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Originally published by Kumamoto University on November 1, 2024 T he trigger for neurodegeneration is the assembly of G4 structures driven by increased intracellular calcium ions (Ca2+) due to cellular stress. α -Synuclein binds directly to G4, shifting into an aggregate-prone structure that employs G4 as a scaffold to form harmful clusters. Therefore, inhibiting G4 assembly can prevent α -synuclein aggregation, helping to protect against neuronal function loss. Credit: Cell (2024). DOI: 10.1016/j.cell.2024.09.037 A team of researchers at Kumamoto University has uncovered a mechanism in the f ormation of harmful protein aggregates that lead to neurodegenerative diseases such as Parkinson's disease. The team, led by Professor Norifumi Shioda and Associate Professor Yasushi Yabuki, identified for the first time that unique RNA structures called G-quadruplexes (G4s) play a central role in promoting the aggregation of α -synuclein , a protein associated with neurodegen

Originally published by Kyoto University, on February 28,2024   'epidecodeR' is a tool that can streamline the analysis of complex epigenome and epitranscriptome data, allowing for the rapid and accurate prediction of the effects of epimarks on gene expression. Credit: Mindy Takamiya/Kyoto University iCeMS Scientists have extensively researched the structure and sequence of genetic material and its interactions with proteins in the hope of understanding h ow our genetics and environment interact with diseases . This research has partly focused on ' epigenetic marks ,' which are chemical modifications to DNA, RNA , and the associated proteins (known as histones ). Epigenetic marks influence when and how genes get switched on or off . They can also instruct cells about how to interpret and use genetic information , influencing various cellular processes. Changes in epigenetic marks, therefore, significantly impact gene regulation and cellular functions, which mea

Originally published by Michaela Kane, Duke University, on December 5, 2023   Credit: Nature Chemical Biology (2023). DOI: 10.1038/s41589-023-01481-5 A team of engineers at Duke University have developed a method to broaden the reach of CRISPR technologies . While the original CRISPR system could only target 12.5% of the human genome, the new method expands access to nearly every gene to potentially target and treat a broader range of diseases through genome engineering. The research involved collaborators at Harvard University, Massachusetts Institute of Technology, University of Massachusetts Medical School, University of Zurich and McMaster University. This work was published on October 4 in the journal Nature Communications . CRISPR-Cas is a bacterial immune system that allows bacteria to use RNA molecules and CRISPR-associated (Cas) proteins to target and destroy the DNA of invading viruses. Since its discovery, researchers have raced to develop an arsenal of new