Card box (Standard) Print Media
- Known as:
- Card box (Standard) Print Media
- Catalog number:
- Box-14-10-7
- Category:
- -
- Supplier:
- Biontex
- Gene target:
- Card box (Standard) Print Media
Ask about this productRelated genes to: Card box (Standard) Print Media
- 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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- Beyond essential roles as central hubs integrating homeostatic cellular metabolism, mitochondria have emerged as critical determinants of infection outcomes. Mitochondrial activities, like MAVS signaling and the release of cytochrome c and mitochondrial DNA, drive host defenses. Across cell types, mitochondrial metabolism and antiviral responses are also increasingly being connected by evidence such as viral-encoded antagonists. Nonetheless, metabolic rewiring in infected cells is still largely viewed as a means to satisfy biosynthetic demands for both viral replication and the host response. However, perturbation of metabolic states within infected and bystander cells seemingly has consequences for outcomes, implying an incompletely understood metabo-immunoregulatory logic. Here, we consider roles for mitochondrial metabolism reprogramming as an active cue that licenses progressive immune states to adapt host responses. In the coming years, integration of mitochondrial biology and new methodologies, including spatial approaches, will illuminate the interplay of mitochondrial metabolism on primary antiviral responses. - Source: PubMed
Publication date: 2026/05/05
Alvarez JessicaHancks Dustin C - As key regulators of inflammation and cell death, gasdermins (GSDMs) play a pivotal role in the pathogenesis of asthma. Through regulation via single nucleotide polymorphisms (SNPs), mediation of pyroptosis, and modulation of signaling pathways such as the MAVS-TBK1 pathway, GSDMs promote mucus hypersecretion, airway epithelial barrier dysfunction, and persistent inflammation, thereby exacerbating airway inflammation, airway remodeling, and pulmonary fibrosis. With the continuous expansion and deepening of research, GSDM-targeted inhibitors show great promise for precision therapy. Meanwhile, GSDM expression levels and specific SNPs may serve as potential biomarkers for the diagnosis and prognosis of asthma, providing novel strategies for asthma management. - Source: PubMed
Publication date: 2026/04/16
Wang ChaopingZhang XuelinCheng FangHuang HaiyingLi Xiao - The mitochondrial anti-viral signaling protein, MAVS, is a central regulator of innate anti-viral immunity. Recently, we demonstrated that MAVS is overexpressed in cancer, where its downregulation resulted in reduced cell proliferation and the expression and nuclear translocation of proteins associated with transcriptional regulation and inflammation. In this study, we demonstrate that CRISPR/Cas9-mediated MAVS depletion in PC-3 prostate cancer cells suppresses proliferation, disrupts immune evasion, and alters the tumor microenvironment. Proteomic profiling of the MAVS-KO cells by LC-MS/MS revealed changes in the expression of proteins associated with immunity, cell signaling, mitochondrial function, metabolism, protein synthesis and degradation, and epigenetic regulation. In contrast to MAVS-expressing cells, MAVS-KO cells implanted subcutaneously in mice formed very small tumors. This inhibited tumor growth was linked to reduced proliferation, and enhanced apoptosis, as indicated by strong TUNEL staining and elevated activated caspase-3. Importantly, the small "tumors" derived from MAVS-KO cells displayed a distinct morphology: diminished cancer stem-cell populations, an altered tumor microenvironment and inflammatory response, increased immune cell infiltration, and reduced PD-L1 expression. Together, these findings establish MAVS as a key mediator of cancer-cell survival, inflammation, and immune regulation, and, thus, its upregulation in tumors makes it a potential anti-cancer target. - Source: PubMed
Publication date: 2026/03/26
Trishna SwetaShteinfer-Kuzmine AnnaChalifa-Caspi VeredShoshan-Barmatz Varda - 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