MDMA (ECSTASY) Card
- Known as:
- MDMA (ECSTASY) Card
- Catalog number:
- ODZ-229
- Product Quantity:
- Tests in kit 20
- Category:
- -
- Supplier:
- Vidia
- Gene target:
- MDMA (ECSTASY) Card
Related genes to: MDMA (ECSTASY) 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: MDMA (ECSTASY) Card
Related articles to: MDMA (ECSTASY) Card
- Atopic dermatitis (AD) and psoriasis (PsO) are chronic inflammatory skin diseases with distinct features, but clinical and molecular overlap exists. These ambiguous phenotypes complicate diagnosis and treatment, and their immunologic basis remains poorly defined. This study aimed to delineate compartment-specific immune profiles in AD-PsO overlap lesions and explore candidate markers associated with molecular stratification. - Source: PubMed
Publication date: 2026/09/25
Lee JongeunChun Yookyung SophieNam Hyo JeongHuh Yun JungKim JaehwanKrueger James GPaik Seung SamKim Hyun JeJin Seon-PilKim Jeong Eun - The DNA damage response (DDR) is increasingly recognized not only as a genome-maintenance network and source of synthetic-lethal vulnerabilities, but also as a regulator of tumor immunity. DDR defects and pharmacologic inhibition can increase neoantigen formation, generate micronuclei and cytosolic nucleic acids, activate cGAS-STING, DNA-PK-NF-κB, and ERV-driven RIG-I/MDA5-MAVS signaling, and alter antigen presentation and immune checkpoint expression. However, the same processes may also promote chronic interferon tolerance, PD-L1 induction, lymphocyte stress, myeloid suppression, extracellular cGAMP degradation, stromal exclusion, and treatment resistance. This review frames DDR targeting around damage-to-immunity conversion, asking when DNA damage becomes a productive antitumor immune signal and when it does not. We summarize targetable DDR modules across cancer types, examine tumor-intrinsic and host-cell sensing mechanisms, and discuss antigen-processing defects, STING regulation, and microenvironmental barriers that shape divergent outcomes. We further review PARP, ATR, WEE1, ATM, and DNA-PK inhibitor combinations with immunotherapy and other treatment modalities, emphasizing clinical evidence, scheduling, and host-cell toxicity. Finally, we propose a modular biomarker framework integrating genomic, functional, immune-context, spatial and dynamic readouts to guide patient selection, treatment adaptation, and precision therapeutic decision-making. - Source: PubMed
Publication date: 2026/09/23
Qiao YihuanKang BoyuZhang JianZhang RuiLi Jipeng - Ebola virus-like particle (EBOV VLP) vaccines composed of glycoprotein (GP), matrix protein VP40, and nucleoprotein (NP) typically require multiple adjuvanted doses to elicit protection. To enhance immunogenicity and mimic live virus infection, retinoic acid-inducible gene I (RIG-I) N-terminal CARD domains (2CARD), which can trigger type I interferon (IFN) production, were fused to the NP C-terminal domain (NP CT). VLPs incorporating 2CARD-NP CT , GP and VP40 triggered a MAVS-dependent IFN response upon infection of A549 cells. In mice, a single immunization elicited robust antibody responses persisting for at least 20 weeks and provided complete protection against lethal challenge with mouse-adapted EBOV, whereas standard VLPs failed to do so. Furthermore, the system successfully incorporated Mycobacterium tuberculosis antigens via fusion to NP CT or VP40. The findings demonstrate that incorporating 2CARD overcomes the low immunogenicity of standard VLPs. This modified EBOV VLP system serves as a potent, single-dose self-adjuvanting vaccine platform adaptable for various non-EBOV antigens. - Source: PubMed
Publication date: 2026/09/16
Thakur NaveenWang LinTsibane TshidiSilvas JesusBorisevich ViktoriyaO'Toole RachelMartinez JasmineGeisbert ThomasCross RobertBasler ChristopherTufariello JoAnn - RNA polymerase III (Pol III) activity is upregulated during herpesvirus infection, yet the functional consequences of this response remain poorly understood. To investigate the role of host Pol III transcription during murine gammaherpesvirus 68 (MHV68) infection, we depleted the Pol III transcription factor Brf1, an essential component of the TFIIIB complex required for transcription from Type I and Type II Pol III promoters. Brf1 depletion enhanced MHV68 replication during low multiplicity of infection (MOI) conditions, resulting in increased viral gene expression, viral protein accumulation, infectious virion production, and extracellular viral genome copies. These effects were confirmed to be Brf1-specific through rescue with an siRNA-resistant Brf1 construct. In contrast, Brf1 depletion produced only modest effects during high-MOI infection, suggesting that Brf1-dependent antiviral activity is most important during multistep viral spread. Transcriptomic analysis revealed accelerated induction of interferon-responsive genes early during infection in Brf1-deficient cells, followed by enhanced host transcript depletion at later stages, consistent with amplified host shutoff. Genetic disruption of the RIG-I/MAVS signaling pathway failed to abolish Brf1 antiviral activity, indicating that this phenotype is independent of MAVS-dependent interferon signaling. Finally, plaque assays demonstrated that Brf1-deficient cells supported larger plaques and increased plaque numbers, suggesting enhanced viral spread and/or entry. Together, our results reveal an unexpected role for Brf1-dependent Pol III activity in controlling gammaherpesvirus spread and suggest that virus-induced Pol III activation contributes to host antiviral defense. - Source: PubMed
Publication date: 2026/09/17
Rapchak KNyberg L SJohnson L AElbert R AHuff C JGrissom Z ADremel S ETucker J M - While mutations in tricarboxylic acid (TCA) cycle enzyme succinate dehydrogenase B (SDHB) are well-established drivers of renal cell carcinoma via the accumulation of the oncometabolite succinate, its precise role in renal fibrosis remains entirely unexplored. In this study, we demonstrate that SDHB is down-regulated in fibrotic kidneys. Tubule-specific knockdown of Sdhb exacerbated fibrosis, mitochondrial dysfunction, and inflammation in unilateral ureteral obstruction (UUO) mice, while its overexpression exerted protective effects. Mechanistically, SDHB deficiency induced succinate accumulation, which directly bound to residue Leu150 (L150) of voltage-dependent anion channel 1 (VDAC1), promoting VDAC1 oligomerization and triggering mitochondrial RNA (mtRNA) leakage. Cytosolic mtRNA activated the retinoic acid-inducible gene I (RIG-I)-mitochondrial antiviral signaling protein (MAVS) pathway, driving proinflammatory responses. Pharmacological inhibition of VDAC1 oligomerization by VBIT-4 attenuated mtRNA release. Furthermore, we identified E2F transcription factor 4 (E2F4) as an upstream transcriptional activator of SDHB, and overexpression of E2f4 restored SDHB expression and ameliorated renal pathology. These findings provide mechanistic insights into how TCA cycle disruptions and mtRNA leakage interactions drive renal inflammation, suggesting SDHB as a potential therapeutic target for renal fibrosis. - Source: PubMed
Publication date: 2026/09/18
Zhu ZijingChen PingShu HongxinZeng QinglinLuo QinghuaZhu WenpingYang LiYan TengFengZhu Xingen