Proteasomes remain intact, but show early focal alteration in their composition in a mouse model of amyotrophic lateral sclerosis.

Proteasomes remain intact, but show early focal alteration in their composition in a mouse model of amyotrophic lateral sclerosis.

Item
http://www.wikidata.org/entity/Q33322191
The complex molecular biology of amyotrophic lateral sclerosis (ALS)The ubiquitin proteasome system in glia and its role in neurodegenerative diseasesp38 mediates mechanical allodynia in a mouse model of type 2 diabetes.A novel small molecule HSP90 inhibitor, NXD30001, differentially induces heat shock proteins in nervous tissue in culture and in vivoMelittin restores proteasome function in an animal model of ALSNerve growth factor mediates mechanical allodynia in a mouse model of type 2 diabetes.Time-Point Dependent Activation of Autophagy and the UPS in SOD1G93A Mice Skeletal MuscleFunctional alterations of the ubiquitin-proteasome system in motor neurons of a mouse model of familial amyotrophic lateral sclerosisChanges in 20S subunit composition are largely responsible for altered proteasomal activities in experimental autoimmune encephalomyelitis.N-acetyl-l-tryptophan, but not N-acetyl-d-tryptophan, rescues neuronal cell death in models of amyotrophic lateral sclerosis.Proteomic characterization of lipid raft proteins in amyotrophic lateral sclerosis mouse spinal cordSequestosome 1/p62 links familial ALS mutant SOD1 to LC3 via an ubiquitin-independent mechanism.Specific induction of Akt3 in spinal cord motor neurons is neuroprotective in a mouse model of familial amyotrophic lateral sclerosis.Cytokine-mediated inflammation mediates painful neuropathy from metabolic syndrome.Impaired proteasome function in sporadic amyotrophic lateral sclerosis.Dysfunctions in endosomal-lysosomal and autophagy pathways underlie neuropathology in a mouse model for Lafora disease.A Metadata Analysis of Oxidative Stress Etiology in Preclinical Amyotrophic Lateral Sclerosis: Benefits of Antioxidant Therapy.
P2860

Proteasomes remain intact, but show early focal alteration in their composition in a mouse model of amyotrophic lateral sclerosis.

Item
http://www.wikidata.org/entity/Q33322191
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
Proteasomes remain intact, but ...... amyotrophic lateral sclerosis.
@ast
Proteasomes remain intact, but ...... amyotrophic lateral sclerosis.
@en
Proteasomes remain intact, but ...... amyotrophic lateral sclerosis.
@nl
type
label
Proteasomes remain intact, but ...... amyotrophic lateral sclerosis.
@ast
Proteasomes remain intact, but ...... amyotrophic lateral sclerosis.
@en
Proteasomes remain intact, but ...... amyotrophic lateral sclerosis.
@nl
prefLabel
Proteasomes remain intact, but ...... amyotrophic lateral sclerosis.
@ast
Proteasomes remain intact, but ...... amyotrophic lateral sclerosis.
@en
Proteasomes remain intact, but ...... amyotrophic lateral sclerosis.
@nl
P1433
P1476
P2093
P2860
P304
P31
P356
P407
P433
P478
P577
P5875
P698
P921
P356
P1433
P1476
Proteasomes remain intact, but ...... amyotrophic lateral sclerosis.
@en
P2093
P2860
P304
P31
P356
10.1111/J.1471-4159.2008.05317.X
P407
P433
P478
P577
P5875
P698
P921