Spectrin mutations that cause spinocerebellar ataxia type 5 impair axonal transport and induce neurodegeneration in Drosophila.
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Spectrin-based skeleton as an actor in cell signalingThe Microtubule Regulatory Protein Stathmin Is Required to Maintain the Integrity of Axonal Microtubules in DrosophilaSpectrin tetramer formation is not required for viable development in DrosophilaMitosis in neurons: Roughex and APC/C maintain cell cycle exit to prevent cytokinetic and axonal defects in Drosophila photoreceptor neuronsCytoplasmic capes are nuclear envelope intrusions that are enriched in endosomal proteins and depend upon βH-spectrin and Annexin B9The p25 subunit of the dynactin complex is required for dynein-early endosome interactionMethods to assay Drosophila behavior.Normal dynactin complex function during synapse growth in Drosophila requires membrane binding by ArfaptinPeriodic actin structures in neuronal axons are required to maintain microtubulesA KCNC3 mutation causes a neurodevelopmental, non-progressive SCA13 subtype associated with dominant negative effects and aberrant EGFR trafficking.Mutant β-III spectrin causes mGluR1α mislocalization and functional deficits in a mouse model of spinocerebellar ataxia type 5.Transgene rescue identifies an essential function for Drosophila beta spectrin in the nervous system and a selective requirement for ankyrin-2-binding activity.Beta-III spectrin mutation L253P associated with spinocerebellar ataxia type 5 interferes with binding to Arp1 and protein trafficking from the Golgi.Ankyrin-B interactions with spectrin and dynactin-4 are required for dystrophin-based protection of skeletal muscle from exercise injury.Prioritizing disease candidate genes by a gene interconnectedness-based approachAutosomal dominant cerebellar ataxia type III: a review of the phenotypic and genotypic characteristics.Neuronal dystonin isoform 2 is a mediator of endoplasmic reticulum structure and function.Microtubule stability, Golgi organization, and transport flux require dystonin-a2-MAP1B interaction.β-III spectrin is critical for development of purkinje cell dendritic tree and spine morphogenesis.βIII spectrin regulates the structural integrity and the secretory protein transport of the Golgi complexA human β-III-spectrin spinocerebellar ataxia type 5 mutation causes high-affinity F-actin binding.Spectrin Breakdown Products (SBDPs) as Potential Biomarkers for Neurodegenerative DiseasesPATHOLOGIES OF AXONAL TRANSPORT IN NEURODEGENERATIVE DISEASESGenetic studies of spectrin in the larval fat body of Drosophila melanogaster: evidence for a novel lipid uptake apparatus.Organelle transport in cultured Drosophila cells: S2 cell line and primary neurons.The synaptic cytoskeleton in development and disease.Mechanisms underlying synaptic vulnerability and degeneration in neurodegenerative disease.Selected recent in vivo studies on chemical measurements in invertebrates.Importance of gene dosage in controlling dendritic arbor formation during development.Cerebellar ataxias: β-III spectrin's interactions suggest common pathogenic pathways.Drosophila Neuronal Injury Follows a Temporal Sequence of Cellular Events Leading to Degeneration at the Neuromuscular Junction.Dystrophin and Spectrin, Two Highly Dissimilar Sisters of the Same Family.Methods to identify and analyze gene products involved in neuronal intracellular transport using Drosophila.Schwannomin-interacting Protein 1 Isoform IQCJ-SCHIP1 Is a Multipartner Ankyrin- and Spectrin-binding Protein Involved in the Organization of Nodes of Ranvier.Glial-derived prodegenerative signaling in the Drosophila neuromuscular system.Case of infantile onset spinocerebellar ataxia type 5.Structural basis for high-affinity actin binding revealed by a β-III-spectrin SCA5 missense mutation.Knockdown of acid-sensing ion channel 1a (ASIC1a) suppresses disease phenotype in SCA1 mouse model.Diverse mitotic functions of the cytoskeletal cross-linking protein Shortstop suggest a role in Dynein/Dynactin activity.A Novel Homozygous Mutation in SPTBN2 Leads to Spinocerebellar Ataxia in a Consanguineous Family: Report of a New Infantile-Onset Case and Brief Review of the Literature.
P2860
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P2860
Spectrin mutations that cause spinocerebellar ataxia type 5 impair axonal transport and induce neurodegeneration in Drosophila.
description
2010 nî lūn-bûn
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2010 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2010年の論文
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2010年論文
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2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
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2010年论文
@wuu
name
Spectrin mutations that cause ...... urodegeneration in Drosophila.
@ast
Spectrin mutations that cause ...... urodegeneration in Drosophila.
@en
type
label
Spectrin mutations that cause ...... urodegeneration in Drosophila.
@ast
Spectrin mutations that cause ...... urodegeneration in Drosophila.
@en
prefLabel
Spectrin mutations that cause ...... urodegeneration in Drosophila.
@ast
Spectrin mutations that cause ...... urodegeneration in Drosophila.
@en
P2093
P2860
P356
P1476
Spectrin mutations that cause ...... eurodegeneration in Drosophila
@en
P2093
Laura P W Ranum
Min-gang Li
Sarah E Mische
Thomas S Hays
P2860
P304
P356
10.1083/JCB.200905158
P407
P577
2010-04-01T00:00:00Z