BAR (BARBITURATES) Card
- Known as:
- BAR (BARBITURATES) Card
- Catalog number:
- ODZ-231
- Product Quantity:
- Tests in kit 20
- Category:
- -
- Supplier:
- Vidia
- Gene target:
- BAR (BARBITURATES) Card
Related genes to: BAR (BARBITURATES) 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: BAR (BARBITURATES) Card
Related articles to: BAR (BARBITURATES) Card
- 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 - Atrazine (ATR) is a widely used herbicide that persists in aquatic environments, raising concerns regarding its long-term immunotoxicity. As a central immune organ, the spleen represents a potential toxicological target, yet the impact of prolonged ATR ingestion via drinking water on splenic apoptosis and immune exhaustion remains unclear. In this study, male C57BL/6 N mice received ATR in drinking water at 0, 1.5 mg/L or 150 mg/L for 24 or 48 weeks. Spleen index, histopathology, peripheral blood leukocytes, serum cytokines, splenocyte apoptosis, T-cell exhaustion-like phenotype-related markers and RIG-I/MAVS signaling were evaluated. Prolonged ATR exposure increased spleen index in a dose- and time-dependent manner and caused progressive white pulp hyperplasia, disruption of splenic architecture, red pulp congestion and macrophage accumulation. Serum IL-6 and TNF-α levels were elevated, accompanied by reduced lymphocyte counts and increased neutrophils and monocytes in peripheral blood. Splenocyte apoptosis was enhanced, with upregulation of Bax, Casp3 and cleaved caspase-3. In parallel, Pdcd1 (PD-1), Ctla4, Lag3 and Tigit expression and PD-1 protein levels were significantly increased, with PD-1-positive regions overlapping with TUNEL-positive cells. RIG-I and Mavs mRNA and RIG-I protein were also upregulated. These results demonstrate that prolonged ATR exposure via drinking water promotes splenic apoptosis and induces an immune exhaustion-like state in mice, associated with the activation of RIG-I/MAVS-linked apoptotic signaling. - Source: PubMed
Publication date: 2026/08/10
Majeed ShoaibDu ChengLi NanTu JieZhu YuSu YingshiQin Lei - The persistent HIV-1 reservoir includes a subset of cells harboring transcriptionally repressed latent HIV-1 that contributes to rebound upon antiretroviral treatment (ART) interruption. However, the majority of the reservoir consists of defective proviral genomes with mutations that prevent production of HIV-1 virions. People with HIV (PWH), even with suppression of viremia, demonstrate comorbidities of the central nervous system, heart, gut, and general aging-associated inflammation. Previously, we identified a transcriptionally active element within the envelope gene () of HIV-1, which mediates the expression of aberrant HIV-1 RNAs. We hypothesize that spurious expression of defective proviruses contributes to the general inflammation that drives these comorbidities. We observed correlations between levels of inflammatory cytokines in serum of PWH and levels of HIV-1 transcripts from this intragenic promoter. To investigate the impact of defective proviruses, we employed CRISPR-Cas9 to render the 5' long terminal repeat (LTR), which acts as the enhancer and promoter for proviral transcription, non-functional. HIV-1-infected cells harboring this deletion produce significantly higher levels of IP-10 and IL-8 in both monocytic cell lines and primary monocyte-derived macrophages. Transcripts generated from the promoter include a 5' cap and polyA tail, and the induction of IP-10 expression was dependent on the cytosolic innate immune sensing pathway components MDA5 and MAVS and not cGAS and RIG-I. We propose that defective HIV proviruses contribute to chronic inflammation in PWH through an MDA5-dependent induction of type I interferon pathways.People with HIV-1 are at higher risk of developing age-associated comorbidities and immune exhaustion even when receiving antiviral treatments and having no detectable viremia. Transcription and translation have been documented from latent and defective proviruses, but their impact on inflammation associated with chronic HIV-1 infection remains poorly understood. The significance of this work is in identifying a role for defective HIV-1 proviruses and correlating their transcription in triggering a type I interferon response. These results highlight the importance of the persistent defective HIV-1 proviruses and understanding their impact on driving chronic inflammation to inform future strategies to assure people with HIV-1 healthy living and aging. - Source: PubMed
Publication date: 2026/08/10
Kilroy Jonathan MDeokar Aparna APatalano SamanthaFuxman Bass Juan ISagar ManishGummuluru SuryaramHenderson Andrew J