Evidence map›Paper›PMID 26876939›Full record

ArticleMolecular cell2016

mTORC1 Coordinates Protein Synthesis and Immunoproteasome Formation via PRAS40 to Prevent Accumulation of Protein Stress.

Young Sung Yun, Kwan Hyun Kim, Barbara Tschida, Zohar Sachs, Klara E Noble-Orcutt, Branden S Moriarity, Teng Ai, Rui Ding, Jessica Williams, Liqiang Chen and 2 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

44 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Proteasome: Role in T Cell Function Regulation.International journal of biological sciences · 2025
    Review
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  13. Review
  14. Role of Proteasomes in Inflammation.Journal of clinical medicine · 2021
    Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. PTEN inhibitor VO-OHpic suppresses TSC2Experimental and therapeutic medicine · 2020
    Article
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

12 authors at 2 institutions in 1 country.

Young Sung YunDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.
Kwan Hyun KimDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.
Barbara TschidaDepartment of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455, USA.
Zohar SachsDivision of Hematology, Oncology, and Transplantation, Department of Medicine, University of Minnesota, Minneapolis, MN 55455, USA; Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA.
Klara E Noble-OrcuttDivision of Hematology, Oncology, and Transplantation, Department of Medicine, University of Minnesota, Minneapolis, MN 55455, USA.
Branden S MoriarityMasonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA; Department of Pediatrics, University of Minnesota, Minneapolis, MN 55455, USA.
Teng AiThe Center for Drug Design, University of Minnesota, Minneapolis, MN 55455, USA.
Rui DingThe Center for Drug Design, University of Minnesota, Minneapolis, MN 55455, USA.
Jessica WilliamsThe Center for Drug Design, University of Minnesota, Minneapolis, MN 55455, USA.
Liqiang ChenThe Center for Drug Design, University of Minnesota, Minneapolis, MN 55455, USA.
David LargaespadaDepartment of Genetics, Cell Biology, and Development, University of Minnesota, Minneapolis, MN 55455, USA; Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA; Department of Pediatrics, University of Minnesota, Minneapolis, MN 55455, USA.
Do-Hyung KimDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA; Masonic Cancer Center, University of Minnesota, Minneapolis, MN 55455, USA. Electronic address: dhkim@umn.edu.
University of Minnesota · USUniversity of Minnesota Medical Center · US

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Jeffrey S. Miller · 1998 to 2026
$100.4M
University of Minnesota Clinical and Translational Science Institute (UMN CTSI)UL1TR000114 · NCATS · UNIVERSITY OF MINNESOTA · PI BLAZAR, BRUCE R · 2012 to 2015
$35.0M
Obesity and Energy Metabolism CoreP30DK050456 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI CROW, SCOTT J · 1995 to 2015
$17.0M
University of Minnesota Clinical and Translational Science Institute (UMN CTSI)KL2TR000113 · NCATS · UNIVERSITY OF MINNESOTA · PI BLAZAR, BRUCE R · 2012 to 2015
$5.4M
Mechanisms of mTOR signaling to early and late stages of autophagyR01GM097057 · NIGMS · UNIVERSITY OF MINNESOTA · PI KIM, DO-HYUNG · 2011 to 2018
$2.7M
NCATS NIH HHS KL2 TR000113NCATS NIH HHS UL1 TR000114NCI NIH HHS P30 CA077598NIDDK NIH HHS DK050456NIDDK NIH HHS P30 DK050456NIGMS NIH HHS GM097057NIGMS NIH HHS R01 GM097057
6 · The paper itself

Abstract

Reduction of translational fidelity often occurs in cells with high rates of protein synthesis, generating defective ribosomal products. If not removed, such aberrant proteins can be a major source of cellular stress causing human diseases. Here, we demonstrate that mTORC1 promotes the formation of immunoproteasomes for efficient turnover of defective proteins and cell survival. mTORC1 sequesters precursors of immunoproteasome β subunits via PRAS40. When activated, mTORC1 phosphorylates PRAS40 to enhance protein synthesis and simultaneously to facilitate the assembly of the β subunits for forming immunoproteasomes. Consequently, the PRAS40 phosphorylations play crucial roles in clearing aberrant proteins that accumulate due to mTORC1 activation. Mutations of RAS, PTEN, and TSC1, which cause mTORC1 hyperactivation, enhance immunoproteasome formation in cells and tissues. Those mutations increase cellular dependence on immunoproteasomes for stress response and survival. These results define a mechanism by which mTORC1 couples elevated protein synthesis with immunoproteasome biogenesis to protect cells against protein stress.

Indexed as

Protein BiosynthesisAdaptor Proteins, Signal TransducingAnimalsCell SurvivalHCT116 CellsHEK293 CellsHumansMechanistic Target of Rapamycin Complex 1MiceMultiprotein ComplexesMutationPhosphoproteinsPhosphorylationProteasome Endopeptidase ComplexPTEN Phosphohydrolaseras ProteinsAdaptor Proteins, Signal TransducingAKT1S1 protein, humanMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesPhosphoproteinsproline-rich Akt substrate, 40 kDa protein, mouseProteasome Endopeptidase ComplexPTEN Phosphohydrolaseras ProteinsTOR Serine-Threonine KinasesTSC1 protein, humanTsc1 protein, mouseTuberous Sclerosis Complex 1 ProteinTumor Suppressor Proteins

Identifiers

PMID26876939
PMCPMC4870089
OpenAlexW2263998250

What OpenQuestion holds

Textmetadata
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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 OpenQuestion graph.