Evidence map›Paper›PMID 20432247›Full record

ArticleJournal of cellular biochemistry2010

The human IGF1R IRES likely operates through a Shine-Dalgarno-like interaction with the G961 loop (E-site) of the 18S rRNA and is kinetically modulated by a naturally polymorphic polyU loop.

Zheng Meng, Nateka L Jackson, Oleg D Shcherbakov, Hyoungsoo Choi, Scott W Blume

Abstract read
In one paragraph

Article in Journal of cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 24% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 35 citations in OpenAlex.

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  14. IRES inhibition induces terminal differentiation and synchronized death in triple-negative breast cancer and glioblastoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Zheng MengDepartment of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Nateka L Jackson
Oleg D Shcherbakov
Hyoungsoo Choi
Scott W Blume
University of Alabama at Birmingham · US

Funding

Dysregulation of IGF-1R Translational ControlR01CA108886 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BLUME, SCOTT W · 2004 to 2015
$2.3M
NCI NIH HHS R01 CA108886
6 · The paper itself

Abstract

IGF1R is a proto-oncogene with potent mitogenic and antiapoptotic activities, and its expression must be tightly regulated to maintain normal cellular and tissue homeostasis. We previously demonstrated that translation of the human IGF1R mRNA is controlled by an internal ribosome entry site (IRES), and delimited the core functional IRES to a 90-nucleotide segment of the 5'-untranslated region positioned immediately upstream of the initiation codon. Here we have analyzed the sequence elements that contribute to the function of the core IRES. The Stem2/Loop2 sequence of the IRES exhibits near-perfect Watson-Crick complementarity to the G961 loop (helix 23b) of the 18S rRNA, which is positioned within the E-site on the platform of the 40S ribosomal subunit. Mutations that disrupt this complementarity have a negative impact on regulatory protein binding and dramatically decrease IRES activity, suggesting that the IGF1R IRES may recruit the 40S ribosome by a eukaryotic equivalent of the Shine-Dalgarno (mRNA-rRNA base-pairing) interaction. The homopolymeric Loop3 sequence of the IRES modulates accessibility and limits the rate of translation initiation mediated through the IRES. Two functionally distinct allelic forms of the Loop3 poly(U)-tract are prevalent in the human population, and it is conceivable that germ-line or somatic variations in this sequence could predispose individuals to development of malignancy, or provide a selectable growth advantage for tumor cells.

Indexed as

Polymorphism, Genetic5' Untranslated RegionsAllelesBase SequenceCell Line, TumorDNA PrimersGene Expression RegulationGenes, ReporterHumansKineticsMutagenesis, Site-DirectedMutationPolymerase Chain ReactionProto-Oncogene MasReceptor, IGF Type 1RNA, Ribosomal, 18S5' Untranslated RegionsDNA PrimersMAS1 protein, humanProto-Oncogene MasReceptor, IGF Type 1RNA, Ribosomal, 18S

Identifiers

PMID20432247
PMCPMC2997104
OpenAlexW2092849727

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Registered trials

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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.