Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Diflunisal stabilizes familial amyloid polyneuropathy-associated transthyretin variant tetramers in serum against dissociation required for amyloidogenesis.

Neuroscience research - 1 Dec 2006

Tojo Kana, Sekijima Yoshiki, Kelly Jeffery W, Ikeda Shu-ichi

Abstract excerpt

Transthyretin (TTR) tetramer dissociation, misfolding and misassembly are required for the process of amyloid fibril formation associated with familial amyloid polyneuropathy (FAP). Preferential stabilization of the native TTR tetramer over the dissociative transition state by small molecule bind...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amyloid beta-Peptides
Share to Amyloid Neuropathies, Familial
Share to Anti-Inflammatory Agents, Non-Steroidal

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chromium

Share to Hydrogen-Ion Concentration

Share to Prealbumin

Share to Protein Denaturation

Source

Identifiers

PMID: 17028027
DOI: 10.1016/j.neures.2006.08.014

Genes

TTR
FAP

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-17028027-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Diflunisal stabilizes familial amyloid polyneuropathy-associated transthyretin variant tetramers in serum against dissociation required for amyloidogenesis.PMID 17028027Read ↗

Native state stabilization by NSAIDs inhibits transthyretin amyloidogenesis from the most common familial disease variants.Semantic proximity Read ↗

Energetic characteristics of the new transthyretin variant A25T may explain its atypical central nervous system pathology.Semantic proximity Read ↗

Tafamidis for transthyretin amyloidosis.Semantic proximity Read ↗

Structural stabilization of transthyretin by a new compound, 6-benzoyl-2-hydroxy-1H-benzo[de]isoquinoline-1,3(2H)-dione.Semantic proximity Read ↗

Disease-Modifying Treatments for Transthyretin Amyloidosis.Semantic proximity Read ↗

Cooperative stabilization of transthyretin by clusterin and diflunisal.Semantic proximity Read ↗

Unusual duplication mutation in a surface loop of human transthyretin leads to an aggressive drug-resistant amyloid disease.Semantic proximity Read ↗

TTR kinetic stabilizers and TTR gene silencing: a new era in therapy for familial amyloidotic polyneuropathiesSemantic proximity Read ↗

Transthyretin (ATTR) amyloidosis nephropathy: lessons from a TTR stabilizer molecule.Semantic proximity Read ↗

Evaluating the effect of mutations and ligand binding on transthyretin homotetramer dynamics.Semantic proximity Read ↗

Thermodynamic Stability and Aggregation Kinetics of EF Helix and EF Loop Variants of Transthyretin.Semantic proximity Read ↗

Probing the Dissociation Pathway of a Kinetically Labile Transthyretin Mutant.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.