Crypto-Giardia Card
- Known as:
- Crypto-Giardia Card
- Catalog number:
- ODZ-055
- Product Quantity:
- Tests in kit 20
- Category:
- -
- Supplier:
- Vidia
- Gene target:
- Crypto-Giardia Card
Related genes to: Crypto-Giardia 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: Crypto-Giardia Card
Related articles to: Crypto-Giardia Card
- This study aims to investigate the inhibitory effect of baicalein on cervical cancer driven by persistent human papillomavirus(HPV) infection and clarify its regulatory mechanism on the mitochondrial antiviral signaling protein(MAVS)-interferon regulatory factor 3(IRF3)-interferon-β(IFN-β) signaling pathway, so as to provide experimental evidence for the clinical transformation of baicalein. AutoDock Vina software was used for molecular docking to predict the binding modes and binding energies of baicalein with MAVS and HPV16 E6 proteins. HPV18-positive HeLa cells and HPV16-positive CaSki cells were cultured in vitro. They were divided into the control group and baicalein groups with low dose(10 μmol·L~(-1)) and high dose(40 μmol·L~(-1)). Meanwhile, the silent MAVS cell model was constructed and divided into the negative control small interfering RNA group(siNC) group, MAVS small interfering RNA(siMAVS) group, siNC + baicalein with high dose(H) group, and siMAVS + baicalein-H group. Cell proliferation and apoptosis were detected by colony formation assay, CCK-8 assay, and flow cytometry. The protein expressions of the MAVS-IRF3-IFN-β pathway and HPV16 E6 were detected by Western blot. A nude mouse model bearing CaSki cell xenografts of cervical cancer was established and randomly divided into five groups with six mice in each group: model group, baicalein with low dose(L) group(10 mg·kg~(-1)), baicalein-H group(40 mg·kg~(-1)), siMAVS + baicalein-H group, and siMAVS + model group. Modeling and administration were completed after anesthesia with pentobarbital sodium. Tumor volume was detected every three days; tumor tissues were stripped and weighed at the end of the experiment; the expressions of pathway-related proteins and oncoproteins in tumor tissues were detected by immunohistochemistry. The results show that the binding energies of baicalein with MAVS and HPV16 E6 proteins are-6.65 and-8.82 kcal·mol~(-1), respectively, with good binding activity. In in vitro experiments, baicalein inhibits the proliferation of HeLa and CaSki cells and promotes their apoptosis in a dose-dependent manner, significantly up-regulating the protein expressions of MAVS, p-IRF3/IRF3, and IFN-β, as well as down-regulating the protein expression of HPV16 E6. After MAVS silencing, the in vitro anti-tumor effect and regulatory pathway effect of baicalein are significantly reversed. In in vivo experiments, there are statistically significant differences in tumor volume, tumor weight, and the expression of related proteins among all groups. The tumor volume and weight in the baicalein-L and baicalein-H groups are significantly lower than those in the model group, with the tumor inhibition rates of 47.22% and 73.61%, respectively. The expressions of MAVS, p-IRF3, and IFN-β in tumor tissues are increased, while the expressions of HPV16 E6 and Ki67 proliferation antigen(Ki67) are decreased. After MAVS silencing, the in vivo tumor inhibition rate of baicalein decreases to 22.22%, and its regulatory pathway effect is significantly weakened. In conclusion, baicalein can directly bind to MAVS and HPV16 E6 proteins and exert an anti-cervical cancer effect driven by persistent HPV infection via activating the MAVS-IRF3-IFN-β mitochondrial antiviral signaling pathway and inhibiting the function of HPV16 E6 oncoprotein. MAVS is a key target for baicalein to exert its anti-tumor effect. - Source: PubMed
Chen JinKang Heng-YuanJiang Yu-HanChen Chen-Chen - The NLRP3 inflammasome is a central signaling pathway of innate immunity that orchestrates host defense and inflammatory responses through the activation of proinflammatory cytokines and the induction of pyroptotic cell death. Accumulating evidence indicates that NLRP3 functions within an extensive network of innate immune and cell death pathways. Reciprocal interactions between NLRP3 and other pattern-recognition receptor pathways, including Toll-like receptors, DNA-sensing cGAS-STING signaling, and RNA-sensing RIG-I/MDA5-MAVS signaling, shape the magnitude and duration of inflammatory responses during pathogen infection. Moreover, substantial crosstalk exists between NLRP3 and other inflammasomes and programmed cell death pathways, reflecting the integrated nature of cellular stress and inflammatory signaling. In this review, we summarize recent advances in our understanding of the molecular mechanisms that mediate these interactions, focusing on shared signaling components, organelle dynamics, posttranslational modifications, and feedback regulatory circuits. We further discuss how these signaling networks contribute to infectious and inflammatory diseases and highlight key unanswered questions and emerging areas of investigation that may guide the development of therapies targeting inflammasome-associated pathologies. - Source: PubMed
