The amyotrophic lateral sclerosis 8 protein VAPB is cleaved, secreted, and acts as a ligand for Eph receptors
about
Intrinsically unstructured domain 3 of hepatitis C Virus NS5A forms a "fuzzy complex" with VAPB-MSP domain which carries ALS-causing mutationsThe ALS8 protein VAPB interacts with the ER-Golgi recycling protein YIF1A and regulates membrane delivery into dendritesVAPB interacts with the mitochondrial protein PTPIP51 to regulate calcium homeostasisCharacterization of the properties of a novel mutation in VAPB in familial amyotrophic lateral sclerosisHuman VAP-C negatively regulates hepatitis C virus propagationSperm and oocyte communication mechanisms controlling C. elegans fertilityRegulated trafficking of the MSP/Eph receptor during oocyte meiotic maturation in C. elegansThe Unfolded Protein Response and the Role of Protein Disulfide Isomerase in NeurodegenerationAutophagy and Neurodegeneration: Insights from a Cultured Cell Model of ALSMolecular motor proteins and amyotrophic lateral sclerosisEph receptor signaling in C. elegansConverging mechanisms in ALS and FTD: disrupted RNA and protein homeostasisDrosophila as a model for unfolded protein response researchOxidative stress and mitochondrial damage: importance in non-SOD1 ALSRedox regulation in amyotrophic lateral sclerosisALS-associated TDP-43 induces endoplasmic reticulum stress, which drives cytoplasmic TDP-43 accumulation and stress granule formationAmyotrophic lateral sclerosis-linked mutant VAPB inclusions do not interfere with protein degradation pathways or intracellular transport in a cultured cell modelEmerging mechanisms of molecular pathology in ALSGlial ephrin-A3 regulates hippocampal dendritic spine morphology and glutamate transport.Structural, stability, dynamic and binding properties of the ALS-causing T46I mutant of the hVAPB MSP domain as revealed by NMR and MD simulationsMutations in the mitochondrial methionyl-tRNA synthetase cause a neurodegenerative phenotype in flies and a recessive ataxia (ARSAL) in humansC-Terminal Auto-Regulatory Motif of Hepatitis C Virus NS5B Interacts with Human VAPB-MSP to Form a Dynamic Replication ComplexBacteria, yeast, worms, and flies: exploiting simple model organisms to investigate human mitochondrial diseasesVAPC, an human endogenous inhibitor for hepatitis C virus (HCV) infection, is intrinsically unstructured but forms a "fuzzy complex" with HCV NS5B.The amyotrophic lateral sclerosis 8 protein, VAP, is required for ER protein quality controlModelling amyotrophic lateral sclerosis: progress and possibilitiesMSP hormonal control of the oocyte MAP kinase cascade and reactive oxygen species signaling.The secreted MSP domain of C. elegans VAPB homolog VPR-1 patterns the adult striated muscle mitochondrial reticulum via SMN-1The C. elegans VAPB homolog VPR-1 is a permissive signal for gonad development.Shared mechanisms between Drosophila peripheral nervous system development and human neurodegenerative diseasesEph receptors and ephrins in cancer: bidirectional signalling and beyond.Drosophila melanogaster in the study of human neurodegeneration.Neurodegenerative models in Drosophila: polyglutamine disorders, Parkinson disease, and amyotrophic lateral sclerosis.Axon guidance and synaptic maintenance: preclinical markers for neurodegenerative disease and therapeuticsResolving the paradox for protein aggregation diseases: NMR structure and dynamics of the membrane-embedded P56S-MSP causing ALS imply a common mechanism for aggregation-prone proteins to attack membranesGenetic heterogeneity of amyotrophic lateral sclerosis: implications for clinical practice and research.VAMP-associated protein B (VAPB) promotes breast tumor growth by modulation of Akt activity.A genetic screen identifies Tor as an interactor of VAPB in a Drosophila model of amyotrophic lateral sclerosis.Flightless flies: Drosophila models of neuromuscular disease.Mechanisms of neuroprotection by protein disulphide isomerase in amyotrophic lateral sclerosis.
P2860
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P2860
The amyotrophic lateral sclerosis 8 protein VAPB is cleaved, secreted, and acts as a ligand for Eph receptors
description
2008 nî lūn-bûn
@nan
2008 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի հունիսին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
name
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@ast
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@en
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@en-gb
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@nl
type
label
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@ast
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@en
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@en-gb
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@nl
prefLabel
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@ast
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@en
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@en-gb
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@nl
P2093
P2860
P921
P1433
P1476
The amyotrophic lateral sclero ...... as a ligand for Eph receptors
@en
P2093
Anthony Zoghbi
Claire Haueter
Hiroshi Tsuda
Hugo J Bellen
Justin Kwan
Kriti Mohan
Michael A Miller
Sung Min Han
Yadollah Harati
P2860
P304
P356
10.1016/J.CELL.2008.04.039
P407
P577
2008-06-01T00:00:00Z