The actin foci are generated by Arp2/3-mediated branched-actin polymerization and stochastically associate with antigen clusters to mediate internalization.
The finding that Arp2/3 complex activity is important for B cell responses to spatially restricted membrane-bound antigens but not for soluble antigens highlights a critical role for Arp2/3 complex-dependent actin remodeling in B cell responses to antigen-presenting cell-bound antigens.
We find that the expression of the actin polymerization complex Arp2/3 is reduced in dysbindin-deficient cells thus affecting actin-dependent phenotypes
Arp2 and Arp3 expression was increased under atherosclerotic conditions both in ApoE-/- mice and in oxidized low-density lipoproteins stimulated human coronary artery endothelial cells (HCAECs).
Dendritic cells possess a mechanism to pass through micrometric constrictions. This mechanism is based on a rapid Arp2/3-dependent actin nucleation around the nucleus that disrupts the nuclear lamina the main structure limiting nuclear deformability.
Arp2/3 complex is an essential regulator of adipocyte development through control of the formation of cortical actin structures which may facilitate nutrient uptake and signalling events.
Show that the Arp2/3 complex localizes to the oocyte cortical cap in a Ran-GTPase-dependent manner and nucleates actin filaments in the cortical cap and a cytoplasmic actin network.
This website requires cookies, and the limited processing of your personal data in order to function. By using the site you are agreeing to this as outlined in our Privacy Notice.