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Inflammatory reflex disruption in COVID-19

Clinical and Experimental Neuroimmunology 2022年第4期13卷 295-301页

作者： Hajiasgharzadeh, Khalil Jafarlou, Mahdi Mansoori, Behzad Dastmalchi, Narges Baradaran, Behzad Khabbazi, Alireza Immunology Research Center Tabriz University of Medical Sciences Tabriz Iran Connective Tissue Diseases Research Center Tabriz University of Medical Sciences Tabriz Iran Cellular and Molecular Oncogenesis Program The Wistar Institute Philadelphia PA United States Department of Biology University College of Nabi Akram Tabriz Iran Pharmaceutical Analysis Research Center Tabriz University of Medical Sciences Tabriz Iran

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was identified in Wuhan, China, in late 2019 and caused coronavirus disease 2019 (COVID-19), which is still a global pandemic. In most infected people, SARS-CoV-2 only causes moderate symptoms, whereas in other patients, it leads to severe illness and eventually death. Although the main clinical manifestation of COVID-19 is often seen in the lungs, this disease affects almost all body organs. The excessive and prolonged release of inflammatory cytokines that might occur in COVID-19 patients, known as cytokine storms, stimulates undesired immune responses and can cause various tissues damage. In the current review article, we focus on the potential advantages of the intrinsic cholinergic anti-inflammatory pathway as the efferent arm of the inflammatory reflex in COVID-19 management. Considering this endogenous protective mechanism against chronic inflammation, we focused on the effects of SARS-CoV-2 in the destruction of this anti-inflammatory system. Several studies showed the interaction of SARS-CoV-2 with the alpha-7 subtype of the nicotinic acetylcholine receptor as the effector molecule of the inflammatory reflex. In contrast, neurological manifestations have increasingly been identified as significant extrapulmonary manifestations of COVID-19. The rational connection between these findings and COVID-19 pathogenesis might be an important issue in both our understanding of and dealing with this disease. COVID-19 is deeply rooted in our daily life and requires an urgent need for the establishment of effective therapeutic options, and all the possible treatments must be considered for the control of such inflammatory conditions. © 2022 Japanese Society for Neuroimmunology.

关键词： autonomic dysfunction cholinergic anti-inflammatory pathway COVID-19 inflammatory reflex SARS-CoV-2

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Common genetic variants in the TP53 pathway and their impact on cancer

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Journal of molecular Cell Biology 2019年第7期11卷 578-585页

作者： Thibaut Barnoud Joshua L.D.Parris Maureen E.Murphy Program in Molecular and Cellular Oncogenesis The