ArticleJournal of molecular and cellular cardiology2012
Arginylation regulates myofibrils to maintain heart function and prevent dilated cardiomyopathy.
Article in Journal of molecular and cellular cardiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 49 citations in OpenAlex.
- Genomic analyses implicate noncoding de novo variants in congenital heart disease.Nature genetics · 2020Trial
- Trypsin exhibits exopeptidase-like activity toward N-terminal arginine that biases proteomic analyses.bioRxiv : the preprint server for biology · 2026Article
- Methods to Study Arginylation of Tubulin.Methods in molecular biology (Clifton, N.J.) · 2026Article
- An unbiased proteomic platform for ATE1-based arginylation profiling.Nature chemical biology · 2025Article
- Arginyltransferase1 drives a mitochondria-dependent program to induce cell death.Cell death & disease · 2025Article
- Arginylation of ⍺-tubulin at E77 regulates microtubule dynamics via MAP1S.The Journal of cell biology · 2025Article
- Identification of an Intrinsically Disordered Region (IDR) in Arginyltransferase 1 (ATE1).Biochemistry · 2024Article
- Identification of an intrinsically disordered region (IDR) in arginyltransferase 1 (ATE1).bioRxiv : the preprint server for biology · 2024Article
- Cardiac-Specific Expression of Cre Recombinase Leads to Age-Related Cardiac Dysfunction Associated with Tumor-like Growth of Atrial Cardiomyocyte and Ventricular Fibrosis and Ferroptosis.International journal of molecular sciences · 2023Article
- Iron-sulfur clusters are involved in post-translational arginylation.Nature communications · 2023Article
- Liquiritin Attenuates Angiotensin II-Induced Cardiomyocyte Hypertrophy via ATE1/TAK1-JNK1/2 Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Glucose and Amino Acid Metabolic Dependencies Linked to Stemness and Metastasis in Different Aggressive Cancer Types.Frontiers in pharmacology · 2021Review
- Regulation of actin isoforms in cellular and developmental processes.Seminars in cell & developmental biology · 2020Review
- Arginyltransferase knockdown attenuates cardiac hypertrophy and fibrosis through TAK1-JNK1/2 pathway.Scientific reports · 2020Article
- Regulation of Mitochondrial Respiratory Chain Complex Levels, Organization, and Function by Arginyltransferase 1.Frontiers in cell and developmental biology · 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
- Protein arginylation of cytoskeletal proteins in the muscle: modifications modifying function.American journal of physiology. Cell physiology · 2019Review
- Cardiac-Specific Cre Induces Age-Dependent Dilated Cardiomyopathy (DCM) in Mice.Molecules (Basel, Switzerland) · 2019Article
- Ate1-mediated posttranslational arginylation affects substrate adhesion and cell migration in Dictyostelium discoideum.Molecular biology of the cell · 2019Article
Corrections and comments
- Commented on by
Authors and funding
14 authors at 5 institutions in 4 countries.
Funding
Abstract
Protein arginylation mediated by arginyltransferase (ATE1) is essential for heart formation during embryogenesis, however its cell-autonomous role in cardiomyocytes and the differentiated heart muscle has never been investigated. To address this question, we generated cardiac muscle-specific Ate1 knockout mice, in which Ate1 deletion was driven by α-myosin heavy chain promoter (αMHC-Ate1 mouse). These mice were initially viable, but developed severe cardiac contractility defects, dilated cardiomyopathy, and thrombosis over time, resulting in high rates of lethality after 6months of age. These symptoms were accompanied by severe ultrastructural defects in cardiac myofibrils, seen in the newborns and far preceding the onset of cardiomyopathy, suggesting that these defects were primary and likely underlay the development of the future heart defects. Several major sarcomeric proteins were arginylated in vivo. Moreover, Ate1 deletion in the hearts resulted in a significant reduction of active and passive myofibril forces, suggesting that arginylation is critical for both myofibril structural integrity and contractility. Thus, arginylation is essential for maintaining the heart function by regulation of the major myofibril proteins and myofibril forces, and its absence in the heart muscle leads to progressive heart failure through cardiomyocyte-specific defects.
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.