ArticleNature communications2026
Control of telomerase recruitment and end protection by independent shelterin components.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Fission yeast RPA-TERT-Tpz1TPP1 complex promotes telomere extension and suppresses telomere recombination.PLoS genetics · 2026Article
- Fission yeast RPA-TERT-Tpz1bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Telomeres are proposed to alternate between "closed" states, in which chromosome ends are protected from DNA damage signaling and inaccessible to telomerase, and "open" states, where they become accessible for telomerase mediated elongation but less protected. Whether these states reflect distinct molecular mechanisms or mutually exclusive structural conformations remains unclear. Here, we develop a single-cell assay to monitor telomerase activity in mouse embryonic stem cells. Using this approach, we demonstrate that the shelterin component TPP1 is essential for telomerase recruitment via its interaction with TIN2, independently of POT1. In contrast, POT1 is dispensable for telomerase function but required for telomere end protection, acting independently of TPP1. These findings challenge the classical open-closed telomere model and reveal that telomerase recruitment and end protection are mediated by genetically and molecularly separable mechanisms.
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Registered trials
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