Publications by authors named "H Dyson"

The transthyretin (TTR) tetramer, assembled as a dimer of dimers, transports thyroxine and retinol binding protein in blood plasma and cerebrospinal fluid. Aggregation of wild type or pathogenic variant TTR leads to transthyretin amyloidosis (ATTR), which is associated with neurodegenerative and cardiac disease. The trigger for TTR aggregation under physiological conditions is unknown.

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  • * The p53 protein is made up of a well-defined DBD and tetramerization domain (TET), along with disordered regions, specifically an N-terminal activation domain (NTAD) and C-terminal regulatory domain (CTD), that play key roles in its function.
  • * Recent findings suggest that these disordered regions work together with the DBD and are influenced by post-translational modifications to regulate p53's activity, especially during cellular stress responses.
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  • Environmental contamination with anthrax spores in pastoral regions poses significant risks to livestock and the local economy, highlighting the need for ongoing monitoring.
  • The study reviewed 232 soil samples from contaminated sites in Kars province, Türkiye, over 14 years, revealing that viable spores were detected in 58.6% of samples, with certain positions showing higher concentrations.
  • The findings indicate that anthrax spores can persist in the soil for over a decade, suggesting that standard burial methods may not effectively decontaminate affected areas, emphasizing the necessity for thorough bacteriological monitoring and appropriate decontamination strategies.
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Aberrant formation and deposition of human transthyretin (TTR) aggregates causes transthyretin amyloidosis. To initialize aggregation, transthyretin tetramers must first dissociate into monomers that partially unfold to promote entry into the aggregation pathway. The native TTR tetramer (T) is stabilized by docking of the F87 sidechain into an interfacial cavity enclosed by several hydrophobic residues including A120.

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The Human papillomavirus (HPV) causes tumors in part by hijacking the host cell cycle and forcing uncontrolled cellular division. While there are >200 genotypes of HPV, 15 are classified as high-risk and have been shown to transform infected cells and contribute to tumor formation. The remaining low-risk genotypes are not considered oncogenic and result in benign skin lesions.

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