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Convergence of Parkin, PINK1, and α-Synuclein on Stress-induced Mitochondrial Morphological Remodeling.

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TLDR
Under moderate mitochondrial stress conditions, parkin stimulates mitochondrial fusion instead of mitophagy by catalyzing K63-linked ubiquitination and inactivating α-synuclein, which provides a physiological context to functionally connect key PARK genes in the pathogenesis of Parkinson disease.
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This article is published in Journal of Biological Chemistry.The article was published on 2015-05-29 and is currently open access. It has received 74 citations till now. The article focuses on the topics: Parkin & PINK1.

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Oxidative stress and Parkinson’s disease

TL;DR: A mini review of the classical pathways involving these mechanisms of neurodegeneration, the biochemical and molecular events that mediate or regulate DA neuronal vulnerability, and the role of PD-related gene products in modulating cellular responses to oxidative stress in the course of the Neurodegenerative process are given.
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Proteinopathy, oxidative stress and mitochondrial dysfunction: cross talk in Alzheimer's disease and Parkinson's disease.

TL;DR: Understanding the common nature of interactions among these three damage mechanisms may help to identify putative neuroprotective strategies that would be beneficial in both the clinical conditions.
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Regulators of mitochondrial dynamics in cancer.

TL;DR: This review focuses on key regulators of mitochondrial dynamics and their role in cancer.
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Serine Availability Influences Mitochondrial Dynamics and Function through Lipid Metabolism

TL;DR: A role for serine in supporting mitochondrial function and cell proliferation through ceramide metabolism is defined, and supplementation of the lipid component of bovine serum or C16:0-ceramide could partially restore defects in cell proliferation and mitochondrial fragmentation induced by serine deprivation.
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Structure, function and toxicity of alpha-synuclein: the Bermuda triangle in synucleinopathies.

TL;DR: Establishing whether alpha‐synuclein has a causative role in all synucleinopathies will enable the identification of targets for the development of novel therapeutic strategies for this devastating group of disorders.
References
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Journal ArticleDOI

Chronic systemic pesticide exposure reproduces features of Parkinson's disease

TL;DR: It is reported that chronic, systemic inhibition of complex I by the lipophilic pesticide, rotenone, causes highly selective nigrostriatal dopaminergic degeneration that is associated behaviorally with hypokinesia and rigidity.
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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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PINK1 is selectively stabilized on impaired mitochondria to activate Parkin.

TL;DR: The authors suggest that PINK1 and Parkin form a pathway that senses damaged mitochondria and selectively targets them for degradation.
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PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1

TL;DR: Functional links between PINK1, Parkin and the selective autophagy of mitochondria, which is implicated in the pathogenesis of Parkinson's disease, are provided.
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Mitofusins Mfn1 and Mfn2 coordinately regulate mitochondrial fusion and are essential for embryonic development

TL;DR: It is concluded that Mfn1 and Mfn2 have both redundant and distinct functions and act in three separate molecular complexes to promote mitochondrial fusion, and by enabling cooperation between mitochondria, has protective effects on the mitochondrial population.
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