ReviewFrontiers in endocrinology2023
From glucose sensing to exocytosis: takes from maturity onset diabetes of the young.
Review in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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.
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
7 citing papers in PubMed, 8 citations in OpenAlex.
- Novel variation in theFrontiers in endocrinology · 2026Review
- Case Report: A novel 1, 171 bp GCK promoter/exon 1 deletion in a Chinese pedigree: correcting a misdiagnosis of MODY10 based on an incidental INS variant.Frontiers in endocrinology · 2026Article
- Article
- Maturity-onset diabetes of the young type 3 complicated with type 5: A case report and literature review.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Assessment of pathogenicity and functional characterization ofWorld journal of diabetes · 2024Article
- Complex rearrangement in TBC1D4 in an individual with diabetes due to severe insulin resistance syndrome.European journal of human genetics : EJHG · 2024Article
- Current views on etiology, diagnosis, epidemiology and gene therapy of maturity onset diabetes in the young.Frontiers in endocrinology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monogenic diabetes gave us simplified models of complex molecular processes occurring within β-cells, which allowed to explore the roles of numerous proteins from single protein perspective. Constellation of characteristic phenotypic features and wide application of genetic sequencing techniques to clinical practice, made the major form of monogenic diabetes - the Maturity Onset Diabetes of the Young to be distinguishable from type 1, type 2 as well as neonatal diabetes mellitus and understanding underlying molecular events for each type of MODY contributed to the advancements of antidiabetic therapy and stem cell research tremendously. The functional analysis of MODY-causing proteins in diabetes development, not only provided better care for patients suffering from diabetes, but also enriched our comprehension regarding the universal cellular processes including transcriptional and translational regulation, behavior of ion channels and transporters, cargo trafficking, exocytosis. In this review, we will overview structure and function of MODY-causing proteins, alterations in a particular protein arising from the deleterious mutations to the corresponding gene and their consequences, and translation of this knowledge into new treatment strategies.
Indexed as
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.