HBsAg Test Card (Serum)
- Known as:
- HBsAg Test Card (Serum)
- Catalog number:
- 4s00090
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Good Biotech Corp - GBC
- Gene target:
- HBsAg Test Card (Serum)
Related genes to: HBsAg Test Card (Serum)
- 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: HBsAg Test Card (Serum)
Related articles to: HBsAg Test Card (Serum)
- HVJ-Envelope (HVJ-E), an inactivated particle derived from the Hemagglutinating virus of Japan, represents a unique virus-based approach for cancer immunotherapy. Unlike replication-competent oncolytic viruses, which exert antitumor effects through viral propagation and tumor cell lysis, HVJ-E lacks replicative capacity and pathogenicity because its viral genome is fragmented. Conversely, although most non-replicative viral vectors are designed primarily as delivery vehicles, HVJ-E itself possesses intrinsic antitumor activity. By preserving the native viral structure and membrane-fusion capacity of the parental virus, HVJ-E enables fragmented viral genomes to enter target cells, thereby inducing antitumor immune activation and tumor cell death. Mechanistic studies have shown that HVJ-E promotes dendritic cell maturation, activates natural killer cells, and stimulates cytotoxic T lymphocytes, leading to systemic antitumor immunity. Clinical trials have demonstrated favorable safety profiles and encouraging signs of efficacy. Furthermore, reverse translational research has identified combination strategies with T cell co-stimulatory signaling and the apolipoprotein system as a downstream mediator that enhances sensitivity to immune attack. This review summarizes the historical development, mechanistic insights, and emerging therapeutic concepts of HVJ-E as a novel cancer immunotherapy platform. A comprehensive literature search was conducted using PubMed for articles related to HVJ-E and cancer published between 2002 and 2025. - Source: PubMed
Publication date: 2026/07/09
Harada AkikazuNimura Keisuke - Flaviviruses, including Dengue, West Nile, Zika, and Japanese encephalitis viruses, are arthropod-borne RNA viruses that pose an increasing global health threat. This review summarizes the role of nonstructural protein 1 (NS1), a multifunctional glycoprotein found in intracellular and secreted forms, as a key regulator of innate immunity. NS1 modulates several pattern recognition receptor pathways, including TLRs, RLRs, SR-B1-related mechanisms, and inflammasome platforms, thereby altering cytokine and interferon responses. Its effects are virus- and context-dependent. WNV NS1 inhibits TLR3/TRIF signaling, reducing IRF3 activation, type I interferon production, and interferon-stimulated gene expression. In contrast, DENV NS1 is linked to inflammatory signaling, particularly through TLR4. At the cytosolic level, NS1 from DENV, WNV, and ZIKV disrupts RIG-I/MDA5-MAVS signaling and weakens IFN-β induction. NS1 also affects inflammasome pathways: DENV promotes IL-1β release through a CD14-dependent mechanism, ZIKV suppresses cGAS-mediated antiviral signaling, and JEV promotes NLRP3 inflammasome assembly. Overall, NS1 selectively dampens interferon-mediated antiviral defenses while sustaining or enhancing inflammation, contributing to endothelial dysfunction, neuroinflammation, and severe disease. - Source: PubMed
Publication date: 2026/06/30
Ferraresi MatteoPezzi GiuliaBeltrami SilviaCianci GiorgiaMaini GloriaLiboni AlessiaBaroni MarcelloBortolotti DariaSchiuma GiovannaRizzo SabrinaStrazzabosco Giovanni - Viral infections trigger cellular stress responses, and host stress proteins play key roles in antiviral defense. Here we identify stress-responsive protein arachidonate lipoxygenase-15 (ALOX15) is a critical component of mitochondrial antiviral innate immunity. Loss of Alox15 impairs mitochondrial antiviral signaling (MAVS)-mediated type I interferon production, resulting in increased susceptibility to influenza virus, an effect reversed by adeno-associated virus-mediated lung delivery of Alox15. ALOX15 translocates to mitochondria in response to H1N1 and other RNA viruses (H3N2 and human coronavirus-229E), independent of its enzymatic activity. This