Influenza A (SWINE FLU) Card
- Known as:
- Influenza A (SWINE FLU) Card
- Catalog number:
- ODZ-221
- Product Quantity:
- Tests in kit 20
- Category:
- -
- Supplier:
- Vidia
- Gene target:
- Influenza (SWINE FLU) Card
Related genes to: Influenza A (SWINE FLU) 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: Influenza A (SWINE FLU) Card
Alkaline Phosphatase Conjugated Affinity Purified anti-Swine IgG (H&L) [Goat] Secondary_Antibodies1250UL TRAY W_INSERT CARD1250UL TRAY W_INSERT CARD14-3-3β/ζ, ~29-30kD, Clone: 22-ii-D8B, Mab anti-Human, Mouse, Rat, Monkey, Dog, Sheep, Swine, Bovine; WB/IH/IC14-3-3β/ζ, ~29-30kD, Clone: 22-ii-D8B, Mab anti-Human, Mouse, Rat, Monkey, Dog, Sheep, Swine, Bovine; WB/IH/IC1H_Purine_2_sulfonyl fluoride, 6_chloro_ 1H_Purine_2_sulfonyl flu1_Fluoro_4_(trifluoromethoxy)benzene 4_(Trifluoromethoxy)flu2,3,3_trifluoroacryloyl fluoride 2,3,3_trifluoroacryloyl flu2-Amino-5-nitro-4-(trifluoromethyl)phenol (FLU-3) C7H5F3N2O3 CAS: 56987-02-12-Amino-5-nitro-4-(trifluoromethyl)phenol (FLU-3) CAS: 56987-02-1 Formula: C7H5F3N2O32_(Trifluoromethoxy)fluorobenzene 2_(Trifluoromethoxy)flu300UL TRAY W_INSERT CARD300UL TRAY W_INSERT CARD3pk, MAPKAPK-3, ~43kD, Rabbit anti-Human, Mouse, Rat, Bovine, Dog, Hamster, Monkey, Sheep, Swine, Rabbit; WB3pk, MAPKAPK-3, ~43kD, Rabbit anti-Human, Mouse, Rat, Bovine, Dog, Hamster, Monkey, Sheep, Swine, Rabbit; WB Related articles to: Influenza A (SWINE FLU) Card
- 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 - Crimean-Congo hemorrhagic fever (CCHF), which is caused by infection with the CCHF virus (CCHFV), is the most widespread hemorrhagic infectious disease. In severe cases, liver damage is a salient manifestation. However, the detailed mechanism is not yet fully understood. To investigate the pathogenesis of CCHF-related liver damage, we infected type I interferon receptor 1 knockout (IFNAR1-/-) mice with Hazara virus (HAZV), which is a surrogate pathogen of CCHFV, as well as with the CCHFV itself. HAZV infection caused CCHF-like symptoms, including severe liver damage, alongside inflammatory responses. HAZV infection in IFNAR1-/- mice additionally lacking mitochondrial antiviral signaling protein (MAVS) induced minimal cytokine responses; however, these mice still exhibited weight loss and liver damage, albeit with a significantly delayed onset of lethal outcomes. We found that loss of liver-resident macrophage, Kupffer cells, occurred prior to viral spread in hepatocytes and liver damage in these mice. Notably, mice lacking IFNAR1 in Kupffer cells, but not mice lacking IFNAR1 in hepatocytes, also lost Kupffer cell population and exhibited lethal liver damage, following HAZV and CCHFV infection. Our findings indicate that IFNAR1 signaling in mononuclear phagocytes, especially Kupffer cells, is essential for preventing viral spread and fatal liver damage and raise the possibility that inflammatory cytokines- and viral replication-mediated Kupffer cell loss synergistically drives both processes. - Source: PubMed
Publication date: 2026/08/18
Yamada ShintaroShimojima MasayukiSaito TakeshiMaruyama JunkiKato Hiroki - VISA/MAVS is a central signaling hub that links viral RNA sensing to type I interferon production and inflammatory responses. Because of its potent signal-amplifying capacity, VISA activity must be precisely controlled: insufficient activation compromises antiviral defense, whereas excessive or spontaneous activation can drive chronic inflammation and autoimmune disease. Recent studies have revealed a complex regulatory network governing VISA signaling, involving post-translational modifications, dynamic protein interactions, selective degradation pathways, metabolic cues, and intrinsic inhibitory mechanisms that collectively determine its activation threshold, signaling duration, and downstream output. In this review, we discuss the molecular mechanisms that regulate VISA activation, signal propagation, signal termination, and quiescence maintenance under resting conditions. We propose that immune homeostasis is achieved not through a simple on-off switch, but through continuous regulation of the VISA signalosome life cycle. This framework provides an integrated view of VISA and offers new insights into the molecular mechanisms underlying immune homeostasis. - Source: PubMed
Publication date: 2026/07/23
Shu Qi-PengLi Shang-Ze