ReviewLeukemia2007
mRNA stability control: a clandestine force in normal and malignant hematopoiesis.
Review in Leukemia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Unlocking mRNA-driven CRISPR-Cas9 gene therapy via optimizing mRNA and the delivery vectors.Molecular therapy. Nucleic acids · 2025Review
- Low RNA stability signifies strong expression regulatability of tumor suppressors.Nucleic acids research · 2023Article
- 3'UTR Diversity: Expanding Repertoire of RNA Alterations in Human mRNAs.Molecules and cells · 2023Review
- Targeting cleavage and polyadenylation specific factor 1 via shRNA inhibits cell proliferation in human ovarian cancer.Journal of biosciences · 2017Article
- Impaired pre-mRNA processing and altered architecture of 3' untranslated regions contribute to the development of human disorders.International journal of molecular sciences · 2013Review
- Wig-1, a novel regulator of N-Myc mRNA and N-Myc-driven tumor growth.Cell death & disease · 2012Article
- Heat shock protein 90 stabilizes nucleolin to increase mRNA stability in mitosis.The Journal of biological chemistry · 2011Article
- The p53 target Wig-1: a regulator of mRNA stability and stem cell fate?Cell death and differentiation · 2011Review
- Modulation of neoplastic gene regulatory pathways by the RNA-binding factor AUF1.Frontiers in bioscience (Landmark edition) · 2011Review
- Article
- Mechanism of regulation of bcl-2 mRNA by nucleolin and A+U-rich element-binding factor 1 (AUF1).The Journal of biological chemistry · 2010Article
- Regulation of tumor suppressor p53 at the RNA level.Journal of molecular medicine (Berlin, Germany) · 2010Review
- The beta subunit of voltage-gated Ca2+ channels interacts with and regulates the activity of a novel isoform of Pax6.The Journal of biological chemistry · 2010Article
- IL-3 and oncogenic Abl regulate the myeloblast transcriptome by altering mRNA stability.PloS one · 2009Article
- The p53 target Wig-1 regulates p53 mRNA stability through an AU-rich element.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- AU-rich elements regulate Drosophila gene expression.Molecular and cellular biology · 2009Article
- Posttranscriptional gene regulation by RNA-binding proteins during oxidative stress: implications for cellular senescence.Biological chemistry · 2008Review
- Staufen-mediated mRNA decay.Wiley interdisciplinary reviews. RNAReview
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review addresses the scope of influence of mRNA decay on cellular functions and its potential role in normal and malignant hematopoiesis. Evidence is emerging that leukemic oncogenes and hematopoietic cytokines interact with mRNA decay pathways. These pathways can co-regulate functionally related genes through specific motifs in the 3'-untranslated region of targeted transcripts. The steps that link external stimuli to transcript turnover are not fully understood, but include subcellular relocalization or post-transcriptional modification of specific transcript-stabilizing or -destabilizing proteins. Improper functioning of these regulators of mRNA turnover can impede normal cellular differentiation or promote cancers. By delineating how subsets of transcripts decay in synchrony during normal hematopoiesis, it may be possible to determine whether this post-transcriptional regulatory pathway is hijacked in leukemogenesis.
Indexed as
Identifiers
17392821What 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.