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The aim of this study is to identify the lncRNA that directly interacts with NLRP3 molecules in RAW264.7 cells infected with S. typhimurium and its role in S. typhimurium-mediated pyroptosis. We have identified LncRNA-Gm17586, which directly interacts with NLRP3 in RAW264.7 cells infected with S. typhimurium. LncRNA-Gm17586 inhibits S. typhimurium-mediated pyroptosis in RAW264.7 cells. Overexpression of LncRNA-Gm17586 not only directly suppresses NLRP3 inflammasome activation but also enhances the binding affinity between Tnip1 and NLRP3, thereby indirectly facilitating Tnip1-mediated inhibition of the NLRP3 inflammasome. Consequently, this dual mechanism effectively inhibits S. typhimurium-induced pyroptosis. Our results demonstrate that LncRNA-Gm17586 directly interacts with NLRP3 during S. typhimurium-mediated pyroptosis and inhibits this process by enhancing the interaction between Tnip1 and NLRP3.
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http://dx.doi.org/10.1038/s41598-025-91296-2 | DOI Listing |
EMBO J
September 2025
New York University Grossman School of Medicine, Microbiology Department, New York, NY, USA.
Serine protease inhibitors (SERPINs) are involved in various physiological processes and diseases, such as inflammation, cancer metastasis, and neurodegeneration. Their role in viral infections is poorly understood, as their expression patterns during infection and the range of proteases they target have yet to be fully characterized. Here, we show widespread expression of human SERPINs in response to respiratory virus infections, both in bronchioalveolar lavages from COVID-19 patients and in polarized human airway epithelial cultures.
View Article and Find Full Text PDFEMBO Mol Med
September 2025
Institute for Regenerative Medicine, Medical Innovation Center and State Key Laboratory of Cardiovascular Diseases, Shanghai East Hospital, National Stem Cell Translational Resource Center & Ministry of Education Stem Cell Resource Center, Frontier Science Center for Stem Cell Research, School of Li
Primary microcephaly, a rare congenital condition characterized by reduced brain size, occurs due to impaired neurogenesis during brain development. Through whole-exome sequencing, we identified compound heterozygous loss-of-function mutations in CENTRIN 3 (CETN3) in a 5-year-old patient with primary microcephaly. As CETN3 has not been previously linked to microcephaly, we investigated its potential function in neurodevelopment in human pluripotent stem cell-derived cerebral organoids.
View Article and Find Full Text PDFMed Eng Phys
October 2025
Department of Engineering Science, University of Oxford, United Kingdom. Electronic address:
Traditionally, clinical devices are designed, tested and improved through lengthy and expensive laboratory experiments and clinical trials [1]. More recently, computational methods have allowed for rapid testing, speeding up the design process and enabling far more complete searches of design space. While computational models cannot fully capture the complexities of biological systems, they provide valuable insights into crucial underlying mechanisms, such as the effects of fluid-structure interactions (FSIs).
View Article and Find Full Text PDFBiochem Pharmacol
September 2025
Department of Biosciences, JIS University, 81, Nilgunj Road, Agarpara, Kolkata, West Bengal 700109, India. Electronic address:
The malignant manifestation of breast cancer is driven by complex molecular alterations that extend beyond genetic mutations to include epigenetic dysregulation. Among these, DNA methylation is a critical and reversible epigenetic modification that significantly influences breast cancer initiation, progression, and therapeutic resistance. This process, mediated by DNA methyltransferases (DNMTs), involves the addition of methyl groups to cytosine residues within CpG dinucleotides, resulting in transcriptional repression of genes.
View Article and Find Full Text PDFCurr Biol
September 2025
Department of Molecular and Cellular Biology, University of California, 1 Shields Avenue, Davis, CA 95616, USA. Electronic address:
Nuclear migration plays a fundamental role in development, requiring precise spatiotemporal control of bidirectional movement through dynein and kinesin motors. Here, we uncover a differential isoform-dependent mechanism for developmental regulation of nuclear migration directionality. The nuclear envelope Klarsicht/ANC-1/Syne homology (KASH) protein UNC-83 in Caenorhabditis elegans exists in multiple isoforms that differentially control motor activity to achieve tissue-specific nuclear positioning.
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