SD Card accessory
- Known as:
- SD Card accessory
- Catalog number:
- 80-3005-00
- Category:
- -
- Supplier:
- Picodrop
- Gene target:
- Card accessory
Related genes to: SD Card accessory
- 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: SD Card accessory
Related articles to: SD Card accessory
- Adenosine deaminase acting on RNA 1 (ADAR1) deaminates adenosine to inosine in dsRNA. ADAR1 RNA editing marks cellular dsRNA as self, preventing aberrant activation of the antiviral dsRNA sensor MDA5. Adar Ifih1 (MDA5) or Adar Mavs double mutant pups escape Adar mutant aberrant interferon induction but die early. Here, we show that long-lived Adar Mavs Eif2ak2 (PKR) mice display a new residual defect: failure to maintain blood CD8+ T cells due to loss of an editing-independent function of ADAR1. Further dsRNA sensor-stripping in Adar Mavs Eif2ak2 Zbp1 mutants shows that loss of blood CD8+ T cells is not prevented. Challenging Adar+/- heterozygous or Adar Mavs Eif2ak2 mice with blood stage Plasmodium yoelii infection led to reduced parasitemia in Adar+/- mice by increased basal interferon. Unexpected reduced parasitemia in Adar Mavs Eif2ak2 mice is also likely due to interferon-related defects specific to hemopoietic cells, leading to altered populations of γδ T cells and other immune cells. The defects observed in this partially dsRNA sensor-stripped mouse suggest that different antiviral dsRNA sensors normally complement each other. - Source: PubMed
Publication date: 2026/05/08
Linhartova PavlaQuin JaclynLoja TomasMelicherova JankaDu QiupeiCherian AnnaVukic DraganaModry DavidTomandlova MarieCervena BarboraStribrnah HelenaOstlund Farrants Ann-KristinKnight AndreaKeegan Liam PeterO'Connell Mary A - Pestivirus bovine viral diarrhea virus (BVDV) is a major causative agent of bovine viral diarrhea-mucosal disease, responsible for substantial economic losses in the global cattle industry. BVDV employs sophisticated strategies to evade host antiviral innate immune responses; however, the precise mechanisms remain incompletely understood. In this study, we demonstrate that BVDV infection induces HIF-1α-mediated glycolytic reprogramming, which, in turn, antagonizes the RIG-I/MAVS pathway and suppresses type I interferon (IFN-I) production, thereby facilitating viral replication. We show that BVDV infection activates endoplasmic reticulum stress, leading to a marked increase in reactive oxygen species (ROS) that promote both the expression and stabilization of HIF-1α. As a key regulator of glycolysis, nuclear translocation of HIF-1α upregulates glycolysis-related proteins, including GLUT1, PFKP, HK2, and LDHA, thereby enhancing glycolytic flux. Furthermore, BVDV-induced glycolysis stimulates the formation of an HK2/MAVS/VDAC1 complex, which disrupts RIG-I-MAVS interaction and impairs pathway activation, inhibiting IFN-I production. Additionally, we found that lactate, a glycolytic byproduct, competitively binds to MAVS, impedes its mitochondrial localization, and consequently disrupts the engagement between RIG-I and MAVS. Collectively, our findings reveal a novel mechanism by which BVDV exploits the ROS-HIF-1α-glycolysis axis to attenuate MAVS-mediated antiviral signaling and promote viral replication. - Source: PubMed
Publication date: 2026/05/07
Li YuanZhou JiangfeiWang JingYan KaiGuan YuemingWang MengmengXiang JiayiLiu YimeiYu HanJia ShuoYang WentaoXu Yigang - 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