Interaction between AP-5 and the hereditary spastic paraplegia proteins SPG11 and SPG15.
about
Complicated spastic paraplegia in patients with AP5Z1 mutations (SPG48).A hereditary spastic paraplegia mouse model supports a role of ZFYVE26/SPASTIZIN for the endolysosomal systemAP2 controls clathrin polymerization with a membrane-activated switchDelving into the complexity of hereditary spastic paraplegias: how unexpected phenotypes and inheritance modes are revolutionizing their nosologyDysfunction of spatacsin leads to axonal pathology in SPG11-linked hereditary spastic paraplegiaIn Vivo Evidence for Lysosome Depletion and Impaired Autophagic Clearance in Hereditary Spastic Paraplegia Type SPG11The cell biology of the endocytic system from an evolutionary perspectiveSpastic paraplegia proteins spastizin and spatacsin mediate autophagic lysosome reformation.Loss of spatacsin function alters lysosomal lipid clearance leading to upper and lower motor neuron degenerationSouffle/Spastizin controls secretory vesicle maturation during zebrafish oogenesis.Lysosomal abnormalities in hereditary spastic paraplegia types SPG15 and SPG11.Adaptor protein complexes and intracellular transport.Toward a comprehensive map of the effectors of rab GTPases.Loss of AP-5 results in accumulation of aberrant endolysosomes: defining a new type of lysosomal storage diseaseHuman Immunodeficiency Virus Type 2 (HIV-2) Gag Is Trafficked in an AP-3 and AP-5 Dependent Manner.Vestiges of Ent3p/Ent5p function in the giardial epsin homolog.Severe axonal neuropathy is a late manifestation of SPG11.Diagnosis, investigation and management of hereditary spastic paraplegias in the era of next-generation sequencing.Endocytic membrane trafficking and neurodegenerative disease.Modeling Axonal Defects in Hereditary Spastic Paraplegia with Human Pluripotent Stem Cells.Subcellular Trafficking of Mammalian Lysosomal Proteins: An Extended View.From all to (nearly) none: Tracing adaptin evolution in FungiAP-4 mediates export of ATG9A from the trans-Golgi network to promote autophagosome formation.Role of the AP-5 adaptor protein complex in late endosome-to-Golgi retrieval.Motor neuron degeneration in spastic paraplegia 11 mimics amyotrophic lateral sclerosis lesions.ALS5/SPG11/KIAA1840 mutations cause autosomal recessive axonal Charcot-Marie-Tooth disease.Neuronal lysosomes.Novel homozygous missense mutation in NT5C2 underlying hereditary spastic paraplegia SPG45.
P2860
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P2860
Interaction between AP-5 and the hereditary spastic paraplegia proteins SPG11 and SPG15.
description
2013 nî lūn-bûn
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2013 թուականի Յուլիսին հրատարակուած գիտական յօդուած
@hyw
2013 թվականի հուլիսին հրատարակված գիտական հոդված
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2013年の論文
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2013年学术文章
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2013年学术文章
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2013年学术文章
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2013年学术文章
@zh-my
2013年学术文章
@zh-sg
2013年學術文章
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name
Interaction between AP-5 and the hereditary spastic paraplegia proteins SPG11 and SPG15.
@ast
Interaction between AP-5 and the hereditary spastic paraplegia proteins SPG11 and SPG15.
@en
type
label
Interaction between AP-5 and the hereditary spastic paraplegia proteins SPG11 and SPG15.
@ast
Interaction between AP-5 and the hereditary spastic paraplegia proteins SPG11 and SPG15.
@en
prefLabel
Interaction between AP-5 and the hereditary spastic paraplegia proteins SPG11 and SPG15.
@ast
Interaction between AP-5 and the hereditary spastic paraplegia proteins SPG11 and SPG15.
@en
P2093
P2860
P50
P356
P1476
Interaction between AP-5 and the hereditary spastic paraplegia proteins SPG11 and SPG15.
@en
P2093
James Edgar
Jennifer Hirst
Margaret S Robinson
Matthias Mann
Robin Antrobus
P2860
P304
P356
10.1091/MBC.E13-03-0170
P577
2013-07-03T00:00:00Z