clathrin and its membrane adaptor AP2 to clathrin coat stiffness, which determines the mechanics of vesicle formation. We found that clathrin coats are less than ten‐fold stiffer than the membrane they enclose, suggesting a ...
And pitstop 2 enhanced the association of ±IIb3 with clathrin, and AP2 indicated that pitstop 2 inhibit platelet activation is probably due to disturbance of the dynamic dissociation of ±IIb3 from clathrin and AP2. Further study demonstrated that Src/PLC/PKC was the key pathway to trigger ...
5P2produced by PIPKIγi2 binds to the AP1B complex to enhance its function in recruiting clathrin coats. PIPKIγi2 also interacts with the β2 subunit of the AP2 complex by a C-terminal sequence conserved in all PIPKIγisoformsthat is close to the junction of the PIPKIγi2 C-termi...
AP-1/σ1B-deficiency causes X-linked intellectual disability. AP-1/σ1B −/− mice have impaired synaptic vesicle recycling, fewer synaptic vesicles and enhanced endosome maturation mediated by AP-1/σ1A. Despite defects in synaptic vesicle recycling
We have used RNA interference to knock down the AP-2 mu2 subunit and clathrin heavy chain to undetectable levels in HeLaM cells. Clathrin-coated pits associated with the plasma membrane were still present in the AP-2-depleted cells, but they were 12-fold less abundant than in control cells...
Clathrin-mediated endocytosis (CME), which occurs at clathrin coated pits (CCPs), requires the major coat proteins, clathrin and AP2 complexes together with a myriad of endocytic accessory factors and lipids. CME proceeds through multiple stages, including initiation, stabilization of nascent CCPs, ...