MOR Morphine Test Card

Price:

624.62 €

Known as:: MOR Morphine Test Card
Catalog number:: MOR-1082
Product Quantity:: 4.0mm (1000 strips in a card) 25cards/box
Category:: -
Supplier:: Innoragen
Gene target:: MOR Morphine Test Card

Related genes to: MOR Morphine 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: MOR Morphine Test Card

Human ELC ELISA KIT 96 TEST (S)_4_[(5_oxo_2_pyrrolidinyl)carbonyl]mor (S)_4_[(5_oxo_2_pyrrolidi* Colonisation Medium w_Dulbecco’s Phosphate Buffer USE For the preparation of suspension of enterotoxigenic Escherichia coli used for HeLa cell test for colonization.*Lactobacilli Broth,AOAC USE For preparation of inocula of test bacteria used in microbiological assays of B vitamins.*Microbial Content Test Agar (Tryptone Soya Agar w_Tween 80 & Lecithin) USE For determining efficiency of sanitization of containers, equipment surfaces,water miscible cosmetics etc.*Niacin Assay Medium USE For microbiological assay of Niacin (Nicotinic acid) or Niacinamide using Lactobacillus plantarum ATCC 8014 as a test organism.*Pantothenate Assay Medium USE For microbiological assay of Pantothenic acid or its salts using Lactobacillus plantarum ATCC 8014 as the test organism.*Pantothenate Assay Medium, AOAC USE For microbiological assay of Pantothenic acid or its salts using Lactobacillus plantarum ATCC 8014 as the test organism.0.02M solution for APTT test1-hour Beef Cow meat adulteration ELISA test (for beef or pig meat; 24 tests)1-hour Beef Cow meat adulteration ELISA test (for beef or pig meat; 48 tests)1-hour Beef Cow meat adulteration ELISA test (for beef or pig meat; 96 tests)1-hour Dog meat adulteration ELISA test (for beef or pig meat; 24 tests)1-hour Dog meat adulteration ELISA test (for beef or pig meat; 48 tests)1-hour Horse meat adulteration ELISA test (for beef or pig meat; 24 tests)

