Results 51 to 60 of about 17,983 (257)
The MFN1 and MFN2 mitofusins promote clustering between mitochondria and peroxisomes
The MFN1 and MFN2 mitofusin proteins localize to the outer mitochondrial membrane, where they may help functionally tether mitochondria to peroxisomes.
Yinbo Huo +4 more
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When, where and how? Focus on neuronal calcium dysfunctions in Alzheimer's Disease. [PDF]
Alzheimer\u2019s disease (AD), since its characterization as a precise form of dementia with its own pathological hallmarks, has captured scientists\u2019 attention because of its complexity.
AGOSTINI, MARIO, FASOLATO, CRISTINA
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Mitofusins as mitochondrial anchors and tethers
Mitochondria have their own genomes and their own agendas. Like their primitive bacterial ancestors, mitochondria interact with their environment and organelle colleagues at their physical interfaces, the outer mitochondrial membrane. Among outer membrane proteins, mitofusins (MFN) are increasingly recognized for their roles as arbiters of mitochondria-
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Pro-diversity mitofusins [PDF]
Affirmative action groups would be proud of Mfn proteins. These fusion proteins work better with diverse partners, say Detmer and Chan (page [405][1]). The results might help explain why only certain neurons are susceptible in Charcot-Marie-Tooth disease 2A (CMT2A).
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Rapid degradation of mutant SLC25A46 by the ubiquitin-proteasome system results in MFN1/2-mediated hyperfusion of mitochondria. [PDF]
SCL25A46 is a mitochondrial carrier protein that surprisingly localizes to the outer membrane and is distantly related to Ugo1. Here we show that a subset of SLC25A46 interacts with mitochondrial dynamics components and the MICOS complex.
Claypool, Steven M +6 more
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Correcting mitochondrial fusion by manipulating mitofusin conformations [PDF]
Mitochondria are dynamic organelles that exchange contents and undergo remodelling during cyclic fusion and fission. Genetic mutations in MFN2 (the gene encoding mitofusin 2) interrupt mitochondrial fusion and cause the untreatable neurodegenerative condition Charcot-Marie-Tooth disease type 2A (CMT2A). It has not yet been possible to directly modulate
Antonietta, Franco +14 more
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αSynuclein control of mitochondrial homeostasis in human-derived neurons is disrupted by mutations associated with Parkinson’s disease [PDF]
The etiology of Parkinson’s disease (PD) converges on a common pathogenic pathway of mitochondrial defects in which α-Synuclein (αSyn) is thought to play a role.
Alloatti, Matías +12 more
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Parkin interacts with Ambra1 to induce mitophagy [PDF]
Mutations in the gene encoding Parkin are a major cause of recessive Parkinson's disease. Recent work has shown that Parkin translocates from the cytosol to depolarized mitochondria and induces their autophagic removal (mitophagy). However, the molecular
Cornelissen, Tom +6 more
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Mitophagy: Mitofusin Recruits a Mitochondrial Killer [PDF]
Parkin is a cytosolic ubiquitin ligase that translocates to damaged mitochondria and promotes their degradation. Recent work demonstrates that a phosphorylated form of the mitochondrial fusion protein Mitofusin 2 serves as a receptor for Parkin translocation to damaged mitochondria.
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Hypertonia is a neurological dysfunction associated with a number of central nervous system disorders, including cerebral palsy, Parkinson’s disease, dystonia, and epilepsy.
Crystal A. Lee, Lih-Shen Chin, Lian Li
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