ArticleThe Biochemical journal2007
Comparative in vitro and ex vivo activities of selected inhibitors of transthyretin aggregation: relevance in drug design.
Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 29 citations in OpenAlex.
- Molecular Tweezers: Supramolecular Hosts with Broad-Spectrum Biological Applications.Pharmacological reviews · 2023Review
- The Transthyretin/Oleuropein Aglycone Complex: A New Tool against TTR Amyloidosis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Repositioning tolcapone as a potent inhibitor of transthyretin amyloidogenesis and associated cellular toxicity.Nature communications · 2016Article
- Transthyretin chemical chaperoning by flavonoids: Structure-activity insights towards the design of potent amyloidosis inhibitors.Biochemistry and biophysics reports · 2015Article
- The flavonoid luteolin, but not luteolin-7-O-glucoside, prevents a transthyretin mediated toxic response.PloS one · 2015Article
- Gene therapy approach to FAP: in vivo influence of T119M in TTR deposition in a transgenic V30M mouse model.Gene therapy · 2014Article
- Molecular tweezers targeting transthyretin amyloidosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2014Article
- Stability of the transthyretin molecule as a key factor in the interaction with a-beta peptide--relevance in Alzheimer's disease.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Destabilization of the tetrameric fold of TTR (transthyretin) is important for aggregation of the protein which culminates in amyloid fibril formation. Many TTR mutations interfere with tetramer stability, increasing the amyloidogenic potential of the protein. The vast majority of proposed TTR fibrillogenesis inhibitors are based on in vitro assays with isolated protein, limiting their future use in clinical assays. In the present study we investigated TTR fibrillogenesis inhibitors using a cellular system that produces TTR intermediates/aggregates in the medium. Plasmids carrying wild-type TTR, V30M or L55P cDNA were transfected into a rat Schwannoma cell line and TTR aggregates were investigated in the medium using a dot-blot filter assay followed by immunodetection. Results showed that, in 24 h, TTR L55P forms aggregates in the medium, whereas, up to 72 h, wild-type TTR and V30M do not. A series of 12 different compounds, described in the literature as in vitro TTR fibrillogenesis inhibitors, were tested for their ability to inhibit L55P aggregate formation; in this system, 2-[(3,5-dichlorophenyl) amino] benzoic acid, benzoxazole, 4-(3,5-difluorophenyl) benzoic acid and tri-iodophenol were the most effective inhibitors, as compared with the reference iododiflunisal, previously shown by ex vivo and in vitro procedures to stabilize TTR and inhibit fibrillogenesis. Among these drugs, 2-[(3,5-dichlorophenyl) amino] benzoic acid and tri-iodophenol stabilized TTR from heterozygotic carriers of V30M in the same ex vivo conditions as those used previously for iododiflunisal. The novel cellular-based test herein proposed for TTR fibrillogenesis inhibitor screens avoids not only lengthy and cumbersome large-scale protein isolation steps but also artefacts associated with most current in vitro first-line screening methods, such as those associated with acidic conditions and the absence of serum proteins.
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