PSA Test Card (Whole Blood/Serum)
- Known as:
- PSA Test Card (Whole Blood/Serum)
- Catalog number:
- 4s00155
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Good Biotech Corp - GBC
- Gene target:
- PSA Test Card (Whole Blood/Serum)
Related genes to: PSA Test Card (Whole Blood/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: PSA Test Card (Whole Blood/Serum)
Related articles to: PSA Test Card (Whole Blood/Serum)
- Enteroviruses initiate infection at the intestinal epithelium but can spread systemically to cause severe disease. Although both MDA5 and TLR3 have been implicated in enterovirus sensing, the mechanisms by which the intestinal epithelium detects these viruses remain poorly defined. To address this, we infected human intestinal organoids (enteroids) with the group B enterovirus echovirus 11 (E11) and compared responses in models differentiated to mimic either crypt-like or villus-like epithelium. Villus-like enteroids produced significantly more type III interferons following E11 infection and exhibited heightened responsiveness to type III interferon signaling. Single-cell RNA sequencing of infected enteroids revealed that E11 broadly infected epithelial cell types, but type III interferon expression was largely restricted to mature enterocytes. Notably, enterocyte differentiation was also associated with upregulation of TLR3 and other innate immune genes. Using CRISPR-Cas9 knockout enteroids, we found that TLR3-TRIF signaling was essential for intestinal type III IFN responses to E11 infection, whereas loss of MAVS, the adaptor for MDA5, had no effect. Together, these data support a model in which mature enterocytes serve as key sensors of enterovirus infection via TLR3-TRIF signaling, triggering a localized type III IFN response that may help restrict viral spread. - Source: PubMed
Publication date: 2026/10/06
Hare David NCoyne Carolyn B - Severe fever with thrombocytopenia syndrome (SFTS), caused by SFTSV, is an emerging tick-borne disease with substantial mortality in East Asia and increasing geographic reach. Here, we provide an updated conceptual framework that integrates classic host recognition via DNA and RNA sensors accompanied with the multifaceted immune evasion strategies orchestrated by the viral components. A central focus is that SFTSV utilizes host receptors for attachment and internalization while hijacking autophagy-related membranes to promote assembly and egress. Its NSs protein forms autophagic inclusion bodies that sequester and degrade innate immune factors, whereas NP and Gn interfere with RIG-I-MAVS and cGAS-STING signaling through autophagy-associated mechanisms. We also examine NS-driven inflammatory regulation and evidence that the microbiota shapes virus transmission and antiviral responses. Collectively, unraveling these intricate host-virus interactions will be pivotal for advancing targeted therapeutic strategies against SFTS. - Source: PubMed
Publication date: 2026/09/24
Ma XueYang SaiWu Zi-MingPang BoKang LongfeiShi LingxueJiang XiaZhou Chuan-Min - The mitochondrial antiviral signaling protein (MAVS; also known as VISA, IPS-1, or Cardif) is the central adaptor of the RIG-I-like receptor (RLR) pathway. Upon viral infection, MAVS forms prion-like aggregates to activate NF-κB and IRF3, thereby inducing type I interferon production and antiviral responses. Here, we identify RNA-binding motif protein 6 (RBM6) as a previously unrecognized positive regulator of MAVS signaling during Sendai virus (SeV) infection. RBM6 overexpression enhanced SeV-induced IFN-β expression, whereas RBM6 deficiency impaired this response. Mechanistically, RBM6 enhanced K63-linked polyubiquitination of MAVS, promoting MAVS aggregation and facilitating the recruitment of TRAF6. Domain-mapping analysis further localized the antiviral activity of RBM6 to its zinc finger (ZnF) domain spanning residues 850-1045. Together, these findings establish RBM6 as an important enhancer of MAVS signalosome assembly and provide new insight into ubiquitin-dependent regulation of the RLR antiviral pathway. - Source: PubMed
Kong De-PingZhong NiZhang JieWang ChenXiao Yan-PingHuang Jing-PingHu TingYu Bo-WenXie Qi-YuLiu MinLi Hui-HongXie Jian-KunXu Liang-Guo - Cancer evolves within tissue ecosystems in which innate immune surveillance and tumor-promoting inflammation jointly shape disease progression and therapeutic response. Innate receptors detect cellular stress, altered-self ligands, damaged-cell products and tumor-derived nucleic acids, thereby initiating cytotoxicity, phagocytosis, antigen presentation and adaptive immune priming. However, tumors can redirect these mechanisms through suppressive cytokines, metabolic competition, hypoxia and dysregulated chemokine networks, promoting immune exclusion, metastasis and treatment resistance. This Review examines innate recognition, immunoediting and innate-adaptive crosstalk. We discuss the heterogeneity, dysfunction and therapeutic targeting of dendritic cells, macrophages, natural killer cells, neutrophils, myeloid-derived suppressor cells, innate lymphoid cells and other tissue-resident populations. We also evaluate Toll-like receptor, cGAS-STING, RIG-I-MAVS, inflammasome and complement pathways as therapeutically actionable but potentially tumor-promoting signaling systems. Finally, we consider how innate adjuvants, antigen selection, delivery technologies and rational combinations can improve therapeutic cancer vaccines. Emerging clinical studies demonstrate feasibility, but inconsistent efficacy and treatment-associated toxicity emphasize the need for biomarker-guided patient selection, spatially restricted delivery and mechanism-based sequencing. Clinical translation will depend on biomarker-guided patient selection, localized delivery and treatment sequencing that preserves antimicrobial defense and tissue homeostasis. - Source: PubMed
Publication date: 2026/09/18
Li XinghanMeng YitongDong JijunMa YueLiu DequanZhang XiaodongZhao Lingjie - Cellular senescence is characterized by irreversible cell-cycle arrest, with cells remaining viable and metabolically active. This state features a proinflammatory senescence-associated secretory phenotype (SASP) that can harm neighboring tissues. Accumulation of senescent cells accelerates age-related physiological decline and associated pathologies. Furthermore, cellular senescence is implicated in various physiological processes, including embryonic development, wound healing, tumor progression, and immune response regulation. The complexity of the aging process arises from its diverse underlying mechanisms, potential reversibility, and intrinsic heterogeneity. Experimental gerontology focuses on identifying pathogenic modulators that regulate the formation and accumulation of senescent cells, as well as investigating their impact on tissue function. Within the field of experimental gerontology, considerable attention is devoted to identifying pathogenic modulators that regulate the formation and accumulation of senescent cells, as well as to investigating their impact on tissue function. Of particular interest is the characterization of novel molecular mechanisms that govern cellular aging. Key pathogenic molecular pathways include the p53-dependent senescence pathway, the p16INK4a/pRb pathway, and non-canonical pathways like IFIH1-MAVS, which contribute to oxidative stress, DNA damage, activation of SASP, and other cellular dysfunction. This study critically examines how viral and bacterial agents induce cellular senescence, particularly in vitro, reviewing the regulatory mechanisms involved. It discusses genetic variants affecting infection susceptibility and categorizes senescence markers. Investigating the molecular mechanisms underlying cellular aging presents promising avenues for the development of targeted and effective therapeutic interventions. Such strategies may include the selective induction of senescence in cancer cells, suppression of senescence to mitigate age-related diseases, or the comprehensive modulation of aging processes to optimize clinical outcomes. - Source: PubMed
Simoroz E VAntonov Y VMuravyov G SVasilevska JRogaev E I