ArticlePloS one2011
GRIM-1, a novel growth suppressor, inhibits rRNA maturation by suppressing small nucleolar RNAs.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- VIRMA-mediated mScience advances · 2025Article
- Review
- Rapid in vivo validation of candidate drivers derived from the PTEN-mutant prostate metastasis genome.Methods (San Diego, Calif.) · 2015Article
- Interferons, signal transduction pathways, and the central nervous system.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- RNA-guided isomerization of uridine to pseudouridine--pseudouridylation.RNA biology · 2014Review
- Regulation of snoRNAs in cancer: close encounters with interferon.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2013Review
- Expression of small nucleolar RNAs in leukemic cells.Cellular oncology (Dordrecht, Netherlands) · 2013Article
- Small nucleolar RNAs in cancer.Biochimica et biophysica acta · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
We have recently isolated novel IFN-inducible gene, Gene associated with Retinoid-Interferon-induced Mortality-1 (GRIM-1), using a genetic technique. Moderate ectopic expression of GRIM-1 caused growth inhibition and sensitized cells to retinoic acid (RA)/IFN-induced cell death while high expression caused apoptosis. GRIM-1 depletion, using RNAi, conferred a growth advantage. Three protein isoforms (1α, 1β and 1γ) with identical C-termini are produced from GRIM-1 mRNA. We show that GRIM-1 isoforms interact with NAF1 and DKC1, two essential proteins required for box H/ACA sno/sca RNP biogenesis and suppresses box H/ACA RNA levels in mammalian cells by delocalizing NAF1. Suppression of these small RNAs manifests as inefficient rRNA maturation and growth suppression. Interestingly, yeast Shq1p also caused growth suppression in mammalian cells. Consistent with its growth-suppressive property, GRIM-1 expression is lost in a number of human primary prostate tumors. Our observations support a recent study that GRIM-1 might act as a co-tumor suppressor in the prostate.
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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.