TB Card Test
- Known as:
- TB Card Test
- Catalog number:
- TC - LF
- Product Quantity:
- 50 Test
- Category:
- -
- Supplier:
- Bhat Biotech India (P) Ltd
- Gene target:
- Card Test
Related genes to: TB Card Test
- 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: TB Card Test
Related articles to: TB Card Test
- - 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 - As an essential intracellular sensor of the RLR family, MDA5 recognizes viral dsRNA and triggers host antiviral immune responses. In this study, we cloned and characterized the MDA5 homolog from large yellow croaker (Larimichthys crocea), named Lc-MDA5. The coding sequence of Lc-MDA5 is 2976 bp and encodes a 991 amino acids (aa) polypeptide, containing two N-terminal CARD motifs, a DEXDc, a HELICc, and a C-terminal RD domain. The gene consists of 16 exons and 15 introns. Tissue expression examination revealed widespread Lc-MDA5 expression in healthy fish, with maximal transcript levels in the liver, followed by the head kidney, gill, and spleen. Lc-MDA5 expression was strongly induced following stimulation with poly I:C, LPS, PGN, or Pseudomonas plecoglossicida. Confocal imaging showed that Lc-MDA5 exhibited cytoplasmic distribution. Co-immunoprecipitation and subcellular co-localization assays demonstrated that Lc-MDA5 interacts with either Lc-MAVS_tv1 or its transmembrane-deficient splice isoform Lc-MAVS_tv2 to form protein complexes. Overexpression of Lc-MDA5 activated the type I interferon (IFNd) promoter and upregulated IRF3 transcript levels. Moreover, SVCV replication was reduced, as indicated by decreased transcript levels of viral glycoprotein (SVCV-G) and matrix protein (SVCV-M). Co-expression of Lc-MDA5 with either Lc-MAVS_tv1 or Lc-MAVS_tv2 amplified promoter activities of IRF3, IRF7, and IFNd, elevated transcription of IRF3, IFNd, and ISG15, and co-expression with Lc-MAVS_tv2 further reduced SVCV-G and SVCV-M transcript levels relative to Lc-MDA5 or Lc-MAVS_tv2 alone. Overall, the present findings revealed that Lc-MDA5 contributes to host antiviral immunity by engaging MAVS and its splicing variant to activate downstream IRF3/7 and IFNd signaling cascades. - Source: PubMed
Publication date: 2026/08/10
Li YingZhang Yi FanChen Xia MingMa QiangZhang Jiao NanHuang Xiao MeiLi Jing XuanZhu Yu XuanGuo Tuan YuZou Peng Fei