NBR1-dependent selective autophagy is required for efficient cell-matrix adhesion site disassembly. Issue 10 (2nd October 2016)

• Record Type: Journal Article
• Authors: Kenific, Candia M.; Debnath, Jayanta
• Is Part Of: Autophagy. Volume 12:Issue 10(2016)
• Page Start: 1958
• Page End: 1959
• Publication Date: 2016-10-02
• Subjects: cell migration -- focal adhesion -- NBR1 -- selective autophagy -- ubiquitin; Autophagic vacuoles -- Periodicals; Apoptosis -- Periodicals; Cell death -- Periodicals; Lysosomes -- Periodicals; Degeneration (Pathology) -- Periodicals; Autophagy -- Periodicals; Cell Death -- Periodicals; Lysosomes -- Periodicals; Periodicals; 571.936
• DOI: 10.1080/15548627.2016.1212789
• Languages: English
• ISSNs: 1554-8627

Abstract

ABSTRACT: Macroautophagy/autophagy has classically been recognized for its vital role in supporting cellular survival during various stresses. However, emerging work has demonstrated that selective autophagy has an impact on diverse cell biological processes by mediating the degradation of various cellular contents during normal cellular homeostasis. We recently established that selective autophagy supports cell migration by promoting the turnover of integrin-based cell-matrix adhesion sites, or focal adhesions (FAs). The autophagy cargo receptor NBR1 acts as a critical mediator of this pathway by promoting targeting of autophagosomes to FAs, leading to their disassembly via the sequestration of FA proteins. Our results demonstrate FAs as a new cellular target for selective autophagy.