ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022
The Endoplasmic Reticulum ATP13A1 is Essential for MAVS-Mediated Antiviral Innate Immunity.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 12 citations in OpenAlex.
- Review
- Tail-anchored protein C-terminal domains stimulate ATP hydrolysis by the P5A-ATPase Spf1p.The Journal of biological chemistry · 2026Article
- Spectrum and functions of ion channels and transporters in osteoclasts.Bone research · 2026Review
- C-terminal tail of MAVS dictates organelle targeting and innate immune response.Cell communication and signaling : CCS · 2026Article
- The APC/C subunit APC7 exerts antiviral effects by targeting the adaptor protein MAVS.Frontiers in immunology · 2026Article
- Human periodontal ligament stem cells-derived small extracellular vesicles mitigate periodontitis by regulating macrophage pyroptosis.Journal of translational medicine · 2025Article
- ATP13A1 engages SEC61 to facilitate substrate-specific translocation.Science advances · 2025Article
- Low-density lipoprotein receptor-related protein 6 ameliorates cardiac hypertrophy by regulating CTSD/HSP90α signaling during pressure overload.Acta pharmacologica Sinica · 2025Article
- Cellular RNA interacts with MAVS to promote antiviral signaling.Science (New York, N.Y.) · 2024Article
- CELLULAR RNA INTERACTS WITH MAVS TO PROMOTE ANTIVIRAL SIGNALING.bioRxiv : the preprint server for biology · 2023Article
- WDR77 inhibits prion-like aggregation of MAVS to limit antiviral innate immune response.Nature communications · 2023Article
- The Endoplasmic Reticulum ATP13A1 is Essential for MAVS-Mediated Antiviral Innate Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Systematic analysis of virus nucleic acid sensor DDX58 in malignant tumor.Frontiers in microbiology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
RIG-I-MAVS signaling pathway is essential for efficient innate immune response against virus infection. Though many components have been identified in RIG-I pathway and it can be partially reconstituted in vitro, detailed mechanisms involved in cells are still unclear. Here, a genome-wide CRISPR-Cas9 screen is performed using an engineered cell line IFNB-P2A-GSDMD-N, and ATP13A1, a putative dislocase located on the endoplasmic reticulum, is identified as an important regulator of RIG-I pathway. ATP13A1 deficiency abolishes RIG-I-mediated antiviral innate immune response due to compromised MAVS stability and crippled signaling potency of residual MAVS. Moreover, it is discovered that MAVS is subject to protease-mediated degradation in the absence of ATP13A1. As homozygous Atp13a1 knockout mice result in developmental retardation and embryonic lethality, Atp13a1 conditional knockout mice are generated. Myeloid-specific Atp13a1-deficient mice are viable and susceptible to RNA virus infection. Collectively, the findings reveal that ATP13A1 is indispensable for the stability and activation of MAVS and a proper antiviral innate immune response.
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.