ArticleEndocrinology2019
Acute Deletion of METTL14 in β-Cells of Adult Mice Results in Glucose Intolerance.
Article in Endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Emerging Role of Epitranscriptomics in Diabetes Mellitus and Its Complications.Frontiers in endocrinology · 2022Pooled it
- NBiomolecules · 2026Review
- Transcriptome-wide N6-methyladenosine methylation dynamic profile in type 1 diabetes progression.Epigenomics · 2025Article
- Exercise induces Mettl14 in iWAT but regulates browning and metabolism independently of Mettl14.BMB reports · 2025Article
- Mettl3 deficiency leads to impaired insulin secretion via regulating Ire1a of mature β-cells in mice.Scientific reports · 2025Article
- Identification of mDiscover oncology · 2025Article
- Circ_0060927 regulates miR-331-3p/ERK/MAPK pathway reaction in non-small cell lung cancer through METTL14-driven methylation.Frontiers in oncology · 2025Article
- Insights into the role of RNA mGenes & diseases · 2024Review
- N6-methyladenine RNA methylation epigenetic modification and diabetic microvascular complications.Frontiers in endocrinology · 2024Review
- Studies on the fat mass and obesity-associated (FTO) gene and its impact on obesity-associated diseases.Genes & diseases · 2023Review
- Adipose METTL14-Elicited NAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- NNature structural & molecular biology · 2023Article
- N6-methyladenosine RNA modification: an emerging molecule in type 2 diabetes metabolism.Frontiers in endocrinology · 2023Review
- The role of mFrontiers in endocrinology · 2023Review
- Glucose Regulates mCells · 2022Article
- The Potential Role of m6A RNA Methylation in the Aging Process and Aging-Associated Diseases.Frontiers in genetics · 2022Review
- Epigenetic regulation of N6-methyladenosine modifications in obesity.Journal of diabetes investigation · 2021Review
- Review
- Biological functions of mCell & bioscience · 2021Review
- The Emerging Role of m6A Modification in Regulating the Immune System and Autoimmune Diseases.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
N6-Methyladenosine (m6A) is the most common and abundant mRNA modification that involves regulating the RNA metabolism. However, the role of m6A in regulating the β-cell function is unclear. Methyltransferase-like 14 (METTL14) is a key component of the m6A methyltransferase complex. To define the role of m6A in regulating the β-cell function, we generated β-cell METTL14-specific knockout (βKO) mice by tamoxifen administration. Acute deletion of Mettl14 in β-cells results in glucose intolerance as a result of a reduction in insulin secretion in β-cells even though β-cell mass is increased, which is related to increased β-cell proliferation. To define the molecular mechanism, we performed RNA sequencing to detect the gene expression in βKO islets. The genes responsible for endoplasmic reticulum stress, such as Ire1α, were among the top upregulated genes. Both mRNA and protein levels of IRE1α and spliced X-box protein binding 1 (sXBP-1) were increased in βKO islets. The protein levels of proinsulin and insulin were decreased in βKO islets. These results suggest that acute METTL14 deficiency in β-cells induces glucose intolerance by increasing the IRE1α/sXBP-1 pathway.
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Identifiers
What OpenQuestion holds
Registered trials
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.