ArticleAmino acids2011
Elevated O-GlcNAc-dependent signaling through inducible mOGT expression selectively triggers apoptosis.
Article in Amino acids, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 65 citations in OpenAlex.
- Review
- Article
- Research progress in pharmacological effects ofZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023Review
- Genetic Ablation of the Nutrient Sensor Ogt in Endocrine Progenitors Is Dispensable for β-Cell Development but Essential for Maintenance of β-Cell Mass.Biomedicines · 2022Article
- Review
- An Epigenetic Role of Mitochondria in Cancer.Cells · 2022Review
- Short O-GlcNAcase Is Targeted to the Mitochondria and Regulates Mitochondrial Reactive Oxygen Species Level.Cells · 2022Article
- Article
- MitochondrialCancers · 2021Article
- Gigaxonin glycosylation regulates intermediate filament turnover and may impact giant axonal neuropathy etiology or treatmentJCI insight · 2020Article
- Functional Analysis ofFrontiers in oncology · 2020Review
- OGA Inhibition Alters Energetics and Nutrient Sensing in Alzheimer's Disease Cytoplasmic Hybrids.Journal of Alzheimer's disease : JAD · 2020Article
- Chemical and Biochemical Strategies To Explore the Substrate Recognition of O-GlcNAc-Cycling Enzymes.Chembiochem : a European journal of chemical biology · 2019Review
- O-GlcNAc in cancer: An Oncometabolism-fueled vicious cycle.Journal of bioenergetics and biomembranes · 2018Review
- O-Linked β-Clinical science (London, England : 1979) · 2018Review
- Nutrient-driven O-GlcNAc in proteostasis and neurodegeneration.Journal of neurochemistry · 2018Review
- O-GlcNAc Glycosylation of nNOS Promotes Neuronal Apoptosis Following Glutamate Excitotoxicity.Cellular and molecular neurobiology · 2017Article
- Potential coordination role between O-GlcNAcylation and epigenetics.Protein & cell · 2017Review
- Impact of protein O-GlcNAcylation on neural tube malformation in diabetic embryopathy.Scientific reports · 2017Article
- MitochondrialThe Journal of biological chemistry · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
O-linked N-acetylglucosamine transferase (OGT) catalyzes O-GlcNAc addition to numerous cellular proteins including transcription and nuclear pore complexes and plays a key role in cellular signaling. One differentially spliced isoform of OGT is normally targeted to mitochondria (mOGT) but is quite cytotoxic when expressed in cells compared with the ncOGT isoform. To understand the basis of this selective cytotoxicity, we constructed a fully functional ecdysone-inducible GFP-OGT. Elevated GFP-OGT expression induced a dramatic increase in intracellular O-GlcNAcylated proteins. Furthermore, enhanced OGT expression efficiently triggered programmed cell death. Apoptosis was dependent upon the unique N-terminus of mOGT, and its catalytic activity. Induction of mOGT expression triggered programmed cell death in every cell type tested including INS-1, an insulin-secreting cell line. These studies suggest that deregulated activity of the mitochondrially targeted mOGT may play a role in triggering the programmed cell death observed with diseases such as diabetes mellitus and neurodegeneration.
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.