Toxicity from different SOD1 mutants dysregulates the complement system and the neuronal regenerative response in ALS motor neurons.
about
Mechanisms of granulin deficiency: lessons from cellular and animal modelsRNA-Seq profiling of spinal cord motor neurons from a presymptomatic SOD1 ALS mouseThe potential of GPNMB as novel neuroprotective factor in amyotrophic lateral sclerosisImproved RNA preservation for immunolabeling and laser microdissection.Progranulin is expressed within motor neurons and promotes neuronal cell survivalDeregulated expression of cytoskeleton related genes in the spinal cord and sciatic nerve of presymptomatic SOD1(G93A) Amyotrophic Lateral Sclerosis mouse model.Axotomy-induced target disconnection promotes an additional death mechanism involved in motoneuron degeneration in amyotrophic lateral sclerosis transgenic mice.Vascular endothelial growth factor prevents G93A-SOD1-induced motor neuron degeneration.Familial amyotrophic lateral sclerosis is associated with a mutation in D-amino acid oxidaseProduction of RNA for transcriptomic analysis from mouse spinal cord motor neuron cell bodies by laser capture microdissection.ALS-causing SOD1 mutants generate vascular changes prior to motor neuron degeneration.Versatility of the complement system in neuroinflammation, neurodegeneration and brain homeostasisThe unfolded protein response in familial amyotrophic lateral sclerosis.Activation of interferon signaling pathways in spinal cord astrocytes from an ALS mouse model.Astrocytes from familial and sporadic ALS patients are toxic to motor neuronsNeuron-specific antioxidant OXR1 extends survival of a mouse model of amyotrophic lateral sclerosisD-amino acid oxidase controls motoneuron degeneration through D-serine.Glycosphingolipids are modulators of disease pathogenesis in amyotrophic lateral sclerosisSpinal cord trauma and the molecular point of no returnLaser capture microscopy coupled with Smart-seq2 for precise spatial transcriptomic profiling.Identification of pharmacological targets in amyotrophic lateral sclerosis through genomic analysis of deregulated genes and pathways.Translational profiling identifies a cascade of damage initiated in motor neurons and spreading to glia in mutant SOD1-mediated ALS.An indicator cell assay for blood-based diagnostics.Motor neuron-immune interactions: the vicious circle of ALS.Complement is dispensable for neurodegeneration in Niemann-Pick disease type C.Current and future directions in genomics of amyotrophic lateral sclerosis.Metabolomic Analysis Reveals Increased Aerobic Glycolysis and Amino Acid Deficit in a Cellular Model of Amyotrophic Lateral Sclerosis.Complement activation at the motor end-plates in amyotrophic lateral sclerosis.Stathmin 1/2-triggered microtubule loss mediates Golgi fragmentation in mutant SOD1 motor neurons.Reduced activity of AMP-activated protein kinase protects against genetic models of motor neuron disease.Schwann cells expressing dismutase active mutant SOD1 unexpectedly slow disease progression in ALS mice.Mitochondrial damage revealed by immunoselection for ALS-linked misfolded SOD1.C1q induction and global complement pathway activation do not contribute to ALS toxicity in mutant SOD1 mice.Dysregulation of synaptogenesis genes antecedes motor neuron pathology in spinal muscular atrophy.Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cellsATF3 expression improves motor function in the ALS mouse model by promoting motor neuron survival and retaining muscle innervation.An enhanced integrated stress response ameliorates mutant SOD1-induced ALS.Analysis of monocyte infiltration in MPTP mice reveals that microglial CX3CR1 protects against neurotoxic over-induction of monocyte-attracting CCL2 by astrocytes.Molecular pathways of motor neuron injury in amyotrophic lateral sclerosis.Cellular therapy to target neuroinflammation in amyotrophic lateral sclerosis.
P2860
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P2860
Toxicity from different SOD1 mutants dysregulates the complement system and the neuronal regenerative response in ALS motor neurons.
description
2007 nî lūn-bûn
@nan
2007 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2007年の論文
@ja
2007年学术文章
@wuu
2007年学术文章
@zh-cn
2007年学术文章
@zh-hans
2007年学术文章
@zh-my
2007年学术文章
@zh-sg
2007年學術文章
@yue
name
Toxicity from different SOD1 m ...... response in ALS motor neurons.
@ast
Toxicity from different SOD1 m ...... response in ALS motor neurons.
@en
type
label
Toxicity from different SOD1 m ...... response in ALS motor neurons.
@ast
Toxicity from different SOD1 m ...... response in ALS motor neurons.
@en
prefLabel
Toxicity from different SOD1 m ...... response in ALS motor neurons.
@ast
Toxicity from different SOD1 m ...... response in ALS motor neurons.
@en
P2860
P356
P1476
Toxicity from different SOD1 m ...... response in ALS motor neurons.
@en
P2093
Christian S Lobsiger
Séverine Boillée
P2860
P304
P356
10.1073/PNAS.0702230104
P407
P577
2007-04-26T00:00:00Z