ArticleRNA (New York, N.Y.)2019
Neither miR-7-5p nor miR-141-3p is a major mediator of iron-responsive transferrin receptor-1 mRNA degradation.
Article in RNA (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
6 citing papers in PubMed, 9 citations in OpenAlex.
- A temporal difference in the stabilization of two mRNAs with a 3' iron-responsive element during iron deficiency.RNA (New York, N.Y.) · 2023Article
- Roquin is a major mediator of iron-regulated changes to transferrin receptor-1 mRNA stability.iScience · 2021Article
- Genome-wide analysis of lncRNA stability in human.PLoS computational biology · 2021Article
- Ironing Out the Details: How Iron Orchestrates Macrophage Polarization.Frontiers in immunology · 2021Review
- Altered Iron Metabolism and Impact in Cancer Biology, Metastasis, and Immunology.Frontiers in oncology · 2020Review
- Iron-induced transferrin receptor-1 mRNA destabilization: A response to "Neither miR-7-5p nor miR-141-3p is a major mediator of iron-responsive transferrin receptor-1 mRNA degradation".RNA (New York, N.Y.) · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transferrin receptor (TfR1) is the principal means of iron importation for most mammalian cells, and regulation of mRNA stability is a major mechanism through which TfR1 expression is controlled in response to changing intracellular iron levels. An endonuclease activity degrades the TfR1 mRNA during iron-repletion, which reduces iron importation and contributes to the restoration of homeostasis. Correct identification of the TfR1 mRNA endonuclease activity is important as it has the potential to be a pharmacological target for the treatment of several pathologies in which iron homeostasis is perturbed. A recent
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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.