Arp3β Inhibitors

Arp3β Inhibitors primarily targets the Arp2/3 complex, a pivotal player in orchestrating actin polymerization and branching within cellular dynamics. Arp3β is an integral subunit of this complex, and thus, while the inhibitors may not single out Arp3β per se, they exhibit profound effects on its functioning by attenuating the overarching activities of the Arp2/3 complex.

CK-666 and CK-869, for instance, work allosterically, meaning they bind to a site other than the active site on the Arp2/3 complex. This binding causes a conformational change, rendering the complex inactive. Wiskostatin specifically disrupts the interaction between N-WASP and the Arp2/3 complex. This interaction is crucial because N-WASP is one of the nucleation-promoting factors (NPFs) that activate the Arp2/3 complex. In contrast, compounds such as Latrunculin A, Cytochalasin D, and Cytochalasin B do not target the Arp2/3 complex directly. Instead, they influence actin dynamics by either inhibiting its polymerization or by capping the filament ends, thereby indirectly affecting the branching process mediated by Arp2/3. In essence, these chemicals, by virtue of their specific or indirect actions on actin dynamics and the Arp2/3 complex, regulate the function of Arp3β as a part of this intricate cellular machinery.