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Despite the virus' error prone polymerase, influenza virus antigenic evolution is rare, even in previously immune hosts, virus replication occurs before producing new antibodies.

Drug resistance in HIV is the result of mutations, which affect fitness depending on epistatic interactions with the entire sequence background that varies within and between patient populations.

A novel Mendelian randomisation framework unravels one gene expression component, correlated with proliferation and genome stability-related features, associated with telomere length in lung adenocarcinoma tumours, which provides insights into how telomere length influences the genetic basis of lung cancer aetiology.

Actin is incorporated into the thin-filament arrays of skeletal muscle sarcomeres in discrete steps, and Fhos, the Drosophila homolog of FHOD-family formins, is an essential player in the process.

A genome-wide association study using whole-genome sequencing data identifies the first known susceptibility genes for posterior urethral valves, the most common cause of kidney failure in boys, implicating the transcription factor TBX5 and planar cell polarity gene PTK7.

Many published findings about population history that rely on inference of admixture graph models fitted to f-statistics are not robust since the method is generally inappropriate for extracting new information about population history.

Two receptors have been identified that can be targeted in melanocytes with selective small molecule agonists to modulate human skin color.

Using unique data from five longitudinal UK birth cohorts, four distinct subsets of genetic variants were identified as differentially associated across wheezing phenotypes from infancy to adolescence with little evidence of genetic associations spanning across different phenotypes.

A certain type of primary cancer may cause another second primary cancer which would be of clinical importance to make a personalized screening plan for certain primary cancer patients.

Genetic and molecular analysis of TP53 exon-6 truncating mutations reveal that these mutations, contrary to current belief, promote tumorigenesis and point towards strategies for treating cancers driven by these prevalent mutations.