COC Cocaine Test Card
- Known as:
- COC Cocaine Test Card
- Catalog number:
- COC-1052
- Product Quantity:
- 4.0mm (1000 strips in a card) 25cards/box
- Category:
- -
- Supplier:
- Innoragen
- Gene target:
- COC Cocaine Test Card
Related genes to: COC Cocaine Test 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: COC Cocaine Test Card
Related articles to: COC Cocaine Test Card
- Parainfluenza virus 5 (PIV5) can establish persistent infections in host cells despite encountering innate immune defenses, including the complement (C') system. The host determinants that enable persistently infected cells (PI) to evade C'-mediated clearance remain largely undefined. Here, we identify the mitochondrial antiviral signaling (MAVS) protein, a central adaptor in double-stranded RNA-triggered antiviral and pro-survival signaling pathways, as a critical mediator of both PIV5 persistence and acquired resistance to C' lysis. Wild-type (WT) PIV5-infected A549 cells were initially sensitive to C'-directed killing, but these cells rapidly establish a PI in culture with ~25% of the cell population becoming resistant to C' lysis by day 2 and ~75% by day 4. In contrast, PIV5-infected A549 MAVS-deficient (MAVS KO) cells exhibited elevated viral gene expression, increased deposition of C3 and the membrane attack complex, and were more susceptible than WT cells to C' killing. PIV5-infected MAVS KO cells showed rapid cytopathic effects and never established a stable PI. While pharmacological suppression of viral gene expression with ribavirin (RBV) restored the survival of PIV5-infected MAVS KO cells into a long-term PI-like state, these RBV-induced PI cells remained sensitive to C' lysis. Collectively, these findings demonstrate a role of MAVS in modulating a PIV5 infection in culture, to facilitate both the conversion of a PIV5 acute infection to a PI and development of resistance to C' killing. - Source: PubMed
Publication date: 2026/03/27
Aquino Jenna RParks Griffith D - Micro air vehicles (MAVs) operating at low Reynolds numbers face aerodynamic and structural challenges that differ significantly from those encountered by conventional aircrafts. Nature provides effective solutions to these constraints, as insects, birds, and bats demonstrate highly efficient flight through integrated interactions between morphology, kinematics, and unsteady aerodynamic mechanisms. This review examines how biological flight principles can inform the design of next-generation MAVs. The study first analyzes biological flight strategies across insects, birds, and bats, with emphasis on scaling laws and physiological adaptations relevant to small-scale flight. It then reviews key unsteady aerodynamic phenomena governing low-Reynolds-number flight, including leading-edge vortex stability, wing-wake interactions, tandem-wing effects, and ground influence, as well as current modeling approaches ranging from quasi-steady methods to high-fidelity Navier-Stokes simulations. Building on these principles, the paper discusses biomimetic design strategies for MAV wings, structural-aerodynamic coupling, and actuation technologies used to replicate flapping flight. Existing MAV demonstrators inspired by biological flyers are analyzed, including concepts relevant to planetary exploration environments. Finally, the review identifies current technological limitations and research gaps in materials, actuation, aerodynamic modeling, and system integration. By synthesizing insights from biology and engineering, this work highlights key directions for the development of efficient, adaptable biomimetic MAV platforms capable of operating in complex environments. - Source: PubMed
Publication date: 2026/04/04
Prisăcariu Emilia GeorgianaDumitrescu Oana - Cancer gene-associated mutations and molecular hallmarks of chromosomal instability (CIN) are unexpectedly common in histologically normal cells and tissues. These emerging findings challenge the binary distinction between "normal" and "cancerous" cells and suggest that early tumorigenesis may commence against a background of widespread yet largely tolerated genomic instability. However, it remains largely unexplored how a cancer gene-associated mutation can initiate the development of CIN-like states in non-malignant cells and drive tumor evolution. , a chromatin remodeling factor, was identified as the most frequently mutated gene in both gastric normal epithelium and tumors. This distinctive molecular convergence presents an opportunity to elucidate the mechanisms by which a cancer-associated gene facilitates the initiation of early CIN phenotypes and develop effective antitumor strategies. In the present study, using primary human gastric organoids, we employed optical genome mapping (OGM) and live-imaging technologies to demonstrate that depletion induced a wide spectrum of structural variants (SVs), copy