Anti HCV Card Immunochromatographic
- Known as:
- Anti Hepatitis C virus Card Immunochromatographic
- Catalog number:
- 172-025
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- GDMS
- Gene target:
- Anti HCV Card Immunochromatographic
Related genes to: Anti HCV Card Immunochromatographic
- 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: Anti HCV Card Immunochromatographic
Alkaline Phosphatase Conjugated Affinity Purified anti-Swine IgG (H&L) [Goat] Secondary_Antibodies(endo,anti)_((rac,anti)-4-Deschloro-sertraline CAS: Formula: C17H18ClN(Tyr1)-Adipokinetic Hormone I, Rabbit anti-Locusta migratoria(Tyr1)-Adipokinetic Hormone I, Rabbit anti-Locusta migratoria, IF Kit(Tyr1)-Adipokinetic Hormone I, Rabbit anti-Locusta migratoria; IH(Tyr1)-Adipokinetic Hormone I, Rabbit anti-Locusta migratoria; RIA1 JAR WITH WIDE BOTTOM PLATE (ANTI-TILT)1 JAR WITH WIDE BOTTOM PLATE (ANTI-TILT)1-step Polymer HISTO-STAT; HRP anti Hamster (Secondary Reagent Component) for staining Hamster antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Chicken (Secondary Reagent Component) for staining Chicken antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Goat (Secondary Reagent Component) for staining Goat antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Mouse Adsorbed (Secondary Reagent Component) for staining Rat antibody- on- Mouse tissues, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Mouse Secondary Reagent Component) for staining Mouse and Rat antibodies, 250 plus slides1-step Polymer HISTO-STAT; HRP anti Rat (SecondaryReagent Component) for staining Rat antibodies, 250 plus slides Related articles to: Anti HCV Card Immunochromatographic
- To explore the nonlinear quadratic relationship between cephalometric measurements and facial attractiveness. - Source: PubMed
Feng XiaofanChen XinRen Hongyu - Our previous clinical data showed that autologous mesenchymal stromal cells (MSCs) can be used as carriers for the systemic delivery of oncolytic adenoviruses in children with advanced cancers, a therapy known as Celyvir. Despite achieving clinical remissions, treatment responses have been heterogeneous. Here, we sought to determine whether intrinsic biological characteristics of carrier MSCs influence therapeutic outcomes. Transcriptomic profiling was performed on MSCs from responder and non-responder patients to identify pathways differentially regulated according to clinical response. Expression of MAVS (mitochondrial antiviral signaling), NF-κB activation, and secretion of pro-inflammatory cytokines were analyzed in MSCs and Celyvir products both at baseline and after adenoviral infection. Among the pathways differentially regulated in MSCs according to treatment response, MAVS was identified as a relevant modulator, showing significantly lower expression in Celyvir products from responder patients. Consistently, MSCs and Celyvir products from responders exhibited reduced NF-κB activation and secreted significantly lower levels of pro-inflammatory cytokines at baseline and post-infection. To validate these findings, immunocompetent mice were treated with murine Celyvir prepared using MAVS-deficient (MAVS) MSCs as a model of "silent cells". Accordingly, murine Celyvir treatment using MAVS MSCs significantly enhanced antitumor efficacy compared to wild-type MSCs. Tumors from animals treated with murine Celyvir MAVS displayed increased infiltration of T cells and NK cells. In summary, carrier MSCs with a diminished antiviral innate immune response-characterized by low MAVS expression and attenuated pro-inflammatory signaling-provide a therapeutic advantage for systemic delivery of oncolytic viruses. These findings support the incorporation of "silent" MSCs, spontaneous or induced, into next-generation clinical trials aiming to optimize cell-based oncolytic virotherapy. - Source: PubMed
Publication date: 2026/04/02
Morales-Molina AlvaroFranco-Luzón LidiaGarcia-Rodriguez PatriciaGonzález-Murillo AfricaGarcía-Castro JavierRamírez Manuel - - Source: PubMed
