🎧 Exciting new discovery from Lingyin Li and postdoctoral researcher Chris Ritchie on PELI2: a protein that functions like noise-canceling headphones for the cGAS-STING pathway. cGAS-STING is a crucial immune defense mechanism for the human body that’s triggered in response to threats like viral and bacterial infections and cancer. But how does it know when to fight and when to stand down? Lingyin and Chris found that PELI2 acts like a sensor, filtering out cellular “white noise” that could chronically trigger STING—and lead to inflammatory conditions like lupus and neurodegeneration. At the same time, PELI2 turns into an amplifier when interferon levels grow above a certain threshold, ensuring that STING turns on at the right time. As Lingyin explains, “This research was highly interdisciplinary, combining “hardcore” biochemistry with immunology, genetics, and computation, but likely would not have received funding under traditional models. It’s the kind of curiosity-driven, interdisciplinary work that we’re uniquely positioned to do at Arc.” Read the full study in MolecularCell: https://lnkd.in/gmj6VDHK
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🧬🔍 Discovering Cretan HLA Genetics: This is our new ASHI Insights article! New research in Human Immunology reveals fascinating connections between Crete's Minoan culture and North Africa & Europe. Dive into the findings! https://lnkd.in/gigENK3m #ASHIInsights
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📃Scientific paper: miR-590-3 and SP1 Promote Neuronal Apoptosis in Patients with Alzheimer's Disease via AMPK Signaling Pathway Abstract: Alzheimer's disease (AD) is a progressive neurological degenerative illness with a hidden onset. Its pathogenesis is complicated, although with molecular biology research on cancer and targeted research on pathogenic mechanisms, good progress has not yet been made. Therefore, this work built a multifactor-driven neuronal apoptosis dysfunction module for the purpose of probing its underlying pathogenic mechanisms. We performed differential expression analysis, coexpression analysis, enrichment analysis, and hypergeometric tests to calculate the underlying regulatory effects of multifactors on the modules by the way of the whole gene expression profile of AD and identify a series of ncRNA (miR-320a) and TF (NFKB1). Additionally, we screened 10 modules corresponding to the Hub gene, which tend to regulate the physiological progress of inflammation, regulation of autophagy, cerebral cortex neuron differentiation, glial cell apoptotic, and so on. Meanwhile, Alzheimer's disease is triggered by signaling pathways such as the MPK signaling pathway. In this study, a dysfunction module is utilized to verify that miR-590-3 and SP1 motility factors can regulate neurons in Alzheimer's disease through the MPK signaling pathway, not only providing new insights into the pathogenesis of Alzheimer's disease but also laying a solid theoretical foundation for the biologists to further cure Alzheimer's disease. Discover the rest of the scientific article on es/iode ➡️https://etcse.fr/XHhw #alzheimer #science #health
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[Current Research] “Hanging on for dear life” DNA molecules in our cells can be damaged by various extrinsic and intrinsic factors called genotoxic stressors; persistent and unchecked damage can lead to developing diseases like cancer. Fortunately, our cells don’t sit idly by and let this happen. In a study published in Cell Death & Disease, a research team led by Professor Shigeomi Shimizu and Project Junior Associate Professor Masatsune Tsujioka of the Department of Pathological Cell Biology, Medical Research Institute, Tokyo Medical and Dental University (TMDU) has uncovered a novel mechanism by which cells can strengthen their adhesion to their surrounding matrix in response to DNA-damaging agents. Focal adhesions, composed of proteins involved in cell-matrix interactions, are remodeled through replacement of focal adhesion kinase (FAK) and FAK-related non-kinase (FRNK) protein following genotoxic stress. While this mechanism helps protect normal tissues, it can also support cancer progression, as FRNK was highly expressed in human metastatic colon cancer samples. The article, “Identification of a novel type of focal adhesion remodelling via FAK/FRNK replacement, and its contribution to cancer progression” was published in Cell Death & Disease at DOI: https://lnkd.in/gY_Z36ny For more information, please visit the following URL. https://lnkd.in/g9KaUZRq #tokyomedicalanddentaluniversity #tmdu #東京医科歯科大学 #医科歯科
