The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity. - Wikidata - awgldk - TriplyDB

The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity.

The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity.

http://www.wikidata.org/entity/Q39681329

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Amyloid-like fibril formation by polyQ proteins: a critical balance between the polyQ length and the constraints imposed by the host protein Biophysical insights into how surfaces, including lipid membranes, modulate protein aggregation related to neurodegeneration.Inversion of the balance between hydrophobic and hydrogen bonding interactions in protein folding and aggregation Characterization of the response of primary cells relevant to dialysis-related amyloidosis to β2-microglobulin monomer and fibrils.Local cooperativity in an amyloidogenic state of human lysozyme observed at atomic resolution.Analysis of the native structure, stability and aggregation of biotinylated human lysozyme.Direct three-dimensional visualization of membrane disruption by amyloid fibrils MetAmyl: a METa-predictor for AMYLoid proteins Structural polymorphism in amyloids: new insights from studies with Y145Stop prion protein fibrils.Serum Amyloid P Component Ameliorates Neurological Damage Caused by Expressing a Lysozyme Variant in the Central Nervous System of Drosophila melanogaster.Phosphorylation induces distinct alpha-synuclein strain formation.Disulfide bonds reduce the toxicity of the amyloid fibrils formed by an extracellular protein.Analysis of Toxic Amyloid Fibril Interactions at Natively Derived Membranes by Ellipsometry.Inflammation protein SAA2.2 spontaneously forms marginally stable amyloid fibrils at physiological temperature.β2-microglobulin amyloid fibrils are nanoparticles that disrupt lysosomal membrane protein trafficking and inhibit protein degradation by lysosomes Activation of innate immunity by lysozyme fibrils is critically dependent on cross-β sheet structure.Biochemical and Electrophysiological Modification of Amyloid Transthyretin on Cardiomyocytes.Effect of curcumin analogs onα-synuclein aggregation and cytotoxicity.Population of nonnative states of lysozyme variants drives amyloid fibril formation.Amyloid Oligomers and Mature Fibrils Prepared from an Innocuous Protein Cause Diverging Cellular Death Mechanisms.Amyloid oligomers and protofibrils, but not filaments, self-replicate from native lysozyme.Lessons learned from protein aggregation: toward technological and biomedical applications.The Significance of the Location of Mutations for the Native-State Dynamics of Human Lysozyme.Molecular dynamics simulations of lysozyme-lipid systems: probing the early steps of protein aggregation.Origin of metastable oligomers and their effects on amyloid fibril self-assembly

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P2860

The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity.

http://www.wikidata.org/entity/Q39681329

description

2010 nî lūn-bûn

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

@zh-tw

2010年论文

@wuu

2010年论文

@zh

2010年论文

@zh-cn

name

The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity.

@en

The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity.

@nl

type

label

The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity.

@en

The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity.

@nl

prefLabel

The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity.

@en

The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity.

@nl

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J.JMB.2010.07.005

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Journal of Molecular Biology

P1476

The non-core regions of human lysozyme amyloid fibrils influence cytotoxicity.

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Angelo Fontana

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Anne Dhulesia

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Erica Frare

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Glyn Devlin

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Janet R Kumita

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Maria F Mossuto

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Mireille Dumoulin

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Patrizia Polverino de Laureto

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P2860

Pre-fibrillar alpha-synuclein variants with impaired beta-structure increase neurotoxicity in Parkinson's disease models

Mechanism of prion propagation: amyloid growth occurs by monomer addition

Rapid colorimetric assay for cellular growth and survival: Application to proliferation and cytotoxicity assays

A camelid antibody fragment inhibits the formation of amyloid fibrils by human lysozyme

Atomic structures of amyloid cross-beta spines reveal varied steric zippers

Instability, unfolding and aggregation of human lysozyme variants underlying amyloid fibrillogenesis

Calculation of protein extinction coefficients from amino acid sequence data

Protein misfolding, functional amyloid, and human disease

Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide

Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis

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783-796

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10.1016/J.JMB.2010.07.005

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5

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402

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Xavier Salvatella

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2010-07-17T00:00:00Z

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45166797

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20624399

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