FSH Test Card
- Known as:
- Follicle-stimulating hormone Test Card
- Catalog number:
- INV-132
- Product Quantity:
- 4.0mm (1000 strips in a card) 25cards/box
- Category:
- -
- Supplier:
- Innoragen
- Gene target:
- FSH Test Card
Related genes to: FSH 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: FSH Test Card
Related articles to: FSH Test Card
- Human trophoblast organoids (TOs) are three-dimensional ex vivo culture models that enable the study of placental development, physiology and pathology. A major limitation of TOs grown in Matrigel or other extracellular matrices is their apical-inward polarity, in which cytotrophoblasts (CTBs) line the outer surface and the multinucleated syncytiotrophoblast (STB) forms the interior layer, opposite to their orientation in vivo. Here we present a detailed protocol to reverse TO polarity, producing organoids that recapitulate the cellular orientation of human chorionic villi. Standard TOs with inward-facing STBs (STB) undergo polarity reversal during suspension culture to generate outward-facing STBs (STB). In parallel, we describe a complementary protocol for CRISPR-Cas9-mediated gene editing in TOs and illustrate its application in generating CGA (hCG) knockout organoids, which disrupt placental hormone secretion, and MAVS knockouts, which impair antiviral signaling. The outward-facing STB protocol can be completed in ~2 weeks, whereas the establishment of stable gene-edited TO lines requires 2-3 months. Successful implementation requires experience in TO culture, lentiviral transduction and CRISPR-Cas9-based genome editing. Together, these protocols provide versatile and reproducible methods for modeling placental architecture and studying gene function in vitro, enabling functional interrogation of trophoblast biology within physiologically oriented organoids. - Source: PubMed
Publication date: 2026/06/29
Yang LihengHatterschide JoshuaWorota Rizban ECooley KailaCoyne Carolyn B - How antiviral immunity first arose in animals is a central question in evolutionary biology. Here, using the sea anemone Nematostella vectensis, we identify CARDIB, a previously uncharacterized gene located next to RLRb-a cnidarian homologue of the vertebrate RIG-I-like receptor family. This conserved genomic linkage across Anthozoa reveals an ancient coupling between immune sensing and regulation. Despite sequence similarity to vertebrate MAVS, CARDIB performs an opposing function: it represses immune genes under basal conditions yet is essential for activation upon viral challenge. CARDIB binds RLRb through a single CARD domain, forming a repressive complex. Loss of either gene abolishes antiviral transcription, disrupts apoptosis and elevates viral load under laboratory conditions. Both genes, as well as the RLRb paralogue RLRa, are essential for antiviral defence under native conditions. Phylogeny places the cnidarian CARDs distinctly from the vertebrate RLR-MAVS families, revealing an ancient mechanism that regulates the antiviral response through CARD-based signalling. - Source: PubMed
Publication date: 2026/06/26
Sharoni TonJaimes-Becerra AdrianBirch SydneyKwak Hee-JinAleshkina DariaLewandowska MagdaSurm Joachim MJustin HannahAharoni ReuvenReitzel Adam MMoran Yehu - Mitochondria are dynamic organelles that continuously remodel their morphology through fusion and fission in response to cellular cues. While this dynamic behavior is essential for diverse cellular functions, how mitochondrial dynamics influence innate immune responses remains incompletely understood. Here, we show that mitochondrial hyperfusion-induced by loss of the fission factor DRP1 or by cellular stress, including cycloheximide or doxorubicin treatment-is associated with activation of a RIG-I-MAVS-dependent innate immune response and BAX-dependent cytosolic release of mitochondrial RNA. Functionally, our data suggest that this pathway contributes to enhanced susceptibility to NK cell-mediated cytotoxicity in vitro and reduced tumor growth in a xenograft model. Collectively, our findings identify mitochondrial hyperfusion-induced mtRNA release as a mechanism that engages innate immune signaling downstream of impaired mitochondrial dynamics. - Source: PubMed
Publication date: 2026/06/26
Yasuda TatsukiIchikawa AoiOnoue KentaOgasawara EmiIshihara TakayaKosako HidetakaIshihara Naotada - Mitochondria are central hubs of antiviral immunity and cellular metabolism, yet the links between SARS-CoV-2-induced mitochondrial remodeling, antiviral gene regulation, and post-translational control remain incompletely understood. Here, we investigated mitochondrial-immune remodeling in SARS-CoV-2-infected lung-derived LC-HK2 cells at 48 and 96 h post-infection using confocal and high-content imaging, colocalization analysis, CellProfiler quantification, RT-qPCR, proteomics, cytokine profiling, and conditioned-medium analysis. Infection induced a time-dependent mitochondrial phenotype. At 48 hpi, cells displayed early mitochondrial stress and fission-associated signatures, including increased DRP1, transient upregulation of mitochondrial respiratory genes, and reduced MFN1/2. At 96 hpi, mitochondria shifted toward elongated perinuclear networks, accompanied by increased fusion/biogenesis markers and partial ISG15-MFN2 colocalization, indicating a spatial association between ISG15-related antiviral/stress responses and mitochondrial remodeling. Antiviral and ISG-related transcripts were consistently upregulated, but IFN-α2 secretion remained limited, suggesting partial uncoupling between antiviral transcriptional activation and downstream interferon output. SUMO2/3 was dynamically modulated and showed time-dependent colocalization with mitochondrial dynamics proteins and MAVS. Together, these data support a coordinated mitochondrial-immune regulatory axis involving mitochondrial remodeling, ISG15-associated responses, and SUMO-dependent regulation during SARS-CoV-2 infection. - Source: PubMed
Publication date: 2026/06/16
Melo Thatiana Corrêa deValerio Hellen PaulaTrevisan-Silva DilzaSouza Marcelo Medina deMelo Amanda Teixeira deAlvarez-Flores Miryam PaolaOliveira Douglas SouzaGomes Renata NascimentoMachado-Santelli Glaucia MariaRibeiro Beatriz Fumelli MontiBotosso Viviane FongaroCalil Jorge Soraia AttieChudzinski-Tavassi Ana Marisa - Persistence of human papillomavirus (HPV) infection leading to cervical carcinogenesis can be attributed to the action of high-risk HPVs, but there are still some unclear factors involved in the mechanisms of either viral clearance or persistence. Although many infections may be self-limiting and cleared successfully by the immune response of the infected individuals, other infections result in persistent HPV infection. Recent studies indicate that microbiota in the gut and cervicovaginal tract modulate host immune status, mucosal inflammation, and epithelial barrier integrity. All these factors determine susceptibility to persistent infection. Inflammation, overproduction of reactive oxygen species (ROS), genomic instability, and impaired antiviral transcription pathways are associated with dysbiosis. In parallel, redox imbalance contributes to mitochondrial dysfunction, impairing mitochondrial antiviral signaling (MAVS)-dependent interferon responses and attenuating induction of interferon-stimulated genes. Additionally, extracellular vesicles (EVs) further promote immune evasion, metabolic programming, and epigenetic regulation by facilitating the intercellular exchange of viral constituents, microRNAs, and signaling molecules. Through this interconnected network of mechanisms, microbial dysbiosis, mitochondrial disruption, and EV signaling collectively shape a niche conducive to persistence. Unlike previous reviews that primarily examine microbiome alterations, oxidative stress (OS), mitochondrial dysfunction, extracellular vesicles, or immune responses as separate processes, this review integrates clinical and omics findings into a systems-based conceptual framework of HPV persistence. By emphasizing the potential interactions among these interconnected biological systems, we aim to identify points of biological convergence, generate mechanistic hypotheses, and highlight opportunities for future biomarker development and therapeutic intervention. - Source: PubMed
Publication date: 2026/06/01
Moustakli EfthaliaMakrydimas StylianosOikonomou Emmanouil DNakou AgniAlbani EleniZagorianakou Nektaria