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      Nix is a selective autophagy receptor for mitochondrial clearance.

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          Abstract

          Autophagy is the cellular homeostatic pathway that delivers large cytosolic materials for degradation in the lysosome. Recent evidence indicates that autophagy mediates selective removal of protein aggregates, organelles and microbes in cells. Yet, the specificity in targeting a particular substrate to the autophagy pathway remains poorly understood. Here, we show that the mitochondrial protein Nix is a selective autophagy receptor by binding to LC3/GABARAP proteins, ubiquitin-like modifiers that are required for the growth of autophagosomal membranes. In cultured cells, Nix recruits GABARAP-L1 to damaged mitochondria through its amino-terminal LC3-interacting region. Furthermore, ablation of the Nix:LC3/GABARAP interaction retards mitochondrial clearance in maturing murine reticulocytes. Thus, Nix functions as an autophagy receptor, which mediates mitochondrial clearance after mitochondrial damage and during erythrocyte differentiation.

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          Author and article information

          Journal
          EMBO Rep
          EMBO reports
          Springer Science and Business Media LLC
          1469-3178
          1469-221X
          Jan 2010
          : 11
          : 1
          Affiliations
          [1 ] Mediterranean Institute for Life Sciences, Mestrovicevo setaliste bb, HR-21000 Split, Croatia.
          Article
          embor2009256
          10.1038/embor.2009.256
          2816619
          20010802
          cd95aeb2-6ba7-4b68-ac33-e6a52b93d66a
          History

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