Evidence map›Paper›PMID 25721046›Full record

ArticleCell death and differentiation2015

Reversible induction of translational isoforms of p53 in glucose deprivation.

D Khan, A Katoch, A Das, A Sharathchandra, R Lal, P Roy, S Das, S Chattopadhyay, S Das

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 10% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Current Practice in Bicistronic IRES Reporter Use: A Systematic Review.International journal of molecular sciences · 2021
    Pooled it
  2. The Dynamic Alliance of p53 and Metabolism in the Tumor Microenvironment Shapes Tumor Evolution.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
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  15. Translational Control inInternational journal of molecular sciences · 2019
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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

9 authors at 2 institutions in 1 country.

D KhanDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
A KatochDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
A DasNational Centre for Cell Science, Ganeshkhind, Pune, India.
A SharathchandraDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
R LalDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
P RoyDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
S DasDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
S ChattopadhyayNational Centre for Cell Science, Ganeshkhind, Pune, India.
S DasDepartment of Microbiology and Cell Biology, Indian Institute of Science, Bangalore, India.
Indian Institute of Science Bangalore · INNational Centre for Cell Science · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor suppressor protein p53 is a master transcription regulator, indispensable for controlling several cellular pathways. Earlier work in our laboratory led to the identification of dual internal ribosome entry site (IRES) structure of p53 mRNA that regulates translation of full-length p53 and Δ40p53. IRES-mediated translation of both isoforms is enhanced under different stress conditions that induce DNA damage, ionizing radiation and endoplasmic reticulum stress, oncogene-induced senescence and cancer. In this study, we addressed nutrient-mediated translational regulation of p53 mRNA using glucose depletion. In cell lines, this nutrient-depletion stress relatively induced p53 IRES activities from bicistronic reporter constructs with concomitant increase in levels of p53 isoforms. Surprisingly, we found scaffold/matrix attachment region-binding protein 1 (SMAR1), a predominantly nuclear protein is abundant in the cytoplasm under glucose deprivation. Importantly under these conditions polypyrimidine-tract-binding protein, an established p53 ITAF did not show nuclear-cytoplasmic relocalization highlighting the novelty of SMAR1-mediated control in stress. In vivo studies in mice revealed starvation-induced increase in SMAR1, p53 and Δ40p53 levels that was reversible on dietary replenishment. SMAR1 associated with p53 IRES sequences ex vivo, with an increase in interaction on glucose starvation. RNAi-mediated-transient SMAR1 knockdown decreased p53 IRES activities in normal conditions and under glucose deprivation, this being reflected in changes in mRNAs in the p53 and Δ40p53 target genes involved in cell-cycle arrest, metabolism and apoptosis such as p21, TIGAR and Bax. This study provides a new physiological insight into the regulation of this critical tumor suppressor in nutrient starvation, also suggesting important functions of the p53 isoforms in these conditions as evident from the downstream transcriptional target activation.

Indexed as

Gene Expression RegulationInternal Ribosome Entry SitesProtein BiosynthesisAnimalsApoptosisCell Cycle CheckpointsCell Cycle ProteinsDNA-Binding ProteinsFemaleGlucoseMiceNuclear ProteinsProtein IsoformsTumor Suppressor Protein p53Banp protein, mouseCell Cycle ProteinsDNA-Binding ProteinsGlucoseInternal Ribosome Entry SitesNuclear ProteinsProtein IsoformsTumor Suppressor Protein p53

Identifiers

PMID25721046
PMCPMC4572868
OpenAlexW2110610312

What OpenQuestion holds

Textmetadata
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Registered trials

None linked

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.