Loss of the m-AAA protease subunit AFG₃L₂ causes mitochondrial transport defects and tau hyperphosphorylation. - Wikidata - wikimedia - TriplyDB

Loss of the m-AAA protease subunit AFG₃L₂ causes mitochondrial transport defects and tau hyperphosphorylation.

Loss of the m-AAA protease subunit AFG₃L₂ causes mitochondrial transport defects and tau hyperphosphorylation.

http://www.wikidata.org/entity/Q34323864

about

Mitochondrial Dysfunction Contributes to the Pathogenesis of Alzheimer's Disease Mitochondrial protein quality control: the mechanisms guarding mitochondrial health YME1L degradation reduces mitochondrial proteolytic capacity during oxidative stress Tau reduction prevents Aβ-induced axonal transport deficits by blocking activation of GSK3β.Mitochondrial Diseases Part II: Mouse models of OXPHOS deficiencies caused by defects in regulatory factors and other components required for mitochondrial function.The Mitochondrial m-AAA Protease Prevents Demyelination and Hair Greying.Loss of Drosophila i-AAA protease, dYME1L, causes abnormal mitochondria and apoptotic degeneration.Disturbed mitochondrial dynamics and neurodegenerative disorders.Genetic landscape remodelling in spinocerebellar ataxias: the influence of next-generation sequencing.New roles for mitochondrial proteases in health, ageing and disease.Mitochondrial Quality Control Proteases in Neuronal Welfare.Mitophagy and Alzheimer's Disease: Cellular and Molecular Mechanisms.Slower Dynamics and Aged Mitochondria in Sporadic Alzheimer's Disease.mPOS is a novel mitochondrial trigger of cell death - implications for neurodegeneration.Inhibition of p25/Cdk5 Attenuates Tauopathy in Mouse and iPSC Models of Frontotemporal Dementia.Mitochondrial diseases: the contribution of organelle stress responses to pathology.m-AAA proteases, mitochondrial calcium homeostasis and neurodegeneration.New practical definitions for the diagnosis of autosomal recessive spastic ataxia of Charlevoix-Saguenay.

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P2860

Loss of the m-AAA protease subunit AFG₃L₂ causes mitochondrial transport defects and tau hyperphosphorylation.

http://www.wikidata.org/entity/Q34323864

description

2014 nî lūn-bûn

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2014 թուականի Մարտին հրատարակուած գիտական յօդուած

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2014 թվականի մարտին հրատարակված գիտական հոդված

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

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2014年论文

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name

Loss of the m-AAA protease sub ...... and tau hyperphosphorylation.

@ast

Loss of the m-AAA protease sub ...... and tau hyperphosphorylation.

@en

Loss of the m-AAA protease sub ...... and tau hyperphosphorylation.

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type

label

Loss of the m-AAA protease sub ...... and tau hyperphosphorylation.

@ast

Loss of the m-AAA protease sub ...... and tau hyperphosphorylation.

@en

Loss of the m-AAA protease sub ...... and tau hyperphosphorylation.

@nl

prefLabel

Loss of the m-AAA protease sub ...... and tau hyperphosphorylation.

@ast

Loss of the m-AAA protease sub ...... and tau hyperphosphorylation.

@en

Loss of the m-AAA protease sub ...... and tau hyperphosphorylation.

@nl

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The EMBO Journal

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Loss of the m-AAA protease sub ...... and tau hyperphosphorylation.

@en

P2093

Anne Korwitz

http://www.w3.org/2001/XMLSchema#string

Astrid C Schauss

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David Herholz

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Michael J Baker

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Nikolay Kladt

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Paola Martinelli

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Sara Montagner

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Shuaiyu Wang

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Thomas Langer

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P2860

Whole-exome sequencing identifies homozygous AFG3L2 mutations in a spastic ataxia-neuropathy syndrome linked to mitochondrial m-AAA proteases

Inducible proteolytic inactivation of OPA1 mediated by the OMA1 protease in mammalian cells

PINK1 and Parkin target Miro for phosphorylation and degradation to arrest mitochondrial motility

Loss of m-AAA protease in mitochondria causes complex I deficiency and increased sensitivity to oxidative stress in hereditary spastic paraplegia

Spastic paraplegia and OXPHOS impairment caused by mutations in paraplegin, a nuclear-encoded mitochondrial metalloprotease

Parkin is recruited selectively to impaired mitochondria and promotes their autophagy

Fission and selective fusion govern mitochondrial segregation and elimination by autophagy

Mitochondrial AAA proteases--towards a molecular understanding of membrane-bound proteolytic machines

The m-AAA protease defective in hereditary spastic paraplegia controls ribosome assembly in mitochondria.

Conserved actin cysteine residues are oxidative stress sensors that can regulate cell death in yeast.

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1011-1026

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scholarly article

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10.1002/EMBJ.201387009

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9

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33

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Elena I Rugarli

Arun Kumar Kondadi

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2014-03-28T00:00:00Z

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