Evidence map›Paper›PMID 28606928›Full record

ArticleThe Journal of cell biology2017

mTOR controls ChREBP transcriptional activity and pancreatic β cell survival under diabetic stress.

Gia Cac Chau, Dong Uk Im, Tong Mook Kang, Jeong Mo Bae, Won Kim, Suhkneung Pyo, Eun-Yi Moon, Sung Hee Um

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 64 citations in OpenAlex.

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  5. A homozygous TARS2 variant is a novel cause of syndromic neonatal diabetes.Diabetic medicine : a journal of the British Diabetic Association · 2025
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  10. Beyond Glucose: The Dual Assault of Oxidative and ER Stress in Diabetic Disorders.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2023
    Review
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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

8 authors at 6 institutions in 1 country.

Gia Cac ChauDepartment of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Gyeonggi-do, Korea.
Dong Uk ImDepartment of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences and Technology, Samsung Medical Center, Sungkyunkwan University, Seoul, Korea.ORCID 0000-0002-1260-6101
Tong Mook KangDepartment of Physiology, Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, Gyeonggi-do, Korea.
Jeong Mo BaeDepartment of Pathology, Seoul National University College of Medicine, Seoul National University Hospital, Seoul Metropolitan Government Boramae Medical Center, Seoul, Korea.
Won KimDivision of Gastroenterology and Hepatology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul Metropolitan Government Boramae Medical Center, Seoul, Korea.
Suhkneung PyoSchool of Pharmacy, Sungkyunkwan University, Suwon, Gyeonggi-do, Korea.
Eun-Yi MoonDepartment of Bioscience and Biotechnology, Sejong University, Seoul, Korea eunyimoon@sejong.ac.kr.
Sung Hee UmDepartment of Molecular Cell Biology, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Suwon, Gyeonggi-do, Korea shum@skku.edu.ORCID 0000-0001-8343-4207
Samsung (South Korea) · KRSungkyunkwan University · KRSamsung Medical Center · KRSejong University · KRSeoul Metropolitan Government · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Impaired nutrient sensing and dysregulated glucose homeostasis are common in diabetes. However, how nutrient-sensitive signaling components control glucose homeostasis and β cell survival under diabetic stress is not well understood. Here, we show that mice lacking the core nutrient-sensitive signaling component mammalian target of rapamycin (mTOR) in β cells exhibit reduced β cell mass and smaller islets. mTOR deficiency leads to a severe reduction in β cell survival and increased mitochondrial oxidative stress in chemical-induced diabetes. Mechanistically, we find that mTOR associates with the carbohydrate-response element-binding protein (ChREBP)-Max-like protein complex and inhibits its transcriptional activity, leading to decreased expression of thioredoxin-interacting protein (TXNIP), a potent inducer of β cell death and oxidative stress. Consistent with this, the levels of TXNIP and ChREBP were highly elevated in human diabetic islets and

Indexed as

Transcription, GeneticAdultAgedAnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBlood GlucoseCarrier ProteinsCell Line, TumorCell SurvivalDiabetes Mellitus, ExperimentalGenotypeHumansInsulinInsulin-Secreting CellsMaleMice, Inbred C57BLBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsBlood GlucoseCarrier ProteinsInsulinMLXIPL protein, humanMlxipl protein, mouseMLX protein, humanMTOR protein, humanmTOR protein, mouseNuclear ProteinsTcfl4 protein, mouseThioredoxinsTOR Serine-Threonine KinasesTranscription FactorsTXNIP protein, humanTxnip protein, mouse

Identifiers

PMID28606928
PMCPMC5496625
OpenAlexW2625225193

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.