Lysophosphatidylcholine modulates fibril formation of amyloid beta peptide (Q24323259)

identical protein binding

GOA release 2020-03-11

1 reference

Amyloid beta-protein and the genetics of Alzheimer's disease

GOA release 2020-03-11

Atsushi Nagai

2

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author name string

Abdullah Md Sheikh

series ordinal

1

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language of work or name

English

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publication date

February 2011

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published in

FEBS Journal

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volume

278

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issue

4

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page(s)

634-42

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cites work

1 reference

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Solution Structures of β Peptide and Its Constituent Fragments: Relation to Amyloid Deposition

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Amyloid A4 protein and its precursor in Down's syndrome and Alzheimer's disease.

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Mutation of the beta-amyloid precursor protein in familial Alzheimer's disease increases beta-protein production

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Release of excess amyloid beta protein from a mutant amyloid beta protein precursor.

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An increased percentage of long amyloid beta protein secreted by familial amyloid beta protein precursor (beta APP717) mutants.

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Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease

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The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics

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Modification of low density lipoprotein by endothelial cells involves lipid peroxidation and degradation of low density lipoprotein phospholipids

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Lysophosphatidylcholine induces glial cell activation: role of rho kinase

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Inflammation in Alzheimer's disease: amyloid-beta oligomers trigger innate immunity defence via pattern recognition receptors

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Cytosolic phospholipase A2 is induced in reactive glia following different forms of neurodegeneration

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Decreased lysophosphatidylcholine/phosphatidylcholine ratio in cerebrospinal fluid in Alzheimer's disease

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Effects of lysophosphatidylcholine on beta-amyloid-induced neuronal apoptosis

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Membrane disruption by Alzheimer beta-amyloid peptides mediated through specific binding to either phospholipids or gangliosides. Implications for neurotoxicity.

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Non-electrostatic binding and self-association of amyloid beta-peptide on the surface of tightly packed phosphatidylcholine membranes.

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Interaction of amyloid beta-protein with anionic phospholipids: possible involvement of Lys28 and C-terminus aliphatic amino acids.

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Lipid-induced conformational transition of the amyloid core fragment Abeta(28-35) and its A30G and A30I mutants

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Conformational dynamics of amyloid beta-protein assembly probed using intrinsic fluorescence.

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Extrinsic fluorescent dyes as tools for protein characterization

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Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis

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Lysophospholipids induce the nucleation and extension of beta2-microglobulin-related amyloid fibrils at a neutral pH.

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The interaction between Alzheimer amyloid beta(1-40) peptide and ganglioside GM1-containing membranes

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Correlation of beta-amyloid aggregate size and hydrophobicity with decreased bilayer fluidity of model membranes

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Detection and characterization of aggregates, prefibrillar amyloidogenic oligomers, and protofibrils using fluorescence spectroscopy

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Oligomerization and toxicity of beta-amyloid-42 implicated in Alzheimer's disease.

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Why Is the C-terminus of Abeta(1-42) more unfolded than that of Abeta(1-40)? Clues from hydrophobic interaction

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Amyloid beta-protein fibrillogenesis. Detection of a protofibrillar intermediate.

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Phosphatidylinositol and inositol involvement in Alzheimer amyloid-beta fibril growth and arrest

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inferred from DOI database lookup

7 January 2021

based on heuristic

MIP-1alpha, MCP-1, GM-CSF, and TNF-alpha control the immune cell response that mediates rapid phagocytosis of myelin from the adult mouse spinal cord

1 reference

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