例如:"lncRNA", "apoptosis", "WRKY"

Rubicon: LC3-associated phagocytosis and beyond.

FEBS J. 2018 Apr;285(8):1379-1388. doi:10.1111/febs.14354. Epub 2017 Dec 29
Sing-Wai Wong 1 , Payel Sil 2 , Jennifer Martinez 2
Sing-Wai Wong 1 , Payel Sil 2 , Jennifer Martinez 2

[No authors listed]

Author information
  • 1 Oral and Craniofacial Biomedicine Curriculum, School of Dentistry, University of North Carolina at Chapel Hill, NC, USA.
  • 2 Immunity, Inflammation, and Disease Laboratory, NIEHS, National Institutes of Health, Research Triangle Park, NC, USA.

摘要


Rubicon (Rubcn) was initially identified as a component of the Class III PI3K complex and a negative regulator of canonical autophagy and endosomal trafficking. However, Rubicon has attracted the most notoriety because of its critical role in LC3-associated phagocytosis (LAP), a form of noncanonical autophagy that utilizes some components of the autophagy machinery to process extracellular cargo. Additionally, Rubicon has been identified as a key modulator of the inflammatory response and viral replication. In this review, we discuss the known functions of Rubicon in LAP and other signaling pathways and examine the disease pathologies associated with Rubicon dysfunction in animal models and humans.

KEYWORDS: LC3-associated phagocytosis, autoimmunity, autophagy, endosome, immunology, interferon