ArticleMolecular and cellular biology2023
The Insulin Receptor and Insulin like Growth Factor Receptor 5' UTRs Support Translation Initiation Independently of EIF4G1.
Article in Molecular and cellular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Structure-informed mutagenesis identifies combinatorial contributions to mouse insulin receptor IRES function.RNA (New York, N.Y.) · 2026Article
- Targeting Cancer Translational Plasticity: IRES-Driven Metabolism and Survival Within the Tumor Microenvironment.Cancers · 2025Review
- The intrinsically disordered region of eIF5B stimulates IRES usage and nucleates biological granule formation.Cell reports · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
IRES mediated translation initiation requires a different repertoire of factors than canonical cap-dependent translation. Treatments that inhibit the canonical translation factor EIF4G1 have little or no effect on the ability of the Insr and Igf1r cellular IRESes to promote translation. Transcripts for two cellular receptors contain RNA elements that facilitate translation initiation without intact EIF4G1. Cellular IRES mechanisms may resemble viral type III IRESes allowing them to promote translate with a limited number of initiation factors allowing them to work under stress conditions when canonical translation is repressed.
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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.