Mutations in SARS-CoV-2 Spike could lead to greater infectivity, study shows
Comparing the original SARS-CoV-2 Spike protein with a mutated version, researchers have potentially revealed why the mutated version is dominant.
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Comparing the original SARS-CoV-2 Spike protein with a mutated version, researchers have potentially revealed why the mutated version is dominant.
Using NMR spectroscopy, researchers have partially observed the structure of heat shock proteins that bind to proteins that cause Huntington's disease.
Discover the latest in SARS-CoV-2 antibody research as we cover three of the most recent developments in this article.
Research has shown that ACE2 and several integrins containing SLiMs are involved in SARS-CoV-2 infection, presenting new therapeutic targets.
In a zebrafish model, researchers have found that the protein NAPMT can trigger muscle stem cells to proliferate and heal muscle damage.
Studies in mice have shown that the drug ProAgio is effective at treating pancreatic cancer and triple-negative breast cancer.
A new therapeutic approach using the protein IL-21 could optimise the immune system, allowing it to combat HIV.
New research has shown that 'hidden' lysis genes in bacteriophages could be used in the development of a new class of antibiotics.
In this article, we explore the findings of a study that suggests a newly identified pathway, the Drp1-HK1-NLRP3 signalling axis, could be a promising target for therapies to prevent Alzheimer’s disease progression.
Using a mouse model, researchers found that cancer progression led to fewer skeletal muscle ribosomes, likely explaining muscle wasting.
Researchers have found that SARS-CoV-2 evades immune responses by deleting parts of its genetic sequence that encode for the Spike protein.
A study has shown that 88 percent of people infected by COVID-19 were able to produce SARS-CoV-2 antibodies after six months.
A new protein can trick SARS-CoV-2 and bind to the Spike protein rather than cell membranes in a kidney organoid.
Disrupting the interaction between the MYC oncogene and its co-factor, host cell factor (HCF)–1, was sufficient to cause Burkitt’s lymphoma cells to self-destruct in vivo.
The N439K mutation improves the interaction between SARS-CoV-2 Spike protein and the viral receptor ACE2 and eludes antibody-mediated immunity, say investigators.