Legionella Card
- Known as:
- Legionella Card
- Catalog number:
- ODZ-189
- Product Quantity:
- Tests in kit 20
- Category:
- -
- Supplier:
- Vidia
- Gene target:
- Legionella Card
Related genes to: Legionella Card
- Gene:
- MAVS NIH gene
- Name:
- mitochondrial antiviral signaling protein
- Previous symbol:
- -
- Synonyms:
- VISA, KIAA1271, IPS-1, Cardif
- Chromosome:
- 20p13
- Locus Type:
- gene with protein product
- Date approved:
- 2009-04-01
- Date modifiied:
- 2017-09-22
Related products to: Legionella Card
Related articles to: Legionella Card
- RNA viruses, major pathogens of humans and animals, are responsible for numerous inflammatory diseases. Commonly, mild RNA virus infection fails to trigger inflammatory diseases due to host immune homeostasis. However, severe RNA virus infection destroys immune homeostasis and causes hyperinflammation. The detail mechanism is still unclear. Here, we reported that SESN1 acts as a critical negative regulator of mitochondrial antiviral signaling protein (MAVS), a central hub protein in RNA-triggered innate immune response, by potentiating MAVS autophagic degradation to repress innate immune response. Upon low dose RNA virus infection, SESN1 level was decreased at infection early stage and was rebounded at late stage, which restrained SESN1-mediated MAVS degradation to clear virus at early stage and enhanced MAVS degradation to prevent excessive cytokines production at late stage. Whereas, SESN1 level was continuously impaired after high dose RNA virus infection, which caused robust cytokines production. Notably, we observed that the expression of SESN1 was markedly downregulated and negatively correlated with cytokine levels in patients with severe influenza. Replenishment of SESN1 effectively inhibited cytokines production in the Human Primary Bronchial/Tracheal Epithelial Cells infected with Influenza A virus PR8 and peripheral blood mononuclear cells of patients with severe influenza. Mechanistically, SESN1 interacted with MAVS and enhanced MAVS autophagic degradation via SQSTM1. Together, these findings revealed SESN1 was an important factor to regulate host innate immune response. - Source: PubMed
Publication date: 2026/08/26
Liu QianghuiChen PeiranHe ChunyanQiu ZuochengZhang YuboWang JiaXu LingxiaoXu YongPan Mingyu - The innate immune response is the first line of host defense against viral infection. RNA virus infection triggers activation of retinoic acid-inducible gene-I (RIG-I)-mitochondrial antiviral signaling protein (MAVS) signaling pathway, resulting in the formation of prion-like aggregates of MAVS and production of type I interferons (IFN-I). Here, we found that APC7, a subunit of the anaphase-promoting complex/cyclosome (APC/C), can significantly restrict the replication of RNA viruses including Enterovirus 71 (EV71) and vesicular stomatitis virus (VSV). Further experiments showed that overexpression of APC7 enhances RNA virus-induced IFN-I expression, whereas knockdown of APC7 reduces it. Moreover, APC7 regulated the innate immune response independently of APC/C catalytic function. Subsequent analysis indicated that APC7 is partly localized to mitochondria, where it interacts with the transmembrane domain of MAVS. Furthermore, we discovered that APC7 promotes K63-linked polyubiquitination and mitochondrial aggregation of MAVS after RNA virus infection. Taken together, these findings demonstrated that APC7 potentiates the antiviral response through activation of MAVS-mediated signaling, which provides new insights into the regulatory mechanisms of innate immunity and viral infections. - Source: PubMed
Publication date: 2026/08/11
Su RuiSun AipingNiu YifanZhao TiesuoWang Hui - Type I interferons (IFN-I) are central to antiviral immunity, but their excessive or sustained production can result in immunopathological damage. RIG-I-like receptor (RLR) signaling is pivotal in regulating RNA virus-induced IFN-I responses and requires precise modulation to maintain immune homeostasis. Here, we report that viral infection induced elevated expression of Eukaryotic translation initiation factor 2 alpha kinase 2 (EIF2AK2), which is an interferon-stimulated gene (ISG) with unclear role in the innate immunity. Using EIF2AK2-deficient mice and cells, we demonstrated that the loss of EIF2AK2 specifically enhances RNA virus-induced IFN-I production in macrophages and suppresses the replication of RNA virus vesicular stomatitis virus (VSV), and that this function is tightly associated with the N-terminal dsRNA binding domain of EIF2AK2. Mechanistically, EIF2AK2 competes with RIG-I for binding viral RNA, thereby inhibiting RIG-I activation. In addition, EIF2AK2 promotes the translocation of p-MLKL to mitochondria via recruiting VAMP8, leading to disruption of mitochondrial membrane potential and dysfunction of MAVS, ultimately inhibiting IFN-I production. These findings identify EIF2AK2 as a critical negative regulator of RLR-mediated innate immune response to RNA viruses via dual inhibitory mechanisms, and suggest its potential as a therapeutic target for controlling dysregulated IFN-I responses. - Source: PubMed
Publication date: 2026/08/24
Chen QinWu JingyiHuang FangbinShen KeZhan WenliZheng Qingliang - - Source: PubMed
Publication date: 2026/08/19
Wu YinLu MeiHou LinsongYang JuanChen QingPan HongZhang Yi - The innate immune response is a first line of defense that allows a rapid reaction to pathogens as well as molecules released from damaged cells. It relies on pathogen-sensing receptors, many of which are nucleic acid-binding proteins, including RNA helicases. Plakophilin 1 (PKP1) is a desmosomal protein essential for strong intercellular adhesion and epithelial barrier integrity. Loss-of-function mutations in PKP1 cause ectodermal dysplasia-skin fragility syndrome (EDSFS), which is characterized by skin fragility, chronic inflammation, and recurrent infections. Here, we report that PKP1, whose role in barrier formation is to function as a critical regulator of innate immune responses. PKP1 sequesters a subset of dsRNAs that sense DExD/H-box RNA helicases-DDX1, DDX3X, DDX21, and DHX15. This limits their ability to activate the MDA5-MAVS signaling axis and prevents excessive activation of IRF3- and NFκB-driven gene expression, including the synthesis of proinflammatory cytokines, mainly IFN-β1, IL6, and TNFα. The inhibitory role of PKP1 is erased during innate immune responses by dsRNA cues, inducing proteasomal PKP1 degradation. This releases sequestered helicases, enabling dsRNA sensing and a rapid inflammatory response. Collectively, these findings identify PKP1 as a key gatekeeper that prevents exaggerated inflammation in quiescent keratinocytes, which is supported by excessive inflammation in EDSFS upon PKP1 loss. In healthy keratinocytes with proinflammatory traits, PKP1 is rapidly degraded, allowing the activation of the MDA5-MAVS signaling cascade by helicases to initiate inflammation. Hence, PKP1 combines two complementary functions essential for epidermal immune homeostasis: it provides a physical barrier preventing substance entry and suppresses innate immune responses in keratinocytes. - Source: PubMed
Publication date: 2026/08/19
Keil RenéMisiak DannyHüttelmaier StefanTellkamp FrederikKrüger MarcusHatzfeld Mechthild