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Nix is a selective autophagy receptor for mitochondrial clearance (CROSBI ID 178530)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Novak, Ivana ; Kirkin, Vladimir ; McEwan, David G. ; Zhang, Ji ; Wild, Philipp ; Rozenknop, Alexis ; Rogov, Vladimir ; Lohr, Frank ; Popovic, Doris ; Occhipinti, Angelo et al. Nix is a selective autophagy receptor for mitochondrial clearance // EMBO reports, 11 (2010), 1; 45-51. doi: 10.1038/embor.2009.256

Podaci o odgovornosti

Novak, Ivana ; Kirkin, Vladimir ; McEwan, David G. ; Zhang, Ji ; Wild, Philipp ; Rozenknop, Alexis ; Rogov, Vladimir ; Lohr, Frank ; Popovic, Doris ; Occhipinti, Angelo ; Reichert, Andreas S. ; Terzić, Janoš ; Doetsch, Volker ; Ney, Paul A. ; Đikić, Ivan

engleski

Nix is a selective autophagy receptor for mitochondrial clearance

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.

reticulocyte maturation; cell-death; structural basis; mitophagy; degradation; ubiquitin; BNIP3; apoptosis; protein; E3

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Podaci o izdanju

11 (1)

2010.

45-51

objavljeno

1469-221X

10.1038/embor.2009.256

Povezanost rada

Biologija

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