The Arp2/3 complex is an evolutionary conserved molecular machine that generates branched actin networks. When activated, the Arp2/3 complex contributes the actin branched junction and thus cross-links the polymerizing actin filaments in a network that exerts a pushing force. The different activators initiate branched actin networks at the cytosolic surface of different cellular membranes to promote their protrusion, movement, or scission in cell migration and membrane traffic. Here we review the structure, function, and regulation of all the direct regulators of the Arp2/3 complex that induce or inhibit the initiation of a branched actin network and that controls the stability of its branched junctions. Our goal is to present recent findings concerning novel inhibitory proteins or the regulation of the actin branched junction and place these in the context of what was previously known to provide a global overview of how the Arp2/3 complex is regulated in human cells. We focus on the human set of Arp2/3 regulators to compare normal Arp2/3 regulation in untransformed cells to the deregulation of the Arp2/3 system observed in patients affected by various cancers. In many cases, these deregulations promote cancer progression and have a direct impact on patient survival.

中文翻译：

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Arp2 / 3调节系统及其在癌症中的放松调控。

Arp2 / 3复合物是进化的保守分子机器，可生成分支的肌动蛋白网络。当被激活时，Arp2 / 3络合物有助于肌动蛋白分支连接，从而在施加推力的网络中交联聚合的肌动蛋白丝。不同的激活剂在不同细胞膜的胞质表面启动分支的肌动蛋白网络，以促进它们在细胞迁移和膜运输中的突出，运动或分裂。在这里，我们审查的结构，功能和Arp2 / 3复杂的所有直接调节剂的诱导或抑制分支肌动蛋白网络的启动，并控制其分支连接的稳定性的调节。我们的目标是提出有关新型抑制蛋白或肌动蛋白支化连接调控的最新发现，并将其置于先前已知的背景下，以提供有关人类细胞中Arp2 / 3复合物调控方式的全面概述。我们将重点放在人类的Arp2 / 3调节剂上，以比较未转化细胞中的正常Arp2 / 3调节与在受各种癌症影响的患者中观察到的Arp2 / 3系统的失调。在许多情况下，这些放松管制会促进癌症进展，并直接影响患者的生存。我们将重点放在人类的Arp2 / 3调节剂上，以比较未转化细胞中的正常Arp2 / 3调节与在受各种癌症影响的患者中观察到的Arp2 / 3系统的失调。在许多情况下，这些放松管制会促进癌症进展，并直接影响患者的生存。我们将重点放在人类的Arp2 / 3调节剂上，以比较未转化细胞中的正常Arp2 / 3调节与在受各种癌症影响的患者中观察到的Arp2 / 3系统的失调。在许多情况下，这些放松管制会促进癌症进展，并直接影响患者的生存。