Evidence map›Paper›PMID 26283179›Full record

ArticleScientific reports2015

OLA1 regulates protein synthesis and integrated stress response by inhibiting eIF2 ternary complex formation.

Huarong Chen, Renduo Song, Guohui Wang, Zonghui Ding, Chunying Yang, Jiawei Zhang, Zihua Zeng, Valentina Rubio, Luchang Wang, Nancy Zu and 8 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

34 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Review
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  7. Review
  8. Article
  9. OLA1 Phosphorylation Governs the Mitochondrial Bioenergetic Function of Pulmonary Vascular Cells.American journal of respiratory cell and molecular biology · 2023
    Article
  10. OLA1 Phosphorylation: A Distress Signal from Damaged Endothelial Mitochondria?American journal of respiratory cell and molecular biology · 2023
    Article
  11. Article
  12. Article
  13. Targeting the methionine addiction of cancer.American journal of cancer research · 2022
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
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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

18 authors at 5 institutions in 2 countries.

Huarong Chen1] Department of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA [2] Cancer Institute, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, China.
Renduo SongDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Guohui WangDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Zonghui DingDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Chunying YangDepartment of Radiation Oncology Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Jiawei ZhangCancer Institute, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, China.
Zihua ZengDepartment of Pathology and Genomic Medicine Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Valentina RubioDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Luchang WangDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Nancy ZuDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Amanda M WeiskoffDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Laurie J MinzeImmunobiology Research Center Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Prince V S JeyabalDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Oula C MansourDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Li BaiDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
William C MerrickBiochemstry Department, Case Western Reserve University, Cleveland, OH 44106, USA.
Shu ZhengCancer Institute, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310009, China.
Zheng-Zheng ShiDepartment of Translational Imaging Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX 77030, USA.
Cornell University · USHouston Methodist · USMethodist Hospital · USSecond Affiliated Hospital of Zhejiang University · CNCase Western Reserve University · US

Funding

PREDOCTORAL TRAINING IN CELLULAR AND MOLECULAR BIOLOGYT32GM007273 · NIGMS · CORNELL UNIVERSITY ITHACA · PI BRETSCHER, ANTHONY P. · 1985 to 2019
$11.6M
Inhibition of OLA1: A Novel Strategy for Anti-Metastasis TherapyR01CA155069 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI SHI, ZHENG-ZHENG · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA155069NCI NIH HHS R01CA155069NIGMS NIH HHS T32 GM007273
6 · The paper itself

Abstract

Translation is a fundamental cellular process, and its dysregulation can contribute to human diseases such as cancer. During translation initiation the eukaryotic initiation factor 2 (eIF2) forms a ternary complex (TC) with GTP and the initiator methionyl-tRNA (tRNAi), mediating ribosomal recruitment of tRNAi. Limiting TC availability is a central mechanism for triggering the integrated stress response (ISR), which suppresses global translation in response to various cellular stresses, but induces specific proteins such as ATF4. This study shows that OLA1, a member of the ancient Obg family of GTPases, is an eIF2-regulatory protein that inhibits protein synthesis and promotes ISR by binding eIF2, hydrolyzing GTP, and interfering with TC formation. OLA1 thus represents a novel mechanism of translational control affecting de novo TC formation, different from the traditional model in which phosphorylation of eIF2α blocks the regeneration of TC. Depletion of OLA1 caused a hypoactive ISR and greater survival in stressed cells. In vivo, OLA1-knockdown rendered cancer cells deficient in ISR and the downstream proapoptotic effector, CHOP, promoting tumor growth and metastasis. Our work suggests that OLA1 is a novel translational GTPase and plays a suppressive role in translation and cell survival, as well as cancer growth and progression.

Indexed as

Adenosine TriphosphatasesCell SurvivalEukaryotic Initiation Factor-2Gene Expression RegulationGTP-Binding ProteinsHEK293 CellsHumansOxidative StressProtein BiosynthesisAdenosine TriphosphatasesEukaryotic Initiation Factor-2GTP-Binding ProteinsOLA1 protein, human

Identifiers

PMID26283179
PMCPMC4539610
OpenAlexW1159297634

What OpenQuestion holds

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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.