(Q42182458)

18 October 2017

Amyloid ion channels: a porous argument or a thin excuse? (English)

1 reference

18 October 2017

David Eliezer

1

1 reference

18 October 2017

1 December 2006

1 reference

The Journal of General Physiology

18 October 2017

1 reference

18 October 2017

128

1 reference

18 October 2017

6

1 reference

18 October 2017

631-633

1 reference

Soluble amyloid oligomers increase bilayer conductance by altering dielectric structure

18 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Are amyloid diseases caused by protein aggregates that mimic bacterial pore-forming toxins?

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Amyloid ion channels: a common structural link for protein-misfolding disease

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Self-propagating, molecular-level polymorphism in Alzheimer's beta-amyloid fibrils

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Inclusion body formation reduces levels of mutant huntingtin and the risk of neuronal death

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Challenging the amyloid cascade hypothesis: senile plaques and amyloid-beta as protective adaptations to Alzheimer disease

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Oligomers on the brain: the emerging role of soluble protein aggregates in neurodegeneration

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Protofibrils, pores, fibrils, and neurodegeneration: separating the responsible protein aggregates from the innocent bystanders

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Conformational Abs recognizing a generic amyloid fibril epitope

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Amyloid beta protein forms ion channels: implications for Alzheimer's disease pathophysiology

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Staphylococcal alpha-hemolysin can form hexamers in phospholipid bilayers

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Fibrillogenesis of synthetic amyloid-beta peptides is dependent on their initial secondary structure

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Alzheimer disease amyloid beta protein forms calcium channels in bilayer membranes: blockade by tromethamine and aluminum

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Alpha-toxin of Staphylococcus aureus

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Alzheimer's disease: the amyloid cascade hypothesis

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

beta-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Contribution of somal Lewy bodies to neuronal death.

26 October 2017

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Permeabilization of lipid bilayers is a common conformation-dependent activity of soluble amyloid oligomers in protein misfolding diseases

29 May 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

Abeta42-peptide assembly on lipid bilayers

17 August 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=2151595

17 August 2018

Identifiers

DOI

10.1085/JGP.200609689

1 reference

18 October 2017

1 reference

PMC publication ID

2151595

18 October 2017

PubMed publication ID

17130516

1 reference

PMC publication ID

2151595