Publication date: 2026/09/02
Xiao NanyangLu ZexuanCooper Destiny KChen Jueqi - Nipah virus (NiV) is a highly lethal zoonotic paramyxovirus harbored by fruit bats (Pteropodidae). The virus spreads through zoonotic spillover via intermediate animal hosts or contaminated environments, and through human-to-human transmission. Since its emergence in 1998, NiV has triggered recurrent outbreaks across South and Southeast Asia, with case-fatality rates of 40-75%. Two genotypes (NiV-M and NiV-B) differ in transmissibility and pathogenicity. WHO-listed as a priority pathogen, NiV has no approved vaccines or antiviral therapeutics. The virus gains entry into host cells through Ephrin-B2/B3 receptors, and evades innate immunity via non-structural proteins (V, W, C) and structural proteins. These evasion strategies disrupt multiple nodes in type I and II interferon (IFN-I/II) signaling pathways, including suppression of RIG-I/MAVS and inhibition of STAT1/STAT2 nuclear translocation, and dysregulation of NF-κB activation. Finally, these mechanisms facilitate viral replication and systemic dissemination. Infection also elicits adaptive immunity, including neutralizing antibodies against viral glycoproteins (G and F) and durable virus-specific CD4⁺ and CD8⁺ T-cell responses. Fatal outcomes correlate with high early viremia, delayed or insufficient antibody production, and dysregulated innate and adaptive immunity. In affected organs, particularly the brain, persistent cytokine storm driven predominantly by CXCL10 recruits inflammatory infiltrates and amplifies immunopathological damage. Current intervention strategies include vaccine candidates (ChAdOx1 Nipah B, mRNA-1215, HeV-sG) and antiviral approaches such as nucleoside analogs, monoclonal antibodies, and fusion inhibitors. This review comprehensively synthesizes current knowledge on NiV epidemiology, pathogenesis, and countermeasure development, providing a conceptual framework to interpret its exceptional virulence and prioritize targets for effective outbreak control. - Source: PubMed
Publication date: 2026/08/31
Sun HaoYuan XinLi JinyanLi XitangJin YuefeiDuan Guangcai - Microglia are the main targets of HIV-1 infection in the central nervous system (CNS) and are considered important contributors to chronic neuroinflammation in people living with HIV (PLWH). In this study, we investigated the mechanisms leading to inflammatory responses during acute HIV-1 infection in an adult human microglia model. - Source: PubMed
Publication date: 2026/08/14
Gaete-Argel AracellyAnanías-Sáez CatarinaRojas-Fuentes CeciliaGiraldo-Ocampo SebastianJara DanielaHernández-Díaz TomásOrtega-Orellana CamilaLópez-Palma DeliaAkiyama HisashiGummuluru SuryaramGonzález Pablo AValiente-Echeverría FernandoSoto-Rifo Ricardo - RNA viruses, major pathogens of humans and animals, are responsible for numerous inflammatory diseases. Commonly, mild RNA virus infection fails to trigger inflammatory diseases due to host immune homeostasis. However, severe RNA virus infection destroys immune homeostasis and causes hyperinflammation. The detail mechanism is still unclear. Here, we reported that SESN1 acts as a critical negative regulator of mitochondrial antiviral signaling protein (MAVS), a central hub protein in RNA-triggered innate immune response, by potentiating MAVS autophagic degradation to repress innate immune response. Upon low dose RNA virus infection, SESN1 level was decreased at infection early stage and was rebounded at late stage, which restrained SESN1-mediated MAVS degradation to clear virus at early stage and enhanced MAVS degradation to prevent excessive cytokines production at late stage. Whereas, SESN1 level was continuously impaired after high dose RNA virus infection, which caused robust cytokines production. Notably, we observed that the expression of SESN1 was markedly downregulated and negatively correlated with cytokine levels in patients with severe influenza. Replenishment of SESN1 effectively inhibited cytokines production in the Human Primary Bronchial/Tracheal Epithelial Cells infected with Influenza A virus PR8 and peripheral blood mononuclear cells of patients with severe influenza. Mechanistically, SESN1 interacted with MAVS and enhanced MAVS autophagic degradation via SQSTM1. Together, these findings revealed SESN1 was an important factor to regulate host innate immune response. - Source: PubMed
Publication date: 2026/08/26
Liu QianghuiChen PeiranHe ChunyanQiu ZuochengZhang YuboWang JiaXu LingxiaoXu YongPan Mingyu