Essential role for Nix in autophagic maturation of erythroid cells

By Héctor Sandoval, P. Thiagarajan, S. Dasgupta, A. Schumacher, J. Prchal, Min Chen, Jin Wang. Nature, 2008

1,162 citations recorded by the source corpus.

Subfields: Epidemiology, Genetics, Physiology

View Paper: https://www.semanticscholar.org/paper/2a5b993a2aedb25f2dd2f11b7da2f15f251514d3

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Citations in the corpus

Atg32 is a mitochondrial protein that confers selectivity during mitophagy (2009, background): “For example, during erythroid cell maturation, mitochondria are eliminated by autophagy when Nix-dependent loss of membrane potential is induced (Sandoval et al., 2008; Schweers et al., 2007).”
Autophagy-Dependent Ferroptosis: Machinery and Regulation (2020, neutral): “, BCL2 interacting protein 3 like [BNIP3L/NIX] (Sandoval et al., 2008), FUN14 domain containing 1 [FUNDC1] (Liu et al.”
A role for ubiquitin in selective autophagy. (2009, background): “In mammals, mitochondria-localized BH3 domain-only protein BNIP3L/NIX (Figure 1) was shown to be critically involved in the entrapment of mitochondria by autophagosomes during the programmed elimination of mitochondria in maturing reticulocytes (Sandoval et al., 2008; Schweers et al., 2007).”
Mitochondrial outer-membrane protein FUNDC1 mediates hypoxia-induced mitophagy in mammalian cells (2012, methodology): “(c) HeLa cells were transfected with (Flag)N-Fundc1(1-155)-C(Myc) or (Flag)N-Fundc1(1-139)C(Myc) vectors, respectively.”
Autophagy and the integrated stress response (2010, positive): “5D) and in mice, BNIP3L/Nix is required for the removal of mitochondria during erythroid maturation (Sandoval et al., 2008).”
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy (2008, background): “Although little is known about the proteins regulating this process in mammalian cells, recently, BNIP3L/NIX was found to promote degradation of mitochondria in reticulocytes by triggering the loss of mitochondrial membrane potential ( Schweers et al., 2007 ; Sandoval et al., 2008 ).”
Oxidative stress and autophagy: the clash between damage and metabolic needs (2014, background): “This is a ‘programmed’ event, independent on any damage response that is required, for example, inmitochondrial elimination during erythrocyte differentiation.(65,66) The second mechanism is activated for the selective dismissal of impaired or dysfunctional mitochondria.”
The pathways of mitophagy for quality control and clearance of mitochondria (2012, background): “mitochondria, but not other organelles that are lost during maturation such as ribosomes and the nucleus.(12,47)”
Molecular definitions of autophagy and related processes (2017, positive): “…on BCL2 interacting protein 3-like (BNIP3L; best known as NIX) and the complete removal of mitochondria may also depend on unconventional secretion (Sandoval et The selective removal of depolarized mitochondria also involves the PINK1-PARK2 system and PHB2 (Clark et al , 2006; Park et al , 2006),…”
The mitophagy pathway and its implications in human diseases (2023, background): “13,106,107 The expression of NIX is upregulated in terminally differentiated erythrocytes.”
The BCL-2 Family Reunion (2010, background): “The mechanism by which BNIP3L induces mitophagy is not known, but the process is BAK and BAX independent (Sandoval et al., 2008).”
Autophagy and Mitophagy in Cardiovascular Disease. (2017, background): “Mitophagy participates in physiological processes, such as the removal of paternal mitochondria from fertilized eggs(17) and the progressive clearance of the mitochondrial network that accompanies the formation of mature erythrocytes.(18) In addition, mitophagy is key for the removal of mitochondria”
Mechanisms of mitophagy (2011, background): “, and mature red blood cells from mice lacking NIX retain residual mitochondri”