ArticleRedox biology2014
Methylglyoxal in cells elicits a negative feedback loop entailing transglutaminase 2 and glyoxalase 1.
Article in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Acetaldehyde and methylglyoxal: comparative analysis of toxic electronic cigarette degradation products in 3D and 2D exposure systems using human bronchial epithelial models.Frontiers in toxicology · 2025Article
- Role of saturated and unsaturated fatty acids on dicarbonyl-albumin derived advanced glycation end products in vitro.Amino acids · 2022Article
- Presence of Circulatory Autoantibodies Against ROS-Modified Histone H1 Protein in Lymphoma Patients.Frontiers in genetics · 2022Article
- Biochemical Regulation of the Glyoxalase System in Response to Insulin Signaling.Antioxidants (Basel, Switzerland) · 2021Article
- Apelin-13 Inhibits Methylglyoxal-Induced Unfolded Protein Responses and Endothelial Dysfunction via Regulating AMPK Pathway.International journal of molecular sciences · 2020Article
- An Azidoribose Probe to Track Ketoamine Adducts in Histone Ribose Glycation.Journal of the American Chemical Society · 2020Article
- Reversible histone glycation is associated with disease-related changes in chromatin architecture.Nature communications · 2019Article
- Activation of Polyamine Catabolism by N¹,NCells · 2018Article
- Redox Signaling by Reactive Electrophiles and Oxidants.Chemical reviews · 2018Review
- Comparative Examination of Temporal Glyoxalase 1 Variations Following Perforant Pathway Transection, Excitotoxicity, and Controlled Cortical Impact Injury.Neurotoxicity research · 2018Article
- Redox Control of Multidrug Resistance and Its Possible Modulation by Antioxidants.Oxidative medicine and cellular longevity · 2016Review
- Effects of methylglyoxal and glyoxalase I inhibition on breast cancer cells proliferation, invasion, and apoptosis through modulation of MAPKs, MMP9, and Bcl-2.Cancer biology & therapy · 2016Article
- Prevention of protein glycation by natural compounds.Molecules (Basel, Switzerland) · 2015Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glyoxalase 1 (GlxI) is the key enzyme that converts the highly reactive α-oxo-aldehydes into the corresponding α-hydroxy acids using l-glutathione as a cofactor. In our preliminary data, GlxI was identified as a substrate of transglutaminase 2 (TG2), a ubiquitous enzyme with multiple functions. According to the catalytic properties of TG2, protein cross-linking, polyamine conjugation, and/or deamidation are potential post-translational modifications. In this article, we have demonstrated that TG2 catalyzes either polyamine conjugation or deamidation to GlxI depending on the presence of polyamines or not. Deamidation leads to activation of GlxI while polyamine conjugation results in activation of GlxI as well as stabilization of GlxI against denaturation treatment. In cultured HeLa cells, methylglyoxal challenge causes increase in intracellular levels of reactive oxygen species (ROS) and calcium leading to TG2 activation and subsequent transamidation and activation of GlxI. The inhibition of TG2 significantly weakens the cell resistance to the methylglyoxal challenge. Thus, GlxI is a novel substrate of TG2 and is activated by TG2 in vitro and in cellulo. Exposure to methylglyoxal elicits a negative feedback loop entailing ROS, calcium, TG2 and GlxI, thus leading to attenuation of the increase in the methylglyoxal level. The results imply that cancer cells highly express TG2 or GlxI can endure the oxidative stress derived from higher glycolytic flux and may gain extra growth advantage from the aerobic glycolysis.
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Registered trials
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