Spectrin mutations that cause spinocerebellar ataxia type 5 impair axonal transport and induce neurodegeneration in Drosophila. - Test2 - elhamkhani - TriplyDB

Spectrin mutations that cause spinocerebellar ataxia type 5 impair axonal transport and induce neurodegeneration in Drosophila.

Spectrin mutations that cause spinocerebellar ataxia type 5 impair axonal transport and induce neurodegeneration in Drosophila.

http://www.wikidata.org/entity/Q33788461

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Spectrin-based skeleton as an actor in cell signaling The Microtubule Regulatory Protein Stathmin Is Required to Maintain the Integrity of Axonal Microtubules in Drosophila Spectrin tetramer formation is not required for viable development in Drosophila Mitosis in neurons: Roughex and APC/C maintain cell cycle exit to prevent cytokinetic and axonal defects in Drosophila photoreceptor neurons Cytoplasmic capes are nuclear envelope intrusions that are enriched in endosomal proteins and depend upon βH-spectrin and Annexin B9 The p25 subunit of the dynactin complex is required for dynein-early endosome interaction Methods to assay Drosophila behavior.Normal dynactin complex function during synapse growth in Drosophila requires membrane binding by Arfaptin Periodic actin structures in neuronal axons are required to maintain microtubules A 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 approach Autosomal 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 complex A human β-III-spectrin spinocerebellar ataxia type 5 mutation causes high-affinity F-actin binding.Spectrin Breakdown Products (SBDPs) as Potential Biomarkers for Neurodegenerative Diseases PATHOLOGIES OF AXONAL TRANSPORT IN NEURODEGENERATIVE DISEASES Genetic 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.

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P2860

Spectrin mutations that cause spinocerebellar ataxia type 5 impair axonal transport and induce neurodegeneration in Drosophila.

http://www.wikidata.org/entity/Q33788461

description

2010 nî lūn-bûn

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2010 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի ապրիլին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Spectrin mutations that cause ...... urodegeneration in Drosophila.

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Spectrin mutations that cause ...... urodegeneration in Drosophila.

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Spectrin mutations that cause ...... urodegeneration in Drosophila.

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Spectrin mutations that cause ...... urodegeneration in Drosophila.

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Spectrin mutations that cause ...... urodegeneration in Drosophila.

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Spectrin mutations that cause ...... urodegeneration in Drosophila.

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Spectrin mutations that cause ...... eurodegeneration in Drosophila

@en

P2093

Laura P W Ranum

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

Min-gang Li

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

Sarah E Mische

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

Thomas S Hays

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P2860

A widely expressed betaIII spectrin associated with Golgi and cytoplasmic vesicles

Spectrin and ankyrin-based pathways: metazoan inventions for integrating cells into tissues

Dynactin is required for coordinated bidirectional motility, but not for dynein membrane attachment.

Golgi localization of Syne-1

An ankyrin-based mechanism for functional organization of dystrophin and dystroglycan

The interaction between cytoplasmic dynein and dynactin is required for fast axonal transport

Regulation of cytoplasmic dynein function in vivo by the Drosophila Glued complex

[Beta]IV-spectrin regulates sodium channel clustering through ankyrin-G at axon initial segments and nodes of Ranvier

Dynactin is required for bidirectional organelle transport

Ankyrin-G coordinates assembly of the spectrin-based membrane skeleton, voltage-gated sodium channels, and L1 CAMs at Purkinje neuron initial segments

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143-158

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189

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Karen R Armbrust

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43023582

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20368622

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2854382

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