ArticleMolecular cell2012
AUF1/HnRNP D RNA binding protein functions in telomere maintenance.
Article in Molecular cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 27 citations in OpenAlex.
- Heterogeneous Nuclear Ribonucleoproteins Involved in the Functioning of Telomeres in Malignant Cells.International journal of molecular sciences · 2019Review
- Cancer cells exploit an orphan RNA to drive metastatic progression.Nature medicine · 2018Article
- NOVA1 regulates hTERT splicing and cell growth in non-small cell lung cancer.Nature communications · 2018Article
- Identification of Elongated Primary Cilia with Impaired Mechanotransduction in Idiopathic Scoliosis Patients.Scientific reports · 2017Article
- Hallmarks of cancer and AU-rich elements.Wiley interdisciplinary reviews. RNA · 2017Review
Corrections and comments
- Comment on
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this issue of Molecular Cell, Pont et al. (2012) show that AUF1/hnRNP D promotes TERT transcription, which is required for telomere maintenance in mice.
Identifiers
What OpenQuestion holds
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.