number variants (CNVs), and chromosomal segregation errors, characteristic features of CIN at a very early stage of gastric tumorigenesis. Mechanistically, ARID1A bound centromere repetitive satellite DNA (satDNA) sequences. Its SWI/SNF-associated chromatin remodeling activity was required for suppressing satDNA transcription and the production of α-SatRNA, through restricting RNAPII elongation. Consequently, depletion led to overexpression of α-SatRNA, and a higher incidence of sister chromatid exchange (SCE), a sensitive indicator of CIN. Importantly, the elevated α-SatRNA expression in -deficient cells further established a dual therapeutic vulnerability for G2/M checkpoint blockade, such as PKMYT1 inhibitor (PKMYTi), by concurrently aggregating CIN-induced cell death and activating self-dsRNA sensing-mediated innate immune response. Notably, PKMYTi markedly promoted α-SatRNA expression, aberrant release of these self-derived dsRNAs into the cytosol and a robust activation of the RIG/MDA5-MAVS-depenent type-I interferon response in -depleted cells. As expected, PKMYTi potentiated the efficacy of immunotherapy in -deficient gastric tumors. Together, our findings reveal that deficiency unleashes centromeric α-SatRNA transcription, which sets the molecular stage for tumor evolution and targeted therapy by coordinately inducing CIN and self-dsRNA-induced innate immune responses. - Source: PubMed
Publication date: 2026/04/13
Li ChengguoCheng XueqianLiu WeizhenZou GengyiNguyen Thi Hong MinhZhao EmilyIra NoemiZeng LiyongFan YiboDhar ShilpaWang GuocanSong ShumeiZhao MingZhang RugangLo Yuan-HungYap Timothy AAjani JafferPeng Guang - Viral myocarditis (VM) is a cardiac inflammatory condition caused by viral infection and serves as a critical precursor to life-threatening complications, such as dilated cardiomyopathy and heart failure. Coxsackievirus B3 (CVB3), a predominant etiological agent of VM, lacks targeted therapeutic interventions despite ongoing antiviral development. Mitophagy is a selective mitochondrial quality control mechanism mediated by PINK1. It has two key roles: maintaining mitochondrial homeostasis and regulating innate antiviral immunity. Here, we employed single-cell RNA sequencing to reveal a significant correlation between impaired mitophagy and cardiomyocyte pathology in CVB3-induced myocarditis. We demonstrated that CVB3 infection suppresses PINK1-dependent mitophagy, while the attenuation of PINK1 reciprocally enhances CVB3 replication. Mechanistically, CVB3 non-structural protein 3C promotes the degradation of mitochondrial antiviral signaling protein (MAVS). MAVS interacts with PINK1 to form a regulatory loop: PINK1 deficiency boosts MAVS reduction, which further promotes viral replication and worsens myocardial injury. Furthermore, we identify the transcription factor FOSL1 as a novel negative regulator of PINK1 transcription through direct promoter binding. Collectively, these findings show that the 3C/FOSL1/PINK1/MAVS signaling axis is a key mechanism in CVB3 pathogenesis. We propose innovative therapeutic targets for viral myocarditis through restoration of mitochondrial homeostasis and modulation of host-virus interactions. - Source: PubMed
Publication date: 2026/04/26
Liu TingjunWan AoXu YinhaiLu HongxiangXie YiweiWu HanWang JiangWang HuaHao TingtingZhang YonggenXu JinfengShen HongxingLi Shibao - Metabolic reprogramming targeting the mevalonate pathway represents an emerging innate immune activation target. However, its regulatory mechanisms remain incompletely elucidated. Here, we target the mevalonate pathway and construct a nano-granulated zoledronate (Nano-ZD) modulator. Following subcutaneous injection, Nano-ZD preferentially accumulates in draining lymph nodes rather than in bone tissues, enabling targeted delivery to innate immune cells. Nano-ZD functions as an immune-metabolic adjuvant, sensitizing and amplifying immune responses. By integrating Nano-ZD with the TLR4 agonist monophosphoryl lipid A (MPLA), MPLA-loaded Nano-ZD (Nano-ZDM) elicits robust humoral and antitumor cellular immunity. Mechanistically, Nano-ZD not only inhibits the isoprenylation of RhoA GTPases but also reduces coenzyme Q (CoQ) biosynthesis. CoQ deficiency disrupts oxidative phosphorylation (OXPHOS) and pyrimidine metabolism, causes mitochondrial ROS accumulation, induces mitochondrial antiviral protein (MAVS) oligomerization, and activates the pyrin inflammasome. This mevalonate-CoQ-OXPHOS/pyrimidine metabolism axis serves as a promising target for screening additional immune-metabolic adjuvants, and nanofabrication offers a paradigm for the lymph-targeted in vivo delivery of such adjuvants. - Source: PubMed
Publication date: 2026/04/22
Chen MeifangJiao XiaojiaYan ZhichengWang YuehengZhang JingWu QinghuaLi MinghuiFan ShuminWang YuanDai WenbingZhang HuaWang XueqingZhang QiangHe Bing