BCMB Allied Program, Weill Cornell Medical College, 1300 York Avenue, New York, NY 10065, USA; Cell Biology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
Semin Cancer Biol. 2013 Oct;23(5):329-36. doi: 10.1016/j.semcancer.2013.05.004. Epub 2013 May 30.
Recent evidence has uncovered cross-regulation of mechanisms of cell engulfment by proteins of the autophagy pathway, in what is called LC3-Associated Phagocytosis, or LAP. By LAP, lysosome fusion to phagosomes and the degradation of engulfed extracellular cargo are facilitated by autophagy proteins that lipidate LC3 onto phagosome membranes. Here we discuss the contexts where LAP is known to occur by focusing on potential roles in tumorigenesis, including predicted consequences of LAP inhibition.
最近的证据揭示了自噬途径中的蛋白质对细胞吞噬机制的交叉调控,这种现象被称为 LC3 相关的吞噬作用,或 LAP。通过 LAP,溶酶体与吞噬体融合,以及吞噬的细胞外货物的降解,是由将 LC3 脂质化到吞噬体膜上的自噬蛋白来促进的。在这里,我们通过关注 LAP 在肿瘤发生中的潜在作用,包括对 LAP 抑制的预测后果,来讨论其已知发生的情况。