Evidence map›Paper›PMID 37903776›Full record

ArticleCell death & disease2023

Talin-1 inhibits Smurf1-mediated Stat3 degradation to modulate β-cell proliferation and mass in mice.

Xiaoting Hou, Yangshan Chen, Bo Zhou, Wanze Tang, Zhen Ding, Litong Chen, Yun Wu, Hongyu Yang, Changzheng Du, Dazhi Yang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 7 citations in OpenAlex.

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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

12 authors at 2 institutions in 2 countries.

Xiaoting Hou *Department of Biochemistry, School of Medicine, Southern University of Science and Technology, Key University Laboratory of Metabolism and Health of Guangdong, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, 518055, China.
Yangshan Chen *Department of Biochemistry, School of Medicine, Southern University of Science and Technology, Key University Laboratory of Metabolism and Health of Guangdong, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, 518055, China.
Bo ZhouDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Key University Laboratory of Metabolism and Health of Guangdong, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, 518055, China.ORCID 0000-0003-4213-726X
Wanze TangDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Key University Laboratory of Metabolism and Health of Guangdong, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, 518055, China.
Zhen DingDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Key University Laboratory of Metabolism and Health of Guangdong, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, 518055, China.ORCID 0000-0002-3759-7520
Litong ChenDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Key University Laboratory of Metabolism and Health of Guangdong, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, 518055, China.
Yun WuDepartment of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital; Guangdong Provincial High-level Clinical Key Specialty; Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment; The Institute of Stomatology, Peking University Shenzhen Hospital, Shenzhen Peking University; The Hong Kong University of Science and Technology Medical Center, Guangdong, China.
Hongyu YangDepartment of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital; Guangdong Provincial High-level Clinical Key Specialty; Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment; The Institute of Stomatology, Peking University Shenzhen Hospital, Shenzhen Peking University; The Hong Kong University of Science and Technology Medical Center, Guangdong, China.ORCID 0000-0002-0367-4938
Changzheng DuDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Key University Laboratory of Metabolism and Health of Guangdong, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, 518055, China.
Dazhi YangThe First Affiliated Hospital, Southern University of Science and Technology, Shenzhen, 518055, China.
Guixing MaDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Key University Laboratory of Metabolism and Health of Guangdong, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, 518055, China. maguixing@live.com.ORCID 0000-0002-9603-8796
Huiling CaoDepartment of Biochemistry, School of Medicine, Southern University of Science and Technology, Key University Laboratory of Metabolism and Health of Guangdong, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Southern University of Science and Technology, Shenzhen, 518055, China. caohl@sustech.edu.cn.ORCID 0000-0002-7728-1774
Southern University of Science and Technology · CNHong Kong University of Science and Technology · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insufficient pancreatic β-cell mass and reduced insulin expression are key events in the pathogenesis of diabetes mellitus (DM). Here we demonstrate the high expression of Talin-1 in β-cells and that deficiency of Talin-1 reduces β-cell proliferation, which leads to reduced β-cell mass and insulin expression, thus causing glucose intolerance without affecting peripheral insulin sensitivity in mice. High-fat diet fed exerbates these phenotypes. Mechanistically, Talin-1 interacts with the E3 ligase smad ubiquitination regulatory factor 1 (Smurf1), which prohibits ubiquitination of the signal transducer and activator of transcription 3 (Stat3) mediated by Smurf1, and ablation of Talin-1 enhances Smurf1-mediated ubiquitination of Stat3, leading to decreased β-cell proliferation and mass. Furthermore, haploinsufficiency of Talin-1 and Stat3 genes, but not that of either gene, in β-cell in mice significantly impairs glucose tolerance and insulin expression, indicating that both factors indeed function in the same genetic pathway. Finally, inducible deletion Talin-1 in β-cell causes glucose intolerance in adult mice. Collectively, our findings reveal that Talin-1 functions as a crucial regulator of β-cell mass, and highlight its potential as a therapeutic target for DM patients.

Indexed as

Glucose IntoleranceTalinAdultAnimalsCell ProliferationHumansInsulinMiceSTAT3 Transcription FactorUbiquitinationUbiquitin-Protein LigasesInsulinSmurf1 protein, mouseStat3 protein, mouseSTAT3 Transcription FactorTalinTln1 protein, mouseUbiquitin-Protein Ligases

Identifiers

PMID37903776
PMCPMC10616178
OpenAlexW4388033704

What Socratic holds

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LicenceCC BY
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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 Socratic graph.