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A Montreal team discovers a new antibody that stimulates the elimination of cancer cells by the immune system. Important work carried out by the team of Dr. André Veillette at the Institut de recherches cliniques de Montréal (IRCM) / Montreal Clinical Research Institute in collaboration with a group of researchers, has just been published in Nature Immunology. The study identified a previously unknown pathway that prevents phagocytosis, a process promoting the immune system's response to cancer. Read: https://lnkd.in/dZvK5svK #sciencesdelavie #biotechnologie #biotechnology #innovation #recherche #sciences #medicaments #research #drugresearch #laboratories #labs #chemistry #chimie #biology #biologie #biopharma #rna #rnatherapeutics #arn #wewillwin
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📃Scientific paper: miR-590-3 and SP1 Promote Neuronal Apoptosis in Patients with Alzheimer's Disease via AMPK Signaling Pathway Abstract: Alzheimer's disease (AD) is a progressive neurological degenerative illness with a hidden onset. Its pathogenesis is complicated, although with molecular biology research on cancer and targeted research on pathogenic mechanisms, good progress has not yet been made. Therefore, this work built a multifactor-driven neuronal apoptosis dysfunction module for the purpose of probing its underlying pathogenic mechanisms. We performed differential expression analysis, coexpression analysis, enrichment analysis, and hypergeometric tests to calculate the underlying regulatory effects of multifactors on the modules by the way of the whole gene expression profile of AD and identify a series of ncRNA (miR-320a) and TF (NFKB1). Additionally, we screened 10 modules corresponding to the Hub gene, which tend to regulate the physiological progress of inflammation, regulation of autophagy, cerebral cortex neuron differentiation, glial cell apoptotic, and so on. Meanwhile, Alzheimer's disease is triggered by signaling pathways such as the MPK signaling pathway. In this study, a dysfunction module is utilized to verify that miR-590-3 and SP1 motility factors can regulate neurons in Alzheimer's disease through the MPK signaling pathway, not only providing new insights into the pathogenesis of Alzheimer's disease but also laying a solid theoretical foundation for the biologists to further cure Alzheimer's disease. Discover the rest of the scientific article on es/iode ➡️https://etcse.fr/XHhw #alzheimer #science #health
miR-590-3 and SP1 Promote Neuronal Apoptosis in Patients with Alzheimer's Disease via AMPK Signaling Pathway
ethicseido.com
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📃Scientific paper: miR-590-3 and SP1 Promote Neuronal Apoptosis in Patients with Alzheimer's Disease via AMPK Signaling Pathway Abstract: Alzheimer's disease (AD) is a progressive neurological degenerative illness with a hidden onset. Its pathogenesis is complicated, although with molecular biology research on cancer and targeted research on pathogenic mechanisms, good progress has not yet been made. Therefore, this work built a multifactor-driven neuronal apoptosis dysfunction module for the purpose of probing its underlying pathogenic mechanisms. We performed differential expression analysis, coexpression analysis, enrichment analysis, and hypergeometric tests to calculate the underlying regulatory effects of multifactors on the modules by the way of the whole gene expression profile of AD and identify a series of ncRNA (miR-320a) and TF (NFKB1). Additionally, we screened 10 modules corresponding to the Hub gene, which tend to regulate the physiological progress of inflammation, regulation of autophagy, cerebral cortex neuron differentiation, glial cell apoptotic, and so on. Meanwhile, Alzheimer's disease is triggered by signaling pathways such as the MPK signaling pathway. In this study, a dysfunction module is utilized to verify that miR-590-3 and SP1 motility factors can regulate neurons in Alzheimer's disease through the MPK signaling pathway, not only providing new insights into the pathogenesis of Alzheimer's disease but also laying a solid theoretical foundation for the biologists to further cure Alzheimer's disease. Discover the rest of the scientific article on es/iode ➡️https://etcse.fr/XHhw #alzheimer #science #health
miR-590-3 and SP1 Promote Neuronal Apoptosis in Patients with Alzheimer's Disease via AMPK Signaling Pathway
ethicseido.com
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Creativity is as important as knowledge / Director, Center for Genetics and Genomics / Director, Ph.D. Program in Sciences and Innovation in Medicine at Universidad del Desarrollo
