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Modulating inhibitors of transthyretin fibrillogenesis via sulfation: polychlorinated biphenyl sulfates as models
Journal article   Open access   Peer reviewed

Modulating inhibitors of transthyretin fibrillogenesis via sulfation: polychlorinated biphenyl sulfates as models

Fabian A Grimm, Hans-Joachim Lehmler, Xianran He, Larry W Robertson and Michael W Duffel
Chemico-biological interactions, Vol.228, pp.1-8
02/25/2015
DOI: 10.1016/j.cbi.2015.01.002
PMCID: PMC4327905
PMID: 25595224
url
https://doi.org/10.1016/j.cbi.2015.01.002View
Published (Version of record) Open Access

Abstract

Small molecules that bind with high affinity to thyroxine (T4) binding sites on transthyretin (TTR) kinetically stabilize the protein's tetrameric structure, thereby efficiently decreasing the rate of tetramer dissociation in TTR related amyloidoses. Current research efforts aim to optimize the amyloid inhibiting properties of known inhibitors, such as derivatives of biphenyls, dibenzofurans and benzooxazoles, by chemical modification. In order to test the hypothesis that sulfate group substituents can improve the efficiencies of such inhibitors, we evaluated the potential of six polychlorinated biphenyl sulfates to inhibit TTR amyloid fibril formation in vitro. In addition, we determined their binding orientations and molecular interactions within the T4 binding site by molecular docking simulations. Utilizing this combined experimental and computational approach, we demonstrated that sulfation significantly improves the amyloid inhibiting properties as compared to both parent and hydroxylated PCBs. Importantly, several PCB sulfates were of equal or higher potency than some of the most effective previously described inhibitors.
Amyloid - antagonists & inhibitors Amyloid - metabolism Prealbumin - metabolism Humans Sulfates - chemistry Molecular Docking Simulation Molecular Structure Structure-Activity Relationship Sulfates - pharmacology Prealbumin - antagonists & inhibitors ISRP Project 3 2015-2020 ISRP Project 1 2015-2020 Synthesis Core

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