ProPrep™ Genomic Blood Card 96
- Known as:
- ProPrep™ Genomic Blood Card 96
- Catalog number:
- PBC-96
- Product Quantity:
- 96 blood spots
- Category:
- Peptides
- Supplier:
- Biotech support group
- Gene target:
- ProPrep™ Genomic Blood Card 96
Related genes to: ProPrep™ Genomic Blood Card 96
- 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: ProPrep™ Genomic Blood Card 96
Related articles to: ProPrep™ Genomic Blood Card 96
- Enterovirus 71 (EV71) infection poses a global public health challenge, especially in infants and young children, with severe cases leading to fatal consequences. EV71 infection modulates various biological processes of the host and evades host immunity through multiple mechanisms. The balance of mitochondrial dynamics is important for cellular homeostasis. However, the mechanisms underlying EV71-induced cellular damage via mitophagy remain unclear. In the current study, we showed that EV71 infection significantly reduced the total and mitochondrial ATP contents in cells, as well as the expression of mitochondrial proteins TOM20 and TIM23. Then, EV71 infection increased the protein levels of PINK1, Parkin, and LC3B, suggesting that EV71 infection triggers the mitophagy. Silencing PINK1 caused a significant reduction in viral replication, while overexpressing Parkin promoted the replication of EV71. Moreover, CsA treatment, as a mitophagy inhibitor, alleviated pathological damage and suppressed the replication of EV71 in vivo. Mechanistic study showed that silencing PINK1 inhibited the cleavage of MAVS by EV71, while overexpressing Parkin enhanced the cleavage of MAVS by EV71, suggesting that PINK1-mediated mitophagy was involved in regulating innate immunity. Furthermore, we found that EV71 infection promoted the release of mitochondria carrying EV71 virions into the extracellular environment, which mediated infection of other cells, thus facilitating virus spreading. In addition, we also demonstrated that the extracellular mitochondria induced the degradation of MAVS and mitophagy promoted the release of mitochondria in EV71-infected HeLa cells. In conclusion, these findings suggest that EV71 infection induces PINK1-mediated mitophagy, which inhibits innate immunity and facilitates virus replication. - Source: PubMed
Tian XiaoyanYuan MengLi LinrunChen DeyanLiu BingxinZou XueHe MiaoWu Zhiwei - Pseudorabies virus (PRV) poses a significant threat to the global swine industry, characterized by high morbidity and a range of sequelae in infected pigs. Mitochondria serve as a crucial platform for innate immunity, playing a pivotal role in a wide array of antiviral responses. In our recent study, we revealed that PRV infection induces mitochondrial disruption, which in turn triggers PINK1/PARKIN-mediated mitophagy. We also show that this process leads to the degradation of the mitochondrial antiviral signaling protein (MAVS) and the inhibition of antiviral interferon production and signaling, ultimately facilitating viral replication. - Source: PubMed
Publication date: 2024/11/27
Zhao YuanZhu ZhenbangWang WenqiangZhang ZhendongWen WeiLi Xiangdong - Ku70 and Ku80 form Ku, a ring-shaped complex that initiates the non-homologous end-joining (NHEJ) DNA repair pathway. Ku binds to double-stranded DNA (dsDNA) ends and recruits other NHEJ factors (e.g., LIG4, DNA-PKcs). While Ku can bind to double-stranded RNA (dsRNA) and trap mutated-DNA-PKcs on ribosomal RNA (rRNA), the physiological role on Ku-RNA interaction in otherwise wildtype cells remains unclear. Intriguingly, Ku is dispensable for murine development but essential in human cells. Despite similar genome sizes, human cells express ~100-fold more Ku than mouse cells, implying functions beyond NHEJ - possibly through a dose-sensitive interaction with dsRNA, which binds Ku 10~100 times weaker than dsDNA. Investigating Ku's essentiality in human cells, we found that Ku-depletion - unlike LIG4 - induces profound interferon (IFN) and NF-kB signaling via dsRNA-sensor MDA5/RIG-I and MAVS. Prolonged Ku-degradation further activates other dsRNA sensors, especially PKR (suppressing translation) and OAS/RNaseL (cleaving rRNA), leading to growth arrest and cell death. MAVS, RIG-I, or MDA5 knockouts suppressed IFN signaling and, like PKR knockouts, all partially rescued Ku-depleted human cells. Ku-irCLIP analyses revealed Ku binding to diverse dsRNA, predominantly stem-loops in primate-specific antisense Alu elements in introns and 3'-UTRs. Ku expression rose sharply in higher primates, correlating tightly with Alu-expansion (r = 0.94/0.95). Thus, Ku plays a vital role in accommodating Alu-expansion in primates by limiting dsRNA-induced innate immunity, explaining both Ku's elevated expression and its essentiality in human cells. - Source: PubMed
Publication date: 2025/05/15
Zhu YimengLi AngelinaMaji SuvrajitLee Brian JKorn Sophie MGertie Jake ADorrity Tyler JWang JianhuaWang Kyle JPelletier AmandineMoakley Daniel FKelly Rachel DHolmes Antony BRabadan RaulEdgell David RPoulter Caroline SchildModesti MauroSteckelberg Anna-LenaHendrickson Eric AChung HachungZhang ChaolinZha Shan - As an evolutionarily conserved and ubiquitous mechanism of host defense, non-immune cells in vertebrates possess the intrinsic ability to autonomously detect and combat intracellular pathogens. This process, termed cell-autonomous immunity, is distinct from classical innate immunity. In this review, we comprehensively examine the defense mechanisms employed by non-immune cells in response to intracellular pathogen invasion. We provide a detailed analysis of the cytosolic sensors that recognize aberrant nucleic acids, lipopolysaccharide (LPS), and other pathogen-associated molecular patterns (PAMPs). Specifically, we elucidate the molecular mechanisms underlying key signaling pathways, including the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway, the retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs)-mitochondrial antiviral signaling (MAVS) axis, and the guanylate-binding proteins (GBPs)-mediated pathway. Furthermore, we critically evaluate the involvement of these pathways in the pathogenesis of various diseases, including autoimmune disorders, inflammatory conditions, and malignancies, while highlighting their potential as therapeutic targets. - Source: PubMed
Publication date: 2025/04/24
Han DanlinZhang BozhengWang ZheMi Yang - Effective antiviral immunity requires a delicate balance between controlling infection and preventing excessive inflammation. NLRX1, an atypical member of the NOD-like receptor family, plays a crucial regulatory role in this process by modulating immune responses to both RNA and DNA viruses. Unlike other NLRs, NLRX1 does not directly activate inflammatory pathways, but rather fine tunes immune responses through interactions with key signaling initiators like MAVS, FAF1, viral RNA, and FBXO6. These interactions allow NLRX1 to influence antiviral pathways in a highly context-dependent manner. In RNA virus infections, NLRX1 can either enhance immune signaling to restrict viral replication or suppress type 1 IFN responses to promote viral persistence. Similarly, in DNA viral infections, NLRX1 exerts either protective or pathogenic effects, though the precise mechanisms remain unclear. Emerging evidence suggests that NLRX1 may also serve as a key regulator of inflammation and metabolic processes during infection, further contributing to its complex role in immunity. By synthesizing current research, this review provides insight into how NLRX1 regulates immune signaling in RNA and DNA viral infections, highlighting its dynamic role in antiviral immunity and the remaining gaps in our understanding. - Source: PubMed
Publication date: 2025/04/28
Woolls Mackenzie KElliott Carley MIvester Hannah MAllen Irving Coy