ArticlePloS one2012
Regulation of the proteasome by AMPK in endothelial cells: the role of O-GlcNAc transferase (OGT).
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 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
19 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Retraction: Regulation of the Proteasome by AMPK in Endothelial Cells: The Role of O-GlcNAc Transferase (OGT).PloS one · 2023Article
- Autophagy and neurodegeneration: Unraveling the role of C9ORF72 in the regulation of autophagy and its relationship to ALS-FTD pathology.Frontiers in cellular neuroscience · 2023Review
- A nexus of lipid andFrontiers in endocrinology · 2022Review
- AMPK controls the axonal regenerative ability of dorsal root ganglia sensory neurons after spinal cord injury.Nature metabolism · 2020Article
- Human and rodent temporal lobe epilepsy is characterized by changes in O-GlcNAc homeostasis that can be reversed to dampen epileptiform activity.Neurobiology of disease · 2019Article
- The Role of Primary Cilia in the Crosstalk between the Ubiquitin⁻Proteasome System and Autophagy.Cells · 2019Review
- Hyperglycemia-Associated Dysregulation of O-GlcNAcylation and HIF1A Reduces Anticancer Action of Metformin in Ovarian Cancer Cells (SKOV-3).International journal of molecular sciences · 2018Article
- Skeletal muscle O-GlcNAc transferase is important for muscle energy homeostasis and whole-body insulin sensitivity.Molecular metabolism · 2018Article
- AMP-Activated Protein Kinase and O-GlcNAcylation, Two Partners Tightly Connected to Regulate Key Cellular Processes.Frontiers in endocrinology · 2018Review
- Crosstalk Between Mammalian Autophagy and the Ubiquitin-Proteasome System.Frontiers in cell and developmental biology · 2018Review
- Article
- Protein Expression of Proteasome Subunits in Elderly Patients with Schizophrenia.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Participation of proteasome-ubiquitin protein degradation in autophagy and the activation of AMP-activated protein kinase.Cellular signalling · 2015Article
- Priming the proteasome by protein kinase G: a novel cardioprotective mechanism of sildenafil.Future cardiology · 2015Review
- Minireview: hey U(PS): metabolic and proteolytic homeostasis linked via AMPK and the ubiquitin proteasome system.Molecular endocrinology (Baltimore, Md.) · 2014Review
- Proteasomal degradation of O-GlcNAc transferase elevates hypoxia-induced vascular endothelial inflammatory response†.Cardiovascular research · 2014Article
- O-GlcNAc transferase is critical for transducin-like enhancer of split (TLE)-mediated repression of canonical Wnt signaling.The Journal of biological chemistry · 2014Article
- RETRACTED: Identification of nitric oxide as an endogenous inhibitor of 26S proteasomes in vascular endothelial cells.PloS one · 2014Article
Corrections and comments
- Retraction · 2023-05-17Duplication of/in Image · Original Data and/or Images not Provided and/or not Available · Unreliable Data ·
- Retracted
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
26S proteasome is a macromolecular multi-subunit complex responsible for recognizing, unfolding, and ultimately destroying proteins. It remains poorly understood how 26S proteasome activity is regulated. The present study was to investigate if AMP-activated protein kinase (AMPK) functions as a physiological suppressor of the 26S proteasome in endothelial cells. 26S proteasome assembly, activity, and O-GlcNAcylation of P700 were assayed in cultured human umbilical vein endothelial cells (HUVEC) and mouse aortas isolated from C57BL6 wild type and AMPKα2 knockout mice with or without being exposed to selective AMPK activators or inhibitors. Pharmacological and genetic activation of AMPK effectively suppresses 26S proteasomes in endothelial cells. Conversely, inactivation of AMPK either pharmacologically or genetically increases 26S proteasome activity; furthermore, the inactivation decreases the O-GlcNAcylation of PA700/S10B (the regulatory complex in 26S proteasomes) and increases the assembly of 26S proteasomes. In contrast, AMPK activation increases levels of O-GlcNAcylated PA700/S10B, likely through enhanced association of PA700 with O-GlcNAc transferase (OGT), the enzyme that catalyzes protein O-GlcNAcylation. Finally, aortas from AMPK-KO vs wild type mice exhibit elevated 26S proteasome activity in parallel with decreased PA700/S10B O-GlcNAcylation and PA700/S10B-OGT association. Taken together, we conclude that AMPK functions as a physiological suppressor of 26S proteasomes.
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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.