ArticleClinical and translational science2010
The RNA editor gene ADAR1 is induced in myoblasts by inflammatory ligands and buffers stress response.
Article in Clinical and translational science, 2010. 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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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.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Characterization of Undiscovered miRNA Involved in Tumor Necrosis Factor Alpha-Induced Atrophy in Mouse Skeletal Muscle Cell Line.International journal of molecular sciences · 2024Article
- What sequencing technologies can teach us about innate immunity.Immunological reviews · 2022Review
- RNA Editing of the Human DNA Glycosylase NEIL1 Alters Its Removal of 5-Hydroxyuracil Lesions in DNA.Biochemistry · 2021Article
- Phosphodiesterase 8A to discriminate in blood samples depressed patients and suicide attempters from healthy controls based on A-to-I RNA editing modifications.Translational psychiatry · 2021Article
- 2'-Fluorinated Hydantoins as Chemical Biology Tools for Base Excision Repair Glycosylases.ACS chemical biology · 2020Article
- MicroRNAs in Skeletal Muscle and Hints on Their Potential Role in Muscle Wasting During Cancer Cachexia.Frontiers in oncology · 2020Review
- Alu-dependent RNA editing of GLI1 promotes malignant regeneration in multiple myeloma.Nature communications · 2017Article
- Inhibition of PKR protects against HScientific reports · 2016Article
- Identification of the long, edited dsRNAome of LPS-stimulated immune cells.Genome research · 2016Article
- Reovirus-mediated induction of ADAR1 (p150) minimally alters RNA editing patterns in discrete brain regions.Molecular and cellular neurosciences · 2014Article
- ADAR1 deaminase contributes to scheduled skeletal myogenesis progression via stage-specific functions.Cell death and differentiation · 2014Article
- ADAR1 promotes malignant progenitor reprogramming in chronic myeloid leukemia.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Identification of widespread ultra-edited human RNAs.PLoS genetics · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Muscle atrophy remains a significant concern in multiple inflammatory conditions, including injury, sepsis, cachexia, and HIV-associated wasting. Herein, we show that inflammatory stressors, including TNF-alpha, IFN-gamma, or lipopolysaccharide, potently induced the novel expression of the RNA editor ADAR1, an observation not previously described in muscle cells. We also observed that cytokine stimulation suppressed muscle-associated microRNAs, an observation also not previously demonstrated. To map potential effects of ADAR1 induction in the muscle program, we conducted knockdown and overexpression studies in the mouse C2C12 muscle precursor cell (MPC) line and in primary human MPCs. We show that knockdown of stress-induced ADAR1 increased inflammation-mediated declines in the muscle differentiation markers Myogenin and myosin heavy chain, and knockdown reduced levels of active phosphorylated Akt (phospho-Akt), but had no effect on microRNA transcript levels, suggesting a role for ADAR1 in buffering inflammatory stress effects on myogenic transcription and protein synthesis pathways. In addition, overexpression of recombinant ADAR1 suppressed active phosphorylated double-stranded RNA (dsRNA)-dependent protein kinase (phospho-PKR), consistent with a role for ADAR1 in limiting inflammation-driven catabolic atrophy pathways. Collectively, these data identify a novel regulatory role for ADAR1 activation under inflammatory stress to both promote muscle protein synthesis pathways and limit atrophy pathways.
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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.