Rab1-dependent ER-Golgi transport dysfunction is a common pathogenic mechanism in SOD1, TDP-43 and FUS-associated ALS.
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The Unfolded Protein Response and the Role of Protein Disulfide Isomerase in NeurodegenerationGolgi Fragmentation in ALS Motor Neurons. New Mechanisms Targeting Microtubules, Tethers, and Transport VesiclesProteomic Analysis of Dynein-Interacting Proteins in Amyotrophic Lateral Sclerosis Synaptosomes Reveals Alterations in the RNA-Binding Protein Staufen1.Protein Quality Control and the Amyotrophic Lateral Sclerosis/Frontotemporal Dementia ContinuumGolgi fragmentation in amyotrophic lateral sclerosis, an overview of possible triggers and consequences.Editorial: Golgi Pathology in Neurodegenerative Diseases.Stathmin 1/2-triggered microtubule loss mediates Golgi fragmentation in mutant SOD1 motor neurons.Interaction between optineurin and Rab1a regulates autophagosome formation in neuroblastoma cells.Old versus New Mechanisms in the Pathogenesis of ALS.Emerging nexus between RAB GTPases, autophagy and neurodegeneration.Stress granules at the intersection of autophagy and ALS.The entangled ER-mitochondrial axis as a potential therapeutic strategy in neurodegeneration: A tangled duo unchained.New links between SOD1 and metabolic dysfunction from a yeast model of amyotrophic lateral sclerosis.ALS/FTD-associated FUS activates GSK-3β to disrupt the VAPB-PTPIP51 interaction and ER-mitochondria associations.TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD.Conserved Oligomeric Golgi and Neuronal Vesicular Trafficking.Characterization of Dopaminergic System in the Striatum of Young Adult Park2-/- Knockout Rats.Causative Genes in Amyotrophic Lateral Sclerosis and Protein Degradation Pathways: a Link to Neurodegeneration.Disrupted ER-to-Golgi Trafficking Underlies Anti-HIV Drugs and Alcohol-Induced Cellular Stress and Hepatic Injury.Autophagy as a common pathway in amyotrophic lateral sclerosis.Rab GTPases and Membrane Trafficking in Neurodegeneration.
P2860
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P2860
Rab1-dependent ER-Golgi transport dysfunction is a common pathogenic mechanism in SOD1, TDP-43 and FUS-associated ALS.
description
2015 nî lūn-bûn
@nan
2015年の論文
@ja
2015年論文
@yue
2015年論文
@zh-hant
2015年論文
@zh-hk
2015年論文
@zh-mo
2015年論文
@zh-tw
2015年论文
@wuu
2015年论文
@zh
2015年论文
@zh-cn
name
Rab1-dependent ER-Golgi transp ...... TDP-43 and FUS-associated ALS.
@en
type
label
Rab1-dependent ER-Golgi transp ...... TDP-43 and FUS-associated ALS.
@en
prefLabel
Rab1-dependent ER-Golgi transp ...... TDP-43 and FUS-associated ALS.
@en
P2093
P50
P1476
Rab1-dependent ER-Golgi transp ...... TDP-43 and FUS-associated ALS
@en
P2093
Katherine A Southam
Manal A Farg
Mark Halloran
Reka P Toth
P2888
P304
P356
10.1007/S00401-015-1468-2
P577
2015-08-23T00:00:00Z
P5875
P6179
1020762468