Synpoptosis: A synthetic biology approach to programmable cell death Cells naturally die (apoptosis, pyroptosis) to eliminate harmful cells and regulate inflammation. Synthetic protein circuits could trigger specific cell death programs in targeted cells, offering a way to eliminate harmful cells while managing immune responses. However, controlling cell death is challenging because cells respond to natural signals. This research introduces "synpoptosis" circuits, inspired by nature, that use protein breakdown to control engineered executioner proteins and mammalian cell death. These circuits direct death modes, respond to protease signals, and eliminate target cells selectively. Additionally, they can be transmitted between cells, enabling the engineering of synthetic killer cells that induce desired death programs without self-destruction. This paves the way for programmable control of mammalian cell death, which has promising applications in cancer and immune disease. The original article was published in Cell: https://lnkd.in/eKm8aScv. #genetics #genomics #precisionmedicine #genomicmedicine #syntheticbiology #apoptosis #celldeath #bioengineering #molecularbiology #biotechnology #cancer #inflammation #immunity #immunology #mitosis #proliferation #therapeutics #innovation #research #science #sciencecommunication
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Phagocytosis involves several sequential stages👇 📎Phagocytes such as macrophages and neutrophils employ pattern-recognition receptors to directly bind to microbes or those coated with complement proteins. 📎This initiates the internalization of the microbes, encapsulating them within phagosome vesicles within the cell's cytosol. Subsequently, these phagosomes merge with lysosomes, exposing the microbes to potent chemicals like ROS and NO, as well as proteolytic enzymes. 📎This process effectively eradicates and breaks down the microbes, ensuring their destruction Image from: Carsten Carlberg, Eunike Velleuer - Molecular Immunology_ How Science Works-Springer (2022) #phagocytosis #microbes #cancerbiology #cancerbiologyresearch
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In the 1970s, BD pioneered flow cytometry, one of the most powerful tools for researchers to study cells and better understand changes linked to disease. Since then, BD Biosciences – celebrating 50 years this year – has enabled researchers to unlock new discoveries. Our cutting-edge technologies enable deeper insights that are changing the future of immunology, cell biology, genomic research, cell-based therapies and more. For example, the BD FACSDiscover™ S8 Cell Sorter with BD CellView™ Image Technology empowers scientists to derive new insights that could lead to more effective treatments for some of the world's most prominent diseases. As the future of healthcare research accelerates at rapid speed, we are delivering products that enable our customers to push the boundaries of science and deliver revolutionary advancements and life-changing discoveries. #BDBiosciences #Flowcytometry #medtechinnovation
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🌟 Weekly Science & Research Update 🌟 Welcome to this week’s roundup of groundbreaking discoveries and innovations in the world of science! Let’s dive into the latest research that is pushing the boundaries of our understanding. Visit these links to know more: Genomics Innovation 🧬 Researchers have achieved de novo scaffolding of chromosome-level haplotypes using Hi-C data to construct the genome of Miscanthus × giganteus. This advancement could enhance biofuel production and genetic research. ( https://lnkd.in/gvNK55qU) Glioma Research 🧠 CCL2-mediated IKZF1 expression promotes M2 polarization of glioma-associated macrophages through the CD84-SHP2 pathway. This finding offers new insights into glioma progression and potential therapeutic targets. (https://lnkd.in/guyY7Htd) Cancer Research 🧬 A CRISPR-based study has dissected the functionality of the microRNA-23a ~ 27a ~ 24-2 cluster in hepatocellular carcinoma, providing new avenues for cancer treatment. (https://lnkd.in/ghaCB_Pi) Plant Pathology 🌱 Scientists have isolated and analyzed the genome of Ceratobasidium theobromae, a new pathogen of cassava in Southeast Asia. Understanding its tissue localization could help in developing strategies to protect this vital crop. (https://lnkd.in/gVx74kh4) Neuroscience Discovery 🧠 Multisensory gamma stimulation has been shown to mitigate the effects of demyelination induced by cuprizone in male mice. This research could lead to new therapies for neurodegenerative diseases. (https://lnkd.in/gS5Jh8EG) Liver Health Breakthrough 🧬 Activation of the pregnane X receptor has been found to protect against cholestatic liver injury by inhibiting hepatocyte pyroptosis. This discovery could lead to new treatments for liver diseases. (https://lnkd.in/gs6Hvpc2) Stay informed and inspired by the latest in research and innovation. 📚✨ #ResearchUpdate #ScientificBreakthroughs #Innovation
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