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Telomerase gene therapy represents a novel effective treatment for pulmonary fibrosis associated with short telomeres by improving pulmonary function, decreasing inflammation and accelerating fiber disappearance in fibrotic lungs.

Preventing premature interactions between microtubules and protein-based structures called kinetochores ensures that chromosomes are segregated by meiosis rather than mitosis in reproductive cells.

Kinesin Kif2C is recruited to DNA damage sites, modulates the mobility and dynamics of DNA damage foci, and promotes DNA double strand break repair.

Biological aging processes and age-related diseases demonstrate sexual dimorphism where complex interactions between underlying aging mechanisms and sex chromosomes and hormones are seen in humans and animals.

Mapping DNA replication timing, allied to genetic analysis of a RecQ repair helicase, reveals that antigenic variation in the African trypanosome may be initiated by locus-specific, replication-derived sequence instability.

Human telomerase unfolds and extends parallel G-quadruplexes using a unique mechanism involving its RNA template.

Knockout of Terc impedes effective immune defense against bacterial lung infections in mice, exacerbating disease course and revealing the critical function of Terc in pulmonary immunity.

Sodium selenate is the first treatment with persistent disease-modifying effects reducing seizures and improving cognitive deficits, in chronically epileptic and drug-resistant TLE animals.

A messenger RNA coding for the histone 1.2 protein negatively regulates telomere elongation by interacting with human telomerase RNA.

HOAP is a telomere-binding protein that has a conserved role in Drosophila, but it also needs to evolve quickly to restrict telomeric retrotransposons.