title: NBR1-dependent selective autophagy is required for efficient cell-matrix adhesion site disassembly.
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.
authors.affiliation: a Department of Pathology and Helen Diller Family Comprehensive Cancer Center , University of California San Francisco , San Francisco , CA , USA.|b Biomedical Sciences Graduate Program , University of California San Francisco , San Francisco , CA , USA.
authors.forename: Candia M
authors.initials: CM
authors.lastname: Kenific
authors.affiliation: a Department of Pathology and Helen Diller Family Comprehensive Cancer Center , University of California San Francisco , San Francisco , CA , USA.
authors.forename: Jayanta
authors.initials: J
authors.lastname: Debnath
mesh_terms: D000818:Animals; D001343:Autophagy; D002465:Cell Movement; D021982:Cell-Matrix Junctions / Q000378:metabolism*; D022001:Focal Adhesions / Q000378:metabolism*; D006801:Humans; D008954:Models, Biological; D011506:Proteins / Q000378:metabolism*
chemical_list: D011506:Proteins
keywords: NBR1; cell migration; focal adhesion; selective autophagy; ubiquitin