ArticleCell death and differentiation2017
Autophagy regulates MAVS signaling activation in a phosphorylation-dependent manner in microglia.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
What it found
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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
55 citing papers in PubMed.
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- Caspase-3 regulates RNA splicing and mitochondrial dynamics in microglia during Parkinson's disease.Cell death & disease · 2026Article
- Review
- Mitochondrial DNA: a molecular switch driving sterile neuroinflammation.Translational neurodegeneration · 2026Review
- A study on oral microbiome characteristics and differences in epilepsy adults with depressive symptoms based on 16S rRNA sequencing.Frontiers in microbiology · 2026Article
- Microglial Rack1 Deficiency Alleviates Alzheimer's Disease Pathology through Enhancing IGF1-Mediated Astrocytic Phagocytosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Old dogs-new tricks: multifaceted functions of MAVS beyond antivirus activity in human health and diseases.Cell & bioscience · 2025Review
- Inflammatory mitochondrial signalling and viral mimicry in cancer.Journal of translational medicine · 2025Review
- Advancements in Proteolysis Targeting Chimeras for Targeted Therapeutic Strategies in Alzheimer's Disease.Molecular neurobiology · 2025Review
- MAVS signaling of long-lived brain-resident myeloid cells is needed during viral encephalitis to adjust the transcriptome of CNS infiltrating CD8Journal of neuroinflammation · 2025Article
- Exploring the role of mitochondrial dysfunction and aging in COVID-19-Related neurological complications.Molecular biology reports · 2025Review
- Exploring the role of mitochondrial antiviral signaling protein in cardiac diseases.Frontiers in immunology · 2025Review
- Autophagy in alzheimer disease pathogenesis and its therapeutic values.Autophagy reports · 2025Review
- Multi-System-Level Analysis with RNA-Seq on Pterygium Inflammation Discovers Association between Inflammatory Responses, Oxidative Stress, and Oxidative Phosphorylation.International journal of molecular sciences · 2024Article
- Advancements in tyrosine kinase-mediated regulation of innate nucleic acid sensing.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Review
- FADD promotes type I interferon production to suppress porcine reproductive and respiratory syndrome virus infection.Frontiers in veterinary science · 2024Article
- Pseudorabies virus causes splenic injury via inducing oxidative stress and apoptosis related factors in mice.Scientific reports · 2023Article
- Activation of cell-free mtDNA-TLR9 signaling mediates chronic stress-induced social behavior deficits.Molecular psychiatry · 2023Article
- Review
- Novel therapeutic targets to halt the progression of Parkinson's disease: an in-depth review on molecular signalling cascades.3 Biotech · 2023Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Mitochondrial antiviral signaling (MAVS) protein has an important role in antiviral immunity and autoimmunity. However, the pathophysiological role of this signaling pathway, especially in the brain, remains elusive. Here we demonstrated that MAVS signaling existed and mediated poly(I:C)-induced inflammation in the brain. Along with the MAVS signaling activation, there was an induction of autophagic activation. Autophagy negatively regulated the activity of MAVS through direct binding of LC3 to the LIR motif Y(9)xxI(12) of MAVS. We also found that c-Abl kinase phosphorylated MAVS and regulated its interaction with LC3. Interestingly, tyrosine phosphorylation of MAVS was required for downstream signaling activation. Importantly, in vivo data showed that the deficiency of MAVS or c-Abl prevented MPTP-induced microglial activation and dopaminergic neuron loss. Together, our findings reveal the molecular mechanisms underlying the regulation of MAVS-dependent microglial activation in the nervous system, thus providing a potential target for the treatment of microglia-driven inflammatory brain diseases.
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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.