Evidence map›Paper›PMID 33906910›Full record

ArticleDiabetes2021

MEK/ERK Signaling in β-Cells Bifunctionally Regulates β-Cell Mass and Glucose-Stimulated Insulin Secretion Response to Maintain Glucose Homeostasis.

Yoshiko Matsumoto Ikushima, Motoharu Awazawa, Naoki Kobayashi, Sho Osonoi, Seiichi Takemiya, Hiroshi Kobayashi, Hirotsugu Suwanai, Yuichi Morimoto, Kotaro Soeda, Jun Adachi and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Diabetes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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  17. Temporal coding of ERK signalling in β-cells.Nature reviews. Endocrinology · 2021
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Yoshiko Matsumoto IkushimaDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Motoharu AwazawaDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Naoki KobayashiDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Sho OsonoiDepartment of Pathology and Molecular Medicine, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Seiichi TakemiyaDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Hiroshi KobayashiDepartment of Stem Cell Biology, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Hirotsugu SuwanaiDepartment of Diabetes, Metabolism and Endocrinology, Tokyo Medical University, Tokyo, Japan.
Yuichi MorimotoLaboratory of Structural Physiology, Center for Disease Biology and Integrative Medicine, Faculty of Medicine, The University of Tokyo, Tokyo, Japan.
Kotaro SoedaDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan.
Jun AdachiLaboratory of Proteome Research, Laboratory of Proteomics for Drug Discovery, Center for Drug Design Research, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka, Japan.
Masafumi MurataniDepartment of Genome Biology, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Jean CharronCentre de Recherche sur le Cancer de l'Université Laval, L'Hôtel-Dieu de Québec, Quebec City, Quebec, Canada.
Hiroki MizukamiDepartment of Pathology and Molecular Medicine, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Noriko TakahashiDepartment of Physiology, Kitasato University School of Medicine, Sagamihara, Japan.
Kohjiro UekiDepartment of Molecular Diabetic Medicine, Diabetes Research Center, Research Institute, National Center for Global Health and Medicine, Tokyo, Japan uekik@ri.ncgm.go.jp.ORCID 0000-0003-1523-8102

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In diabetic pathology, insufficiency in β-cell mass, unable to meet peripheral insulin demand, and functional defects of individual β-cells in production of insulin are often concurrently observed, collectively causing hyperglycemia. Here we show that the phosphorylation of ERK1/2 is significantly decreased in the islets of

Indexed as

HomeostasisInsulin SecretionAnimalsBlood GlucoseCell LineDiet, High-FatExocytosisExtracellular Signal-Regulated MAP KinasesHumansInsulin-Secreting CellsMaleMiceMice, Inbred C57BLMitogen-Activated Protein Kinase KinasesPhosphorylationSignal TransductionBlood GlucoseExtracellular Signal-Regulated MAP KinasesMitogen-Activated Protein Kinase Kinases

Identifiers

PMID33906910

What OpenQuestion holds

Textmetadata
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.