mitochondrial localization is also strikingly observed in peripheral blood mononuclear cells from influenza-infected individuals. Mechanistically, ALOX15 is recruited to mitochondria by polymerized MAVS, displacing the deubiquitinase USP19 and sustaining MAVS K63-linked ubiquitination and aggregation. Leveraging these insights, we developed a synergistic ALOX15 regulation-based therapeutic strategy for influenza infection by combining the ALOX15 transcriptional activator songorine with its enzymatic inhibitor PD146176. Together, our findings establish ALOX15 as an essential component of mitochondrial antiviral immunity and a promising host-directed target for antiviral therapy. - Source: PubMed
Publication date: 2026/07/08
Weng Jing-YuChen Xin-XingYe Hui-ErZeng Ying-YingLiang Wan-LiZhang Yin-CiZong Xin-YuYan Chang-YuYe YueWu Yan-PingSun Wan-YangDuan Wen-JunLiang LeiYan YuqiCao Yun-FengDai YiKurihara HiroshiGao HaoOuyang Shu-HuaLi Yi-FangHe Rong-Rong - The global rise in chronic inflammatory and autoimmune disorders has intensified research to understand cellular stress response pathways that drive immune dysregulation. Mitochondria have emerged not only as central hubs of cellular metabolism but also as active modulators of immunity and inflammation. Mitochondrial proteases are essential regulators of mitochondrial protein quality control, dynamics, and stress responses. By selectively degrading misfolded or damaged proteins, they maintain mitochondrial function and bioenergetic capacity. Beyond housekeeping roles, mitochondrial proteases also influence immune signaling by modulating mitochondrial stress pathways, reactive oxygen species production, and the release of mitochondrial-derived danger signals. Dysregulation of these proteases has been linked to chronic inflammation and contributes to the pathogenesis of inflammatory diseases. This review summarizes current knowledge on the role of mitochondrial proteases CLPXP, LONP1, i-AAA, m-AAA, as well as processing peptidase OMA1, in immune cells and inflammatory pathologies. We explore the molecular mechanisms by which these mitochondrial proteases regulate immune signaling, integrating the results from immune cells as well as other non-immune cell types, including those involved in cancer, neurodegeneration, renal injury, and other inflammatory pathologies. We explore mitochondrial proteases function as context-dependent regulators of immunometabolic signaling, with effects shaped by cell type, metabolic state, and stress conditions. Finally, we discuss emerging small molecules and drugs targeting mitochondrial proteases to highlight their potential therapeutic role in modulating inflammation. By situating mitochondrial proteases at the crossroads of immunometabolism and therapeutic intervention, this review underscores their untapped potential in the development of innovative anti-inflammatory strategies. - Source: PubMed
Publication date: 2026/06/23
Ferreira Anna Rebeka OliveiraDay Emily A - Renal fibrosis is a critical step in chronic kidney disease (CKD) progression, but fibrosis induction is still not understood well. We found that IFN-λ is a profibrotic factor that is upregulated in fibrotic human and mouse kidneys. IFN-λ receptor deficiency ameliorated renal fibrosis in mice while exogenous IFN-λ exacerbated disease, establishing a detrimental role of IFN-λ signaling in renal fibrosis. Mechanistically, we found that IFN-λ promotes fibrosis by preferentially acting on renal fibroblasts, inducing their activation and migration through ERK/JNK-dependent synthesis of TGF-β and activation of the TGF-β-SMAD2/3 signaling pathway. Renal tubular epithelial cell (TEC)-derived IFN-λ induced by RIG-I/MAVS signaling emerged as a critical driver of renal fibroblast activation and fibrogenesis. Importantly, neutralizing antibodies against IFN-λ strongly attenuated renal fibrosis in mice. Thus, the renal TEC-IFN-λ-fibroblast axis is a previously unrecognized pathway of renal fibrosis induction that represents an attractive novel target for mitigating CKD progression. - Source: PubMed
Publication date: 2026/07/06
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