M6A modification is crucial for HIV-1 survival
The discovery of three m6A modifications and their exact locations could lead to the development of drugs that inhibit viral RNA and protein production.
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The discovery of three m6A modifications and their exact locations could lead to the development of drugs that inhibit viral RNA and protein production.
In this Q&A, Associate Professor Dr Mete Civelek shares insights from the University of Virginia’s exciting recent study identifying several potential therapeutic targets for accelerating translational research in cardiovascular disease treatment, with a focus on proteins associated with the extracellular matrix (ECM) secretion by smooth muscle cells (SMCs).
The combination therapy worked faster and was lessened the number of leukaemia cells compared to asparaginase or venetoclax alone.
Dr Fernández-Capetillo shares his insights from a recent study conducted at the CNIO, elucidating how the expression of (PR)arginine-rich peptides affects ribosomal protein translation and accumulation, and how accelerated aging can be alleviated.
IFNβ could be developed into a new therapy, following an improved understanding of how innate immunity affects the brain during chronic HIV infection.
A new proof-of-principle study demonstrates the DCAF5 protein is a promising target, which could avoid the need for toxic therapies.
The discovery of two proteins that effectively mature hiPSCs into endothelial cells may have a range of research and clinical benefits.
New understanding of the CRC and its interaction with STAT3 could lead to novel therapeutics and combination strategies.
A single change in the amino acid structure of the transmembrane segment can either enhance or diminish the inhibitory function of PD-1 in immune responses.
Researchers discover that fusion proteins and a gene regulatory protein complex interact through disordered domains.
Proteins regulating plasminogen-plasmin levels can be used to identify patients at risk of progressing to a severe stage of COVID-19.
Using tumour organoids, researchers identified that overexpression of Engrailed-1 blocked genes associated with natural cell death.
A novel cellular mechanism has been uncovered with the use of CRISPR gene-tiling technology, which could advance oncologic therapies.
Researchers suggest that DA histology slowly emerges by accumulating burdens of DNA damage and copy number aberrations.
Distinct macrophage signatures that align specifically with regeneration could offer novel therapies to enhance wound healing.