ArticleeLife2013
The insulin receptor cellular IRES confers resistance to eIF4A inhibition.
Article in eLife, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 34 citations in OpenAlex.
- Programmed cell death protein 4 (PDCD4): a pleiotropic regulator in cardiovascular diseases.Journal of physiology and biochemistry · 2026Review
- Structure-informed mutagenesis identifies combinatorial contributions to mouse insulin receptor IRES function.RNA (New York, N.Y.) · 2026Article
- The intrinsically disordered region of eIF5B stimulates IRES usage and nucleates biological granule formation.Cell reports · 2023Article
- The Insulin Receptor and Insulin like Growth Factor Receptor 5' UTRs Support Translation Initiation Independently of EIF4G1.Molecular and cellular biology · 2023Article
- Article
- Oxidised metabolites of the omega-6 fatty acid linoleic acid activate dFOXO.Life science alliance · 2020Article
- IRES Trans-Acting Factors, Key Actors of the Stress Response.International journal of molecular sciences · 2019Review
- Insulin Receptor Isoforms in Cancer.International journal of molecular sciences · 2018Review
- IRES-mediated translation of cofilin regulates axonal growth cone extension and turning.The EMBO journal · 2018Article
- CTLA-4-mediated posttranslational modifications direct cytotoxic T-lymphocyte differentiation.Cell death and differentiation · 2017Article
- Focal Adhesion- and IGF1R-Dependent Survival and Migratory Pathways Mediate Tumor Resistance to mTORC1/2 Inhibition.Molecular cell · 2017Article
- Translation of CircRNAs.Molecular cell · 2017Article
- A researcher's guide to the galaxy of IRESs.Cellular and molecular life sciences : CMLS · 2017Review
- 4E-BP is a target of the GCN2-ATF4 pathway during Drosophila development and aging.The Journal of cell biology · 2017Article
- dFOXO Activates Large and Small Heat Shock Protein Genes in Response to Oxidative Stress to Maintain Proteostasis in Drosophila.The Journal of biological chemistry · 2016Article
- FOXO regulates RNA interference in Drosophila and protects from RNA virus infection.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Targeting Translation Initiation Bypasses Signaling Crosstalk Mechanisms That Maintain High MYC Levels in Colorectal Cancer.Cancer discovery · 2015Article
- Article
- Small molecule inhibitors of IRES-mediated translation.Cancer biology & therapy · 2015Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Under conditions of stress, such as limited growth factor signaling, translation is inhibited by the action of 4E-BP and PDCD4. These proteins, through inhibition of eIF4E and eIF4A, respectively, impair cap-dependent translation. Under stress conditions FOXO transcription factors activate 4E-BP expression amplifying the repression. Here we show that Drosophila FOXO binds the PDCD4 promoter and stimulates the transcription of PDCD4 in response to stress. We have shown previously that the 5' UTR of the Drosophila insulin-like receptor (dINR) supports cap-independent translation that is resistant to 4E-BP. Using hippuristanol, an eIF4A inhibitor, we find that translation of dINR UTR containing transcripts are also resistant to eIF4A inhibition. In addition, the murine insulin receptor and insulin-like growth factor receptor 5' UTRs support cap-independent translation and have a similar resistance to hippuristanol. This resistance to inhibition of eIF4E and eIF4A indicates a conserved strategy to allow translation of growth factor receptors under stress conditions. DOI:http://dx.doi.org/10.7554/eLife.00542.001.
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.