Ovulation Urine Card
- Known as:
- Ovulation Urine Card
- Catalog number:
- INV-122
- Product Quantity:
- 4.0mm (1000 strips in a card) 25cards/box
- Category:
- -
- Supplier:
- Innoragen
- Gene target:
- Ovulation Urine Card
Related genes to: Ovulation Urine 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
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- Autophagy-associated protein 13 (ATG13) plays a pivotal role in regulating the assembly of the autophagy initiation complex. However, the function and mechanism of action of ATG13 during influenza virus infection remain incompletely understood. This study elucidates that ATG13 restricts influenza A virus (IAV) replication while potentiating the activation of the type I interferon (IFN-I) pathway. Mechanistically, coimmunoprecipitation assays revealed that ATG13 interacts with MAVS and recruits the E3 ubiquitin ligase ASB1 to catalyze K63-linked polyubiquitination at the K348 residue, thereby amplifying the downstream antiviral signaling cascade. Furthermore, through dual-luciferase reporter assays and pharmacological inhibition of autophagy, we confirmed that this novel immunomodulatory function of ATG13 is independent of the canonical autophagy pathway. The present study identifies ATG13 as a novel host restriction factor against IAV and reveals a nonautophagic role for ATG13 in antiviral innate immunity. - Source: PubMed
Publication date: 2026/09/07
Lu YiyuanChen JialeXiao HuiminLi JinzeWang HaixuLiang TianhaoWang JiaruiPang XueyiCheng MingyangSun YuCui TongPu FeiyangZhan JiaxingZhao YiboBao HongyuYang WentaoJiang YanlongYang GuilianWang JianzhongCao XinWang ChunfengBai XueZeng Yan - 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