Protein modification by O-linked β-N-acetylglucosamine (O-GlcNAc) is a critical cell signaling modality, but identifying signal-specific O-GlcNAcylation events remains a significant experimental challenge. Here, we describe a method for visualizing and analyzing organelle- and stimulus-specific O-GlcNAcylated proteins and use it to identify the mitochondrial voltage-dependent anion channel 2 (VDAC2) as an O-GlcNAc substrate. VDAC2(-/-) cells resist the mitochondrial dysfunction and apoptosis caused by global O-GlcNAc perturbation, demonstrating a functional connection between O-GlcNAc signaling and mitochondrial physiology through VDAC2. More broadly, our method will enable the discovery of signal-specific O-GlcNAcylation events in a wide array of experimental contexts.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869705 | PMC |
| http://dx.doi.org/10.1016/j.celrep.2013.08.048 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
A New target of ischemic ventricular arrhythmias-ITFG2.
Eur J Pharmacol
January 2025
Department of Basic Medicine, Institute of Respiratory Diseases Xiamen Medical College, Xiamen Medical College, Xiamen, Fujian 361023, P. R. China; State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD), Harbin Medical University, Harbin, Heilongjiang 150081, P. R. China. Electronic address:
ITFG2 is an intracellular protein known to modulate the immune response of T-cells. Our previous investigation revealed that ITFG2 specifically targets ATP5b to regulate ATP energy metabolism and maintain mitochondrial function, thereby protecting the heart from ischemic injury. However, the role of ITFG2 in ischemic ventricular arrhythmias and its underlying mechanisms have not been previously reported.
View Article and Find Full Text PDFVDAC1: A Key Player in the Mitochondrial Landscape of Neurodegeneration.
Biomolecules
December 2024
Department of Physiology and Cell Biology, Faculty of Health Sciences, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 84105, Israel.
Voltage-Dependent Anion Channel 1 (VDAC1) is a mitochondrial outer membrane protein that plays a crucial role in regulating cellular energy metabolism and apoptosis by mediating the exchange of ions and metabolites between mitochondria and the cytosol. Mitochondrial dysfunction and oxidative stress are central features of neurodegenerative diseases. The pivotal functions of VDAC1 in controlling mitochondrial membrane permeability, regulating calcium balance, and facilitating programmed cell death pathways, position it as a key determinant in the delicate balance between neuronal viability and degeneration.
View Article and Find Full Text PDFSuppression of PCK1 attenuates neuronal injury and improves post-resuscitation outcomes.
Biochim Biophys Acta Mol Basis Dis
January 2025
Department of Cardiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, China. Electronic address:
Cardiac arrest (CA) is a critical medical emergency that can occur in both patients with preexisting conditions and otherwise healthy individuals. Despite successful resuscitation through cardiopulmonary resuscitation (CPR), many survivors are at significant risk of developing post-cardiac arrest syndrome (PCAS), a complex systemic response to CA that includes brain injury as a major component. Phosphoenolpyruvate carboxykinase 1 (PCK1), the first rate-limiting enzyme in gluconeogenesis, has been implicated in various diseases.
View Article and Find Full Text PDFVoltage-dependent anion channel 1 oligomerization regulates PANoptosis in retinal ischemia-reperfusion injury.
Neural Regen Res
January 2025
Department of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, Hunan Province, China.
Ischemia-reperfusion injury is a common pathophysiological mechanism in retinal degeneration. PANoptosis is a newly defined integral form of regulated cell death that combines the key features of pyroptosis, apoptosis, and necroptosis. Oligomerization of mitochondrial voltage-dependent anion channel 1 is an important pathological event in regulating cell death in retinal ischemia-reperfusion injury.
View Article and Find Full Text PDFCalcium-mediated mitochondrial fission and mitophagy drive glycolysis to facilitate arterivirus proliferation.
PLoS Pathog
January 2025
Key Laboratory of Animal Diseases Diagnostic and Immunology, Ministry of Agriculture, MOE International Joint Collaborative Research Laboratory for Animal Health & Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, China.
Mitochondria, recognized as the "powerhouse" of cells, play a vital role in generating cellular energy through dynamic processes such as fission and fusion. Viruses have evolved mechanisms to hijack mitochondrial function for their survival and proliferation. Here, we report that infection with the swine arterivirus porcine reproductive and respiratory syndrome virus (PRRSV), manipulates mitochondria calcium ions (Ca2+) to induce mitochondrial fission and mitophagy, thereby reprogramming cellular energy metabolism to facilitate its own replication.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!