Publication date: 2026/04/01
Min YukunO'Neill Luke A J - LGP2 is a key regulator within the RIG-I-like receptor (RLR) pathway with dual roles in antiviral immunity, but its function under basal conditions and its evolutionary variation among fish species require further investigation. In this study, we constructed a zebrafish lgp2 knockout model using CRISPR/Cas9. Knockout lgp2 led to upregulation of key RLR signaling components (mda5, mavs), type I interferons (ifnphi1, ifnphi3, ifnphi4), and the interferon-stimulated gene mxa. Transcriptomic profiling of 3 dpf embryos identified 3,186 differentially expressed genes (DEGs), including significantly elevated expression of five claudin-family genes. Protein-protein interaction (PPI) analysis of DEGs indicated that irf7 and claudin b exhibit an interaction at the protein level. Gene ontology analysis showed that LGP2 was enriched in terms such as helicase activity and ATPase activity, and was also significantly enriched in extracellular structure terms. Comparative sequence analysis revealed conserved DEXDc, HELICc and CTD domains in LGP2 from zebrafish, grass carp and barbel chub, with notable species-specific sequence variations. Functional rescue experiments demonstrated that all three LGP2 orthologs could restore lgp2 expression and modulate downstream interferon responses in lgp2 embryos; however, induction of the transcription factor irf7 was specifically mediated only by zebrafish-derived LGP2. These results provide insights into the functional diversity of LGP2 in teleost immunity and inform strategies for selective breeding aimed at disease resistance. - Source: PubMed
Publication date: 2026/03/30
Liao Yi JianLi Yao GuoLi Yi Lin - The neurotropic betacoronavirus porcine hemagglutinating encephalomyelitis virus (PHEV) subverts early innate defenses to establish persistent neuronal infection. We show that PHEV activates RIG-I-MAVS signaling but hijacks this pathway to induce a delayed IRF7-dependent interferon (IFN-I) response (>12 h post-infection), permitting unchecked replication prior to late-phase immunity. Mechanistically, the viral nucleocapsid (N) protein directly engages RIG-I's caspase activation and recruitment domain (CARD) via its C-terminal domain (CTD), competitively blocking TRIM25-mediated K63-linked ubiquitination and silencing RIG-I activation. Concurrently, N protein disrupts IRF3 activation by disrupting homodimerization, phosphorylation, and nuclear translocation, abrogating its function as the dominant early antiviral mediator. Consequently, inadequate IRF7-driven IFN induction (<3-fold at mRNA level) fails to compensate for IRF3 inactivation, creating an immune-permissive window. Pharmacological blockade of replication (Remdesivir or Lopinavir) abolished RIG-I-IRF7 activation and IFN induction, confirming replication-derived dsRNA as the essential immune trigger. Thus, PHEV deploys its N protein to simultaneously sabotage RIG-I sensing and IRF3 effector functions, enabling covert immune evasion critical for neurotropic pathogenesis.IMPORTANCEPorcine hemagglutinating encephalomyelitis virus (PHEV) causes lethal encephalomyelitis in piglets by exploiting neuronal immune vulnerabilities. We reveal that PHEV nucleocapsid (N) protein directly binds RIG-I to block its antiviral activation signal (K63-ubiquitination) and concurrently disabling IRF3-the master regulator of early interferon defense. This unique strategy, distinct from nonstructural protein-mediated evasion in other coronaviruses, allows unchecked viral replication during critical early infection. Our work identifies the N protein as a central immunosuppressor evolved for neurotropism and exposes the RIG-I-IRF3 interface as a druggable target. These findings provide a blueprint for countermeasures against PHEV and related neuroinvasive coronaviruses threatening human and animal health. - Source: PubMed
Publication date: 2026/03/30
Mu ShaoqianBai YuanmaoQiu RuizhaoZhang FeilinShi JunchaoLan YungangGao FengHe WenqiLi Zi