Related articles to: MOR Morphine Test Card

Lactylation in influenza a virus infection: Current evidence, knowledge gaps, and future perspectives.
Influenza A virus (IAV) is a major respiratory pathogen causing seasonal epidemics and pandemics, posing serious threats to public health and livestock. The high mutation rate of IAV leads to vaccine mismatches and drug-resistant variants, underscoring the need for novel antiviral strategies. This review examines the role of lactylation in IAV-host interactions, focusing on three core questions: how IAV induces lactylation, how lactylation reshapes antiviral immunity, and how IAV exploits lactylation for immune evasion. Key findings include lactylation of viral vRNP components required for efficient replication and the host deacetylase SIRT1, which suppresses IAV replication by removing these lactyl groups. IAV counteracts this defense by downregulating SIRT1 expression. Lactylation also regulates cGAS-STING, RLR-MAVS, and IFN signaling pathways. The therapeutic potential of targeting lactate metabolism and SIRT1 is discussed. Understanding lactylation in IAV infection may open new avenues for antiviral drug development. - Source: PubMed
Publication date: 2026/08/02
Yan Yu-Mei ChenLi ZhijunHe HaiyanWu ModingYang HaolinWei Fanhua
African swine fever virus pMGF360-3 L suppresses innate immunity by facilitating CMA-dependent SKP1 degradation to promote BNIP3-mediated mitophagy.
African swine fever (ASF) is an acute, hemorrhagic, and highly contagious disease caused by African swine fever virus (ASFV), which causes severe economic losses in the swine industry. ASFV has evolved multiple strategies to evade host antiviral immune responses. Here, we report that ASFV pMGF360-3 L promotes host mitophagy by manipulating chaperone-mediated autophagy (CMA), thereby inhibiting the production of type I interferon (IFNB/IFN-β). Mechanistically, pMGF360-3 L targets the SKP1 protein its N-terminal ankyrin (ANK) repeat domain, promoting the degradation of SKP1 through the CMA pathway, which inhibits the proteasomal degradation of BNIP3 to increase its expression level in mitochondria. Subsequently, BNIP3 binds to MAP1LC3B/LC3B to induce mitophagy, a process that leads to the degradation of mitochondria. Notably, the CMA-mediated degradation of SKP1 depends on its K94 site, and the SKP1-BNIP3 axis is critical for pMGF360-3 L-mediated IFNB inhibition. In summary, our study reveals a mechanism through which ASFV pMGF360-3 L facilities CMA-dependent degradation of the E3 complex component SKP1. This stabilizes mitochondrial BNIP3 to initiate mitophagy and block IFNB production. This deepens our understanding of the immune evasion strategies of ASFV and provides potential drug targets for controlling viral infection.: 3-MA: 3-methyladenine; ASFV: African swine fever virus; BafA1: bafilomycin A; BNIP3: BCL2 interacting protein 3; CMA: chaperone-mediated autophagy; co-IP: co-immunoprecipitation; CQ: chloroquine; CHX: cycloheximide; CUL1: cullin 1; DAPI: 4', 6-diamidino-2'-phenylindole; EV: emptor vector; FBXL4: F-box and leucine rich repeat protein 4; hpi: hours post-infection; IFNB: interferon beta; ISGs: IFN-stimulated genes; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MG132: cbz-leu-leu-leucinal; MAVS: mitochondrial antiviral signaling protein; MOI: multiplicity of infection; PAMs: porcine alveolar macrophages; PPTC7: protein phosphatase targeting COQ7; RBX1: ring-box 1; RT-PCR: real-time polymerase chain reaction; siRNA: small interfering RNA; SKP1: S-phase kinase associated protein 1; TCID: 50% tissue culture infectious doses; Ub: ubiquitin; WCL: whole-cell lysate; WT: wild-type. - Source: PubMed
Publication date: 2026/08/02
Lin SizhanLiang JingtaoYe JiafangChen MinpingZhang MingyuHuang ZhaoGao QiLiu YingnanChen HongjunZhang GuihongGong Lang
Molecular mechanism by which SARS-CoV-2 Orf9b suppresses the Tom70-Hsp90 interaction to evade innate immunity.
The Tom70-Hsp90 interaction is critical for MAVS-mediated interferon (IFN) production. Upon RNA virus infection, cytosolic Hsp90 recruits key innate immune signaling proteins to MAVS on mitochondria through its interaction with Tom70. To evade this innate immune response, SARS-CoV-2 Orf9b binds to Tom70, thereby disrupting the Tom70-Hsp90 interaction and suppressing IFN production. Despite its importance, the molecular mechanism underlying the Orf9b-mediated IFN antagonism has remained unclear. Here, using an integrative approach including cryo-electron microscopy and F NMR spectroscopy, we show that Orf9b inhibits the Tom70-Hsp90 interaction through a bipartite mechanism. Through comprehensive structural, thermodynamic, and kinetic analyses, we reveal a previously unrecognized interplay between the rigid and dynamically disordered regions of Orf9b that blocks Hsp90 access to Tom70. Collectively, our results provide a high-resolution mechanistic framework for understanding Orf9b-mediated suppression of the host innate immune response. - Source: PubMed
Publication date: 2026/07/31
Sherer NoahBastiray AbhishekChen Xiao-RuMolugu Trivikram RYadav Gaya PIgumenova Tatyana ICho Jae-Hyun
Topical Glycolysis Inhibition Restores MAVS-Associated Antiviral Signaling in Herpes Simplex Keratitis.
Herpes simplex keratitis (HSK) is a leading cause of infectious corneal blindness. Host antiviral responses, particularly type I interferon (IFN) signaling, are impaired during corneal herpes simplex virus type 1 (HSV-1) infection, partly due to viral immune evasion and metabolic reprogramming. This study investigated if topical glycolysis inhibition restores mitochondrial antiviral signaling (MAVS)-associated innate antiviral signaling and improves HSK outcomes. - Source: PubMed
Xu WeiLiu HuiruCheng ZihanLi QixinWu XiaoqingHe ZeshengXiao DechengJiang DanChen Wei
Hypoxia Differentially Regulates Ferroptosis Sensitivity and Tumor Cell-Intrinsic Type I Interferon Signaling in Pancreatic Ductal Adenocarcinoma Cells.
Ferroptosis has emerged as a promising strategy to overcome resistance to conventional cancer therapies. Pancreatic ductal adenocarcinoma (PDAC) is characterized by hypoxia, therapy resistance, and an immunosuppressive microenvironment. Although hypoxia is likely to influence ferroptosis susceptibility and the associated inflammatory pathways that regulate antitumor immunity, their impact on ferroptosis sensitivity and innate immune responses remains poorly understood. In this study, we investigated the effects of hypoxia on the induction of ferroptosis and immune-related signaling in PDAC cell lines. We examined how hypoxia affects the responses of Panc-1, BxPC3, and Capan-1 cells to the ferroptosis inducers RAS-selective lethal 3 (RSL3)/Imidazole ketone erastin (IKE) under normoxic and hypoxic (0.1% O) conditions. Cell viability assays were used to assess ferroptosis sensitivity, and rescue experiments were performed using liproxstatin-1 (LIP). Gene expression analysis was conducted to evaluate changes in immune, interferon, inflammatory, and hypoxia-related genes following ferroptosis induction. Panc-1 cells were the most sensitive, whereas Capan-1 cells were resistant, particularly under hypoxia. Ferroptosis triggered cell line-specific responses involving interferon signaling, inflammation, and stress pathways. Panc-1 cells showed over-expression of and , particularly under hypoxia, indicating activation of Type I interferon (IFN)-associated transcriptional program. BxPC3 cells demonstrated broader cytokine induction, including , , , , and , whereas Capan-1 cells were minimally responsive. Hypoxia also increased and expression following ferroptosis induction. These findings show that hypoxia differentially affects ferroptosis sensitivity and immune responses in PDAC, revealing complex interactions among ferroptosis, innate immunity, and the tumor microenvironment. - Source: PubMed
Publication date: 2026/07/18
Das ShubhankarMahmood Ayda ShahChouaib Salem

MOR Morphine Test Card

Related genes to: MOR Morphine Test Card

Related products to: MOR Morphine Test Card

Related articles to: MOR Morphine Test Card

Lactylation in influenza a virus infection: Current evidence, knowledge gaps, and future perspectives.

African swine fever virus pMGF360-3 L suppresses innate immunity by facilitating CMA-dependent SKP1 degradation to promote BNIP3-mediated mitophagy.

Molecular mechanism by which SARS-CoV-2 Orf9b suppresses the Tom70-Hsp90 interaction to evade innate immunity.

Topical Glycolysis Inhibition Restores MAVS-Associated Antiviral Signaling in Herpes Simplex Keratitis.

Hypoxia Differentially Regulates Ferroptosis Sensitivity and Tumor Cell-Intrinsic Type I Interferon Signaling in Pancreatic Ductal Adenocarcinoma Cells.