Loss of iron triggers PINK1/Parkin‐independent mitophagy
TLDR
A mitophagy pathway is identified and characterized, the induction of which could prove beneficial as a potential therapy for several neurodegenerative diseases in which mitochondrial clearance is advantageous.Abstract:
In this study, we develop a simple assay to identify mitophagy inducers on the basis of the use of fluorescently tagged mitochondria that undergo a colour change on lysosomal delivery. Using this assay, we identify iron chelators as a family of compounds that generate a strong mitophagy response. Iron chelation-induced mitophagy requires that cells undergo glycolysis, but does not require PINK1 stabilization or Parkin activation, and occurs in primary human fibroblasts as well as those isolated from a Parkinson's patient with Parkin mutations. Thus, we have identified and characterized a mitophagy pathway, the induction of which could prove beneficial as a potential therapy for several neurodegenerative diseases in which mitochondrial clearance is advantageous.read more
Citations
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A Glance on the Role of Bacterial Siderophore from the Perspectives of Medical and Biotechnological Approaches.
TL;DR: Roles and applications of bacterial siderophore are discussed, which include the ability to chelate various other metal particles that have collocated away to focus the use of sidersophores on wound care items.
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ATPase activity of DFCP1 controls selective autophagy
Viola Nähse,Camilla Raiborg,Kia Wee Tan,Sissel Mørk,Maria Lyngaas Torgersen,Eva Maria Wenzel,Mireia Nàger,Veijo T. Salo,Terje Johansen,Elina Ikonen,Kay Oliver Schink,Harald Stenmark +11 more
TL;DR: It is demonstrated that DFCP1 is an ATPase that dimerizes in an ATP-dependent fashion and mediates ATPase-driven constriction of omegasomes to release autophagosomes for selective autophagy.
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Acute action of rotenone on excitability of catecholaminergic neurons in rostral ventrolateral medulla.
TL;DR: Results suggest that rotenone-induced electrophysiological changes of RVLM catecholaminergic neurons are caused by the opening of K-ATP channels, which are partly related to ROS generation.
Journal ArticleDOI
Comment on "mt-Keima detects PINK1-PRKN mitophagy in vivo with greater sensitivity than mito-QC".
TL;DR: One aspect of selective Autophagy that has garnered intense interest is mitochondrial autophagy (mitophagy), particularly PINK1-PRKN-mediated mitophagy as this has direct implications for Parkinson's disease.
Journal ArticleDOI
Mitophagy in the aging nervous system
Anna Rappe,Thomas G. McWilliams +1 more
TL;DR: The recent profiling of mitophagy reporter mice has revealed variegated vistas of steady-state mitochondrial destruction across different tissues, which have considerable implications for targetingMitophagy and other degradative pathways in age-related neurological disease.
References
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Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
TL;DR: It is shown that Parkin is selectively recruited to dysfunctional mitochondria with low membrane potential in mammalian cells and this recruitment promotes autophagy of damaged mitochondria and implicate a failure to eliminate dysfunctional mitochondira in the pathogenesis of Parkinson's disease.
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Sulforhodamine B colorimetric assay for cytotoxicity screening
TL;DR: The sulforhodamine B (SRB) assay is used for cell density determination, based on the measurement of cellular protein content, which is an efficient and highly cost-effective method for screening.
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Mitochondria: In Sickness and in Health
TL;DR: This work provides a current view of how mitochondrial functions impinge on health and disease and identifies mitochondrial dysfunction as a key factor in a myriad of diseases, including neurodegenerative and metabolic disorders.
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Dissection of the Autophagosome Maturation Process by a Novel Reporter Protein, Tandem Fluorescent-Tagged LC3
TL;DR: Using this method, evidence that overexpression of a dominant negative form of Rab7 prevented the fusion of autophagosomes with lysosomes is provided, suggesting that Rab7 is involved in this step.
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Reactive oxygen species are essential for autophagy and specifically regulate the activity of Atg4
TL;DR: The role of reactive oxygen species (ROS) as signaling molecules in starvation‐induced autophagy is described and a cysteine residue located near the HsAtg4 catalytic site is specified as a critical for this regulation.