ArticleEMBO reports2017
TZAP-ing telomeres down to size.
Article in EMBO reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- Prognostic Value of Telomeric Zinc Finger-Associated Protein Expression in Adenocarcinoma and Squamous Cell Carcinoma of Lung.Medicina (Kaunas, Lithuania) · 2021Article
- Telomeric zinc-finger associated protein (TZAP) in cancer biology: friend or foe?Molecular biology research communications · 2021Article
- Clinical and Prognostic Significance of TZAP Expression in Cervical Cancer.Medicina (Kaunas, Lithuania) · 2020Article
- Telomere Length Dynamics and the Evolution of Cancer Genome Architecture.International journal of molecular sciences · 2018Review
- Metabolic and genomic adaptations to winter fattening in a primate species, the grey mouse lemur (Microcebus murinus).International journal of obesity (2005) · 2018Article
- The 11th C2H2 zinc finger and an adjacent C-terminal arm are responsible for TZAP recognition of telomeric DNA.Cell research · 2018Article
- Telomeric zinc-finger associated protein (TZAP): a new player in telomere diseases?Annals of translational medicine · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The phenomenon of gradual telomere shortening has become a paradigm for how we understand the biology of aging and cancer. Cell proliferation is accompanied by cumulative telomere loss, and the aged cell either senesces, dies or transforms toward cancer. This transformation requires the activation of telomere elongation mechanisms in order to restore telomere length such that cell death or senescence programs are not induced. Most of the time, this occurs through telomerase reactivation. In other rare cases, the Alternative lengthening of telomeres (ALT) pathway hijacks DNA recombination-associated mechanisms to hyperextend telomeres, often to more than 50 kb. Why telomere length is restricted and what sets their maximal length has been a long-standing puzzle in cell biology. Two recent studies published in this issue of
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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.