Legionella Card
- Known as:
- Legionella Card
- Catalog number:
- ODZ-189
- Product Quantity:
- Tests in kit 20
- Category:
- -
- Supplier:
- Vidia
- Gene target:
- Legionella Card
Related genes to: Legionella 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: Legionella Card
Related articles to: Legionella Card
- 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 - Infectious bovine rhinotracheitis (IBR) is a globally recognized infectious disease. The causative agent infects the respiratory and reproductive tracts of cattle, resulting in substantial economic losses to the cattle industry. Endoplasmic reticulum stress (ERS) and mitophagy play critical roles in maintaining cellular homeostasis during viral infections. However, whether Infectious bovine rhinotracheitis virus (IBRV) infection activates ERS and regulates the initiation of mitophagy remains unclear. In this study, IBRV infection robustly activates the ERS unfolded protein response (UPR) pathway and concurrently induces mitophagy and the innate immune pathway mediated by RIG-I-MAVS. Pharmacological inhibition of ERS, 4-PBA significantly abrogated IBRV-induced mitophagy. Further investigations revealed that inhibition of PERK with GSK2606414 and IRE1 with STF-083010 reverse IBRV-induced mitophagy, whereas the ATF6 inhibitor AEBSF had no such effect. Collectively, these findings suggested that IBRV-induced ER stress promotes mitophagy, at least in part, through the PERK and IRE1 pathways. Additionally, the mitophagy induced by IBRV may be related to the weakened transmission of type I interferon pathway mediated by RIG-I-MAVS, thereby establishing a permissive intracellular microenvironment for viral replication. These results implied the mechanism by which IBRV facilitates self-replication by impairing innate immunity through the induction of endoplasmic reticulum stress-mediated activation of mitophagy, likely offering novel insights for the prevention and control of IBRV infection. - Source: PubMed
Publication date: 2026/09/29
Li ShifanZhao YinaMo RongqianLiu YiLv XiweiWang TuoZhang QiWang WeixuanZhao QianzhiZhou HongchaoXu Xingang - Birds routinely solve high-speed, three-dimensional collision-avoidance problems that remain a central challenge for autonomous micro-aerial vehicles (MAVs). While pairwise avoidance is well studied in budgerigars, comparatively little is known about how avoidance kinematics change when more than two birds must simultaneously resolve a potential collision-the regime in which distributed control becomes attractive for MAV swarms. Using an openly available stereo-camera dataset (n = 150 1v1, n = 80 2v2, n = 30 3v3 trials), we extracted nine kinematic indices per encounter and tested for group-size effects using dual statistical frameworks supplemented by stratified, subsampling-robustness and noise-floor sensitivity analyses. The two most robust findings are (i) that the optic-flow time-to-contact margin τ is qualitatively conserved across group sizes (the time-course is preserved while the absolute margins compress with group size), and (ii) that the minimum inter-bird separation does not shrink with group size and in fact grows mildly. By contrast, evidence that birds in the 3v3 condition react later, modulate forward speed less, or fly more curved paths is conditionally supported at best: the reaction-distance effect replicates in only 19.5% of subsampled iterations, and the path-complexity effects are significant only after trial-level aggregation. The agility metrics (peak lateral acceleration and minimum turn radius) are heavily confounded with tracking noise; a majority of 3v3 encounters fall below the empirical noise floor and these values should not be used as an engineering target. These observations are consistent with-but do not strongly mandate-a bioinspired design hypothesis in which a fixed τ-based visual policy is paired with a group-size- adaptive reaction threshold. A proof-of-concept multi-agent simulation of this controller resolves pairwise head-on encounters reliably (100% collision-free) but degrades sharply with group size and density, indicating that a purely reactive single-threat policy is insufficient for swarm-scale operation and that an explicit multi-threat coordination mechanism is required. - Source: PubMed
Publication date: 2026/09/30
Tawhid S MMohim Abdul KaderAli Sk ShahedHaque Tanzil Kazi TanzizulBhowmik AbhijitKarmaker Debajyoti