The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
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Multifunctional Mitochondrial AAA ProteasesThe Mitochondrial m-AAA Protease Prevents Demyelination and Hair Greying.The Function of the Mitochondrial Calcium Uniporter in Neurodegenerative Disorders.New insights into the role of mitochondrial calcium homeostasis in cell migration.Structure, Activity Regulation, and Role of the Mitochondrial Calcium Uniporter in Health and Disease.Permeability transition in human mitochondria persists in the absence of peripheral stalk subunits of ATP synthase.Pathological consequences of MICU1 mutations on mitochondrial calcium signalling and bioenergetics.Commentary: The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria.Proteolytic control of the mitochondrial calcium uniporter complex.Processing of SMDT1Identification of Physiological Substrates and Binding Partners of the Plant Mitochondrial Protease FTSH4 by the Trapping Approach.Multi-omic Mitoprotease Profiling Defines a Role for Oct1p in Coenzyme Q Production.Mitochondrial cardiomyopathies feature increased uptake and diminished efflux of mitochondrial calcium.ATAD3 proteins: brokers of a mitochondria-endoplasmic reticulum connection in mammalian cells.Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.Metalloproteases of the Inner Mitochondrial Membrane.m-AAA proteases, mitochondrial calcium homeostasis and neurodegeneration.C2orf47:AFG3L2 binds the transit peptide of SMDT1PMPCA:PMPCB cleaves the transit peptide of proSMDT1 (proEMRE)SMDT1 assists in assembling MCU; MCUB; MICU1; MICU2 (or MICU3) yielding the MCU complexAFG3L2 (m-AAA protease) degrades SMDT1 that is not assembled in MCUYME1L1 proteolyzes unassembled proSMDT1Loss of the Drosophila m-AAA mitochondrial protease paraplegin results in mitochondrial dysfunction, shortened lifespan, and neuronal and muscular degeneration.The still uncertain identity of the channel-forming unit(s) of the mitochondrial permeability transition poreUBXD1 is a mitochondrial recruitment factor for p97/VCP and promotes mitophagy
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P248
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P2860
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
description
2016 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2016 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
artículu científicu espublizáu en 2016
@ast
im Oktober 2016 veröffentlichter wissenschaftlicher Artikel
@de
scientific journal article
@en
vedecký článok (publikovaný 2016/10/06)
@sk
vědecký článek publikovaný v roce 2016
@cs
wetenschappelijk artikel (gepubliceerd op 2016/10/06)
@nl
наукова стаття, опублікована в жовтні 2016
@uk
مقالة علمية (نشرت في 6-10-2016)
@ar
name
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
@ast
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
@en
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
@nl
type
label
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
@ast
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
@en
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
@nl
prefLabel
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
@ast
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
@en
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
@nl
P2093
P50
P921
P1433
P1476
The m-AAA Protease Associated with Neurodegeneration Limits MCU Activity in Mitochondria
@en
P2093
Angela Paggio
Anne Korwitz
Kavya Bakka
Mareike Mühlmeister
Maria Patron
Philipp A Lampe
Ricarda Richter-Dennerlein
Simon E Tröder
Thorsten Decker
P304
P356
10.1016/J.MOLCEL.2016.08.020
P50
P577
2016-09-15T00:00:00Z