Evidence map›Paper›PMID 25866880›Full record

ArticleNature structural & molecular biology2015

Translational control of the cytosolic stress response by mitochondrial ribosomal protein L18.

Xingqian Zhang, Xiangwei Gao, Ryan Alex Coots, Crystal S Conn, Botao Liu, Shu-Bing Qian

Open access · greenAbstract read
In one paragraph

Article in Nature structural & molecular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

60 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
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  9. The translatome of glioblastoma.Molecular oncology · 2025
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  16. An HSF1-JMJD6-HSP feedback circuit promotes cell adaptation to proteotoxic stress.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  17. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Xingqian ZhangDivision of Nutritional Sciences, Cornell University, Ithaca, New York, USA.
Xiangwei GaoDivision of Nutritional Sciences, Cornell University, Ithaca, New York, USA.
Ryan Alex Coots1] Division of Nutritional Sciences, Cornell University, Ithaca, New York, USA. [2] Graduate Field of Nutritional Sciences, Cornell University, Ithaca, New York, USA.
Crystal S ConnGraduate Field of Genetics, Genomics and Development, Cornell University, Ithaca, New York, USA.
Botao LiuGraduate Field of Genetics, Genomics and Development, Cornell University, Ithaca, New York, USA.
Shu-Bing Qian1] Division of Nutritional Sciences, Cornell University, Ithaca, New York, USA. [2] Graduate Field of Nutritional Sciences, Cornell University, Ithaca, New York, USA. [3] Graduate Field of Genetics, Genomics and Development, Cornell University, Ithaca, New York, USA.
Cornell University · US

Funding

Engineering Ubiquitin Ligases to Investigate Protein Aggregation and NeurodegenerDP2OD006449 · OD · CORNELL UNIVERSITY · PI QIAN, SHU-BING · 2009 to 2009
$2.3M
Linking Nutrient Signaling and Protein Homeostasis in Mammalian AgingR01AG042400 · NIA · CORNELL UNIVERSITY · PI QIAN, SHU-BING · 2013 to 2017
$1.6M
NIA NIH HHS R01 AG042400NIA NIH HHS R01AG042400NIH HHS DP2 OD006449
6 · The paper itself

Abstract

In response to stress, cells attenuate global protein synthesis but permit efficient translation of mRNAs encoding heat-shock proteins (HSPs). Although decades have passed since the first description of the heat-shock response, how cells achieve translational control of HSP synthesis remains enigmatic. Here we report an unexpected role for mitochondrial ribosomal protein L18 (MRPL18) in the mammalian cytosolic stress response. MRPL18 bears a downstream CUG start codon and generates a cytosolic isoform in a stress-dependent manner. Cytosolic MRPL18 incorporates into the 80S ribosome and facilitates ribosome engagement on mRNAs selected for translation during stress. MRPL18 knockdown has minimal effects on mitochondrial function but substantially dampens cytosolic HSP expression at the level of translation. Our results uncover a hitherto-uncharacterized stress-adaptation mechanism in mammalian cells, which involves formation of a 'hybrid' ribosome responsible for translational regulation during the cytosolic stress response.

Indexed as

Cell Line, TumorCodon, InitiatoreIF-2 KinaseGene Expression RegulationHeat-Shock ProteinsHeat-Shock ResponseHeLa CellsHumansPhosphorylationProtein BiosynthesisProtein IsoformsRibosomal ProteinsRibosomesRNA InterferenceRNA, Small InterferingStress, PhysiologicalCodon, InitiatorEIF2AK1 protein, humaneIF-2 KinaseHeat-Shock ProteinsProtein Isoformsribosomal protein L18Ribosomal ProteinsRNA, Small Interfering

Identifiers

PMID25866880
PMCPMC4424103
OpenAlexW1988207317

What OpenQuestion holds

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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.