Rubicon: LC3‐associated phagocytosis and beyond. (29th December 2017)

• Record Type: Journal Article
• Authors: Wong, Sing‐Wai; Sil, Payel; Martinez, Jennifer
• Is Part Of: FEBS journal. Volume 285:Number 8(2018)
• Page Start: 1379
• Page End: 1388
• Publication Date: 2017-12-29
• Subjects: autoimmunity -- autophagy -- endosome -- immunology -- interferon -- LC3‐associated phagocytosis; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Pathology, Molecular -- Periodicals; 572
• DOI: 10.1111/febs.14354
• Languages: English
• ISSNs: 1742-464X

Abstract

Abstract : 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. Abstract : Originally discovered as an inhibitor of canonical autophagy, we now recognize the Rubicon can function in multiple biological pathways, including endosomal trafficking, LC3‐associated phagocytosis, and autoimmune and inflammatory diseases. Exploration into how these pathways converge and how to target Rubicon pharmacologically is of great interest.