Protein-misfolding diseases and chaperone-based therapeutic approaches.
about
A blood-brain barrier (BBB) disrupter is also a potent α-synuclein (α-syn) aggregation inhibitor: a novel dual mechanism of mannitol for the treatment of Parkinson disease (PD)The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodiesLongevity of animals under reactive oxygen species stress and disease susceptibility due to global warmingEmerging novel concept of chaperone therapies for protein misfolding diseasesModulation of the maladaptive stress response to manage diseases of protein foldingEndoplasmic reticulum stress in chondrodysplasias caused by mutations in collagen types II and XMutation in the key enzyme of sialic acid biosynthesis causes severe glomerular proteinuria and is rescued by N-acetylmannosamineADP-ribosylation factor 6 mediates E-cadherin recovery by chemical chaperonesThe proteome response to amyloid protein expression in vivoThe effect of chemical chaperones on the assembly and stability of HIV-1 capsid proteinPhosphoproteomics and bioinformatics analyses of spinal cord proteins in rats with morphine toleranceIdentification and glycerol-induced correction of misfolding mutations in the X-linked mental retardation gene CASKA multiparametric computational algorithm for comprehensive assessment of genetic mutations in mucopolysaccharidosis type IIIA (Sanfilippo syndrome)Derlin-2-deficient mice reveal an essential role for protein dislocation in chondrocytesPhytochemical approach and bioanalytical strategy to develop chaperone-based medicationsToward resolution of ambiguity for the unfolded state.Compared effects of missense mutations in Very-Long-Chain Acyl-CoA Dehydrogenase deficiency: Combined analysis by structural, functional and pharmacological approaches.Molecular dynamics simulations reveal structural instability of human trypsin inhibitor upon D50E and Y54H mutations.Characterization of the protein unfolding processes induced by urea and temperatureMinireview: the intimate link between calcium sensing receptor trafficking and signaling: implications for disorders of calcium homeostasis.Biophysical characterization of the olfactomedin domain of myocilin, an extracellular matrix protein implicated in inherited forms of glaucoma.Endoplasmic reticulum quality control is involved in the mechanism of endoglin-mediated hereditary haemorrhagic telangiectasia.Functional rescue of Kallmann syndrome-associated prokineticin receptor 2 (PKR2) mutants deficient in traffickingCharge-rich regions modulate the anti-aggregation activity of Hsp90.Proteasomal inhibition restores biological function of mis-sense mutated dysferlin in patient-derived muscle cells.Evidence that proteosome inhibitors and chemical chaperones can rescue the activity of retinol dehydrogenase 12 mutant T49M.Rescue of functional CFTR channels in cystic fibrosis: a dramatic multivalent effect using iminosugar cluster-based correctors.Identification and characterization of pharmacological chaperones to correct enzyme deficiencies in lysosomal storage disorders.Ligands for glaucoma-associated myocilin discovered by a generic binding assayDealing with misfolded proteins: examining the neuroprotective role of molecular chaperones in neurodegeneration.Disease specific therapies in leukodystrophies and leukoencephalopathies.OS9 Protein Interacts with Na-K-2Cl Co-transporter (NKCC2) and Targets Its Immature Form for the Endoplasmic Reticulum-associated Degradation Pathway.POLG2 disease variants: analyses reveal a dominant negative heterodimer, altered mitochondrial localization and impaired respiratory capacity.Endoplasmic Reticulum Stress and Unfolded Protein Response Pathways: Potential for Treating Age-related Retinal DegenerationMutations in the Yeast Hsp70, Ssa1, at P417 Alter ATP Cycling, Interdomain Coupling, and Specific Chaperone Functions.Protein quality control: the who's who, the where's and therapeutic escapes.Genetic basis for correction of very-long-chain acyl-coenzyme A dehydrogenase deficiency by bezafibrate in patient fibroblasts: toward a genotype-based therapyUnfolding the Therapeutic Potential of Chemical Chaperones for Age-related Macular DegenerationInhibition of proteasome activity promotes the correct localization of disease-causing alpha-sarcoglycan mutants in HEK-293 cells constitutively expressing beta-, gamma-, and delta-sarcoglycan.Chaperonopathies and chaperonotherapy.
P2860
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P2860
Protein-misfolding diseases and chaperone-based therapeutic approaches.
description
2006 nî lūn-bûn
@nan
2006 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
name
Protein-misfolding diseases and chaperone-based therapeutic approaches.
@ast
Protein-misfolding diseases and chaperone-based therapeutic approaches.
@en
Protein-misfolding diseases and chaperone-based therapeutic approaches.
@nl
type
label
Protein-misfolding diseases and chaperone-based therapeutic approaches.
@ast
Protein-misfolding diseases and chaperone-based therapeutic approaches.
@en
Protein-misfolding diseases and chaperone-based therapeutic approaches.
@nl
prefLabel
Protein-misfolding diseases and chaperone-based therapeutic approaches.
@ast
Protein-misfolding diseases and chaperone-based therapeutic approaches.
@en
Protein-misfolding diseases and chaperone-based therapeutic approaches.
@nl
P2860
P1433
P1476
Protein-misfolding diseases and chaperone-based therapeutic approaches.
@en
P2093
Subhankar Paul
Tapan K Chaudhuri
P2860
P304
P356
10.1111/J.1742-4658.2006.05181.X
P407
P577
2006-04-01T00:00:00Z