Evidence map›Paper›PMID 38738857›Full record

ArticleeLife2024

mTORC1/S6K1 signaling promotes sustained oncogenic translation through modulating CRL3

Dongyue Jiao, Huiru Sun, Xiaying Zhao, Yingji Chen, Zeheng Lv, Qing Shi, Yao Li, Chenji Wang, Kun Gao

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Long non-coding RNA (lncRNA)Translational cancer research · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Dongyue Jiao *State Key Laboratory of Genetic Engineering, Shanghai Stomatological Hospital & School of Stomatology, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, China.ORCID https://orcid.org/0009-0002-4061-0578
Huiru Sun *State Key Laboratory of Genetic Engineering, Shanghai Stomatological Hospital & School of Stomatology, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, China.
Xiaying ZhaoState Key Laboratory of Genetic Engineering, Shanghai Stomatological Hospital & School of Stomatology, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, China.ORCID https://orcid.org/0009-0002-4067-9655
Yingji ChenState Key Laboratory of Genetic Engineering, Shanghai Stomatological Hospital & School of Stomatology, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, China.
Zeheng LvDepartment of Clinical Laboratory, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, China.ORCID https://orcid.org/0009-0009-6355-9374
Qing ShiState Key Laboratory of Genetic Engineering, Shanghai Stomatological Hospital & School of Stomatology, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, China.
Yao LiState Key Laboratory of Genetic Engineering, Shanghai Stomatological Hospital & School of Stomatology, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, China.
Chenji WangState Key Laboratory of Genetic Engineering, Shanghai Stomatological Hospital & School of Stomatology, MOE Engineering Research Center of Gene Technology, Shanghai Engineering Research Center of Industrial Microorganisms, School of Life Sciences, Fudan University, Shanghai, China.ORCID https://orcid.org/0000-0002-5752-6439
Kun GaoDepartment of Clinical Laboratory, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, China.

Funding

National Natural Science Foundation of China 32370726National Natural Science Foundation of China 81872109National Natural Science Foundation of China 81972396National Natural Science Foundation of China 82272992National Natural Science Foundation of China 91954106National Natural Science Foundation of China 91957125National Natural Science Foundation of China 92357301National Science Foundation of Shanghai 22ZR1406600National Science Foundation of Shanghai 22ZR1449200Open Research Fund of State Key Laboratory of Genetic Engineering, Fudan University No. SKLGE-2111Open Research Fund of the Shanghai Key Laboratory of Maternal and Fetal Medicine mfmkf202204Science and Technology Research Program of Shanghai 9DZ2282100State Key Development Programs of China 2022YFA1104200
6 · The paper itself

Abstract

Enhanced protein synthesis is a crucial molecular mechanism that allows cancer cells to survive, proliferate, metastasize, and develop resistance to anti-cancer treatments, and often arises as a consequence of increased signaling flux channeled to mRNA-bearing eukaryotic initiation factor 4F (eIF4F). However, the post-translational regulation of eIF4A1, an ATP-dependent RNA helicase and subunit of the eIF4F complex, is still poorly understood. Here, we demonstrate that IBTK, a substrate-binding adaptor of the Cullin 3-RING ubiquitin ligase (CRL3) complex, interacts with eIF4A1. The non-degradative ubiquitination of eIF4A1 catalyzed by the CRL3

Indexed as

Eukaryotic Initiation Factor-4AMechanistic Target of Rapamycin Complex 1Protein BiosynthesisRibosomal Protein S6 Kinases, 70-kDaSignal TransductionUbiquitinationAnimalsCell Line, TumorHumansMiceEIF4A1 protein, humanEukaryotic Initiation Factor-4AMechanistic Target of Rapamycin Complex 1ribosomal protein S6 kinase, 70kD, polypeptide 1Ribosomal Protein S6 Kinases, 70-kDacancer biologycell biologyhumanmTORC1/S6K1 signalingphosphorylationtranslationtumorigenesisubiquitination

Identifiers

PMID38738857
PMCPMC11090508

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.