ArticleThe Journal of biological chemistry2012
Characterization of arginylation branch of N-end rule pathway in G-protein-mediated proliferation and signaling of cardiomyocytes.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 51 citations in OpenAlex.
- Acylamino acid-releasing enzyme, a bifunctional protease with a potential role in aging.Journal of experimental botany · 2025Review
- Global profiling of N-terminal cysteine-dependent degradation mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- N-recognins UBR1 and UBR2 as central ER stress sensors in mammals.Molecules and cells · 2024Article
- Molecular Regulation of the Response of Brain Pericytes to Hypoxia.International journal of molecular sciences · 2023Review
- RGS5: a novel role as a hypoxia-responsive protein that suppresses chemokinetic and chemotactic migration in brain pericytes.Biology open · 2022Article
- The Final Maturation State of β-actin Involves N-terminal Acetylation by NAA80, not N-terminal Arginylation by ATE1.Journal of molecular biology · 2022Article
- The Antipsychotic Drug Clozapine Suppresses the RGS4 Polyubiquitylation and Proteasomal Degradation Mediated by the Arg/N-Degron Pathway.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Arginyltransferase (Ate1) regulates the RGS7 protein level and the sensitivity of light-evoked ON-bipolar responses.Scientific reports · 2021Article
- R-catcher, a potent molecular tool to unveil the arginylome.Cellular and molecular life sciences : CMLS · 2021Article
- Arginylation Regulates G-protein Signaling in the Retina.Frontiers in cell and developmental biology · 2021Article
- Modulation of CaChannels (Austin, Tex.) · 2020Article
- Arginyltransferase knockdown attenuates cardiac hypertrophy and fibrosis through TAK1-JNK1/2 pathway.Scientific reports · 2020Article
- Posttranslational Arginylation Enzyme Arginyltransferase1 Shows Genetic Interactions With Specific Cellular PathwaysFrontiers in physiology · 2020Article
- Quantification of intracellular N-terminal β-actin arginylation.Scientific reports · 2019Article
- Article
- Genetic Analysis of Rare Human Variants of Regulators of G Protein Signaling Proteins and Their Role in Human Physiology and Disease.Pharmacological reviews · 2018Review
- Group VII Ethylene Response Factors in Arabidopsis: Regulation and Physiological Roles.Plant physiology · 2018Review
- PARK7 modulates autophagic proteolysis through binding to the N-terminally arginylated form of the molecular chaperone HSPA5.Autophagy · 2018Article
- p62/SQSTM1/Sequestosome-1 is an N-recognin of the N-end rule pathway which modulates autophagosome biogenesis.Nature communications · 2017Article
- Article
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
Abstract
The N-end rule pathway is a proteolytic system in which destabilizing N-terminal amino acids of short lived proteins are recognized by recognition components (N-recognins) as an essential element of degrons, called N-degrons. In eukaryotes, the major way to generate N-degrons is through arginylation by ATE1 arginyl-tRNA-protein transferases, which transfer Arg from aminoacyl-tRNA to N-terminal Asp and Glu (and Cys as well in mammals). We have shown previously that ATE1-deficient mice die during embryogenesis with defects in cardiac and vascular development. Here, we characterized the arginylation-dependent N-end rule pathway in cardiomyocytes. Our results suggest that the cardiac and vascular defects in ATE1-deficient embryos are independent from each other and cell-autonomous. ATE1-deficient myocardium and cardiomyocytes therein, but not non-cardiomyocytes, showed reduced DNA synthesis and mitotic activity ~24 h before the onset of cardiac and vascular defects at embryonic day 12.5 associated with the impairment in the phospholipase C/PKC-MEK1-ERK axis of Gα(q)-mediated cardiac signaling pathways. Cardiac overexpression of Gα(q) rescued ATE1-deficient embryos from thin myocardium and ventricular septal defect but not from vascular defects, genetically dissecting vascular defects from cardiac defects. The misregulation in cardiovascular signaling can be attributed in part to the failure in hypoxia-sensitive degradation of RGS4, a GTPase-activating protein for Gα(q). This study is the first to characterize the N-end rule pathway in cardiomyocytes and reveals the role of its arginylation branch in Gα(q)-mediated signaling of cardiomyocytes in part through N-degron-based, oxygen-sensitive proteolysis of G-protein regulators.
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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.