ArticlePediatric reports2011
The role of haploinsufficiency of RPS14 and p53 activation in the molecular pathogenesis of the 5q- syndrome.
Article in Pediatric reports, 2011. 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, 16 citations in OpenAlex.
- Understanding the Continuum between High-Risk Myelodysplastic Syndrome and Acute Myeloid Leukemia.International journal of molecular sciences · 2023Review
- Pathophysiologic and clinical implications of molecular profiles resultant from deletion 5q.EBioMedicine · 2022Article
- Targeting Myc Interacting Proteins as a Winding Path in Cancer Therapy.Frontiers in pharmacology · 2021Review
- GRWD1, a new player among oncogenesis-related ribosomal/nucleolar proteins.Cell cycle (Georgetown, Tex.) · 2017Review
- Efficacy and Mechanism of Action of Low Dose Emetine against Human Cytomegalovirus.PLoS pathogens · 2016Article
- Methylation of promoters of microRNAs and their host genes in myelodysplastic syndromes.Leukemia & lymphoma · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years we have gained great insight into the molecular pathogenesis of the 5q- syndrome, a distinct subtype of myelodysplasia. The demonstration of haploinsufficiency of the ribosomal gene RPS14 (mapping to the commonly deleted region) and the finding that this is the cause of the erythroid defect in the 5qsyndrome represent major advances. A mouse model of the human 5q- syndrome generated by large-scale deletion of the Cd74-Nid67 interval (containing RPS14) further supports a critical role for RPS14 haploinsufficiency. It is widely accepted that ribosomal deficiency results in p53 activation and defective erythropoiesis and the crossing of the '5q- mice' with p53 deficient mice ameliorated the erythroid progenitor defect. Emerging data suggests that the p53 activation observed in the mouse model may also apply to the human 5q- syndrome.
Indexed as
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.