ArticleAging cell2021
A novel p53 regulator, C16ORF72/TAPR1, buffers against telomerase inhibition.
Article in Aging cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Exploring the role of β2-microglobulin in the relationship between physical activity and DNAm-predicted PhenoAge: Evidence from a population-based and mice single-cell RNA-sequencing study.Journal of advanced research · 2026Article
- G-quadruplex homeostasis is a determinant of PARP inhibitor toxicity in BRCA2-deficient cells.Nature communications · 2026Article
- Interplay of telomerase non-canonical functions in NK cell resistance to iCasp9-mediated apoptosis.Cell death discovery · 2026Article
- Navigating the Landscape of Translational Geroscience in Canada: A Comprehensive Evaluation of Current Progress and Future Directions.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- Genome-wide CRISPR screens identify novel regulators of wild-type and mutant p53 stability.Molecular systems biology · 2024Article
- Tight regulation of a nuclear HAPSTR1-HUWE1 pathway essential for mammalian life.Life science alliance · 2024Article
- Article
- A CRISPR base editing approach for the functional assessment of telomere biology disorder-related genes in human health and aging.Biogerontology · 2024Article
- C16orf72/HAPSTR1/TAPR1 functions with BRCA1/Senataxin to modulate replication-associated R-loops and confer resistance to PARP disruption.Nature communications · 2023Article
- HAPSTR1 localizes HUWE1 to the nucleus to limit stress signaling pathways.Cell reports · 2023Article
- Review
- Article
- Cellular Senescence as a Brake or Accelerator for Oncogenic Transformation and Role in Lymphatic Metastasis.International journal of molecular sciences · 2023Review
- The HAPSTR2 retrogene buffers stress signaling and resilience in mammals.Nature communications · 2023Article
- Stable methylation loci are associated with systolic blood pressure in a Croatian island population.Epigenomics · 2022Article
- Tieing together loose ends: telomere instability in cancer and aging.Molecular oncology · 2022Review
- C16orf72/HAPSTR1 is a molecular rheostat in an integrated network of stress response pathways.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Integrating multi-omics data reveals function and therapeutic potential of deubiquitinating enzymes.eLife · 2022Article
- Novel Epigenetic Clock Biomarkers of Age-Related Macular Degeneration.Frontiers in medicine · 2022Article
- Telomere Attrition and p53 Response 1 (TAPR1): a new player in cancer biology?Clinics (Sao Paulo, Brazil) · 2021Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Telomere erosion in cells with insufficient levels of the telomerase reverse transcriptase (TERT), contributes to age-associated tissue dysfunction and senescence, and p53 plays a crucial role in this response. We undertook a genome-wide CRISPR screen to identify gene deletions that sensitized p53-positive human cells to telomerase inhibition. We uncovered a previously unannotated gene, C16ORF72, which we term Telomere Attrition and p53 Response 1 (TAPR1), that exhibited a synthetic-sick relationship with TERT loss. A subsequent genome-wide CRISPR screen in TAPR1-disrupted cells reciprocally identified TERT as a sensitizing gene deletion. Cells lacking TAPR1 or TERT possessed elevated p53 levels and transcriptional signatures consistent with p53 upregulation. The elevated p53 response in TERT- or TAPR1-deficient cells was exacerbated by treatment with the MDM2 inhibitor and p53 stabilizer nutlin-3a and coincided with a further reduction in cell fitness. Importantly, the sensitivity to treatment with nutlin-3a in TERT- or TAPR1-deficient cells was rescued by loss of p53. These data suggest that TAPR1 buffers against the deleterious consequences of telomere erosion or DNA damage by constraining p53. These findings identify C16ORF72/TAPR1 as new regulator at the nexus of telomere integrity and p53 regulation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.