DNA methylation could determine liver disease progression
DNA methylation at specific genomic sites was found to correlate with non-fatty liver disease and could be used to diagnose severity.
List view / Grid view
Genomics is the branch of molecular biology concerned with the structure, function, evolution, and mapping of genomes.
DNA methylation at specific genomic sites was found to correlate with non-fatty liver disease and could be used to diagnose severity.
A breaking discovery has revealed the gene HSD3B1 that regulates the production of sex hormones is linked to atopic dermatitis (AD).
The decreased expression of PTEN in mouse models was found to make rhabdomyosarcoma tumours more aggressive, highlighting new treatment approaches.
Researchers have established an organoid biobank to search for genes that are essential for the spreading of SARS-CoV-2 infection.
New technology system of drug-based markers for the selection or counter-selection of genes may advance genetic screening methods.
Researchers discovered that glioblastoma cells rely on biotin distribution for growth, leading to possible future drug combinations.
New genomic study reveals that the microbiome could predict rheumatoid arthritis prognosis, potentially advancing treatments.
A novel gene therapy has fully corrected whole-body alterations in a rat model, paving the way for Morquio A therapies.
Researchers have identified a spider-like antibacterial mechanism by immune cells that could inspire Staphylococcus aureus treatments.
An NIH team have built a cellular map of chronic multiple sclerosis (MS) lesions to identify cells that drive inflammation and potential therapies.
The Gut Cell Atlas comprises 428,000 cells in the gut and sheds light on the origin of Crohn’s disease and other intestinal diseases.
An NIH study used whole genome sequencing to describe three molecular subtypes of lung cancer in non-smokers, possibly improving treatments.
Stanford researchers have developed a multi-purpose “mini” CRISPR system, called CasMINI, that may be easier to deliver into human cells.
A genetic defect in patients with inflammatory bowel disease (IBD) was found to affect how intestinal epithelial cells maintain a barrier.
A new study has found mutations originating in blood progenitor cells, possibly leading to Waldenstrom macroglobulinemia (WM) therapies.