The TEN-domain of human telomerase mediates the direct interaction with TPP1 to drive telomerase recruitment to telomeres.

The roles of key telomerase active site residues were elucidated to determine how telomerase selects the correct from the incorrect nucleotide to maintain telomere integrity.

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.

TRF1 suppresses replication fork stalling, which triggers break induced replication at telomeres associated with DNA damage response, alteration in the telomere chromatin environment, and re-localisation of telomeres to PML bodies.

Telomere dysfunction in iPSC-derived type II alveolar epithelial cells causes senescence and gene expression changes including Wnt-related changes that GSK3 inhibition can rescue, providing insight into pulmonary fibrosis pathogenesis.

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

The Cajal body chaperone TCAB1 and scaffold protein Coilin are not required for telomerase activity in human cells.

Comprehensive analysis of telomere maintenance from transcriptomic, epigenetic, and loss-of-function profiles of cancer cell lines elucidates features of telomere regulation in cancer.

In yeast, the secondary pathway for recruiting telomerase to chromosome ends requires a component of telomeric transcriptionally silent chromatin.

A telomerase recruitment mechanism delivers cell cycle information to the telomere-telomerase interface to ensure timely telomerase engagement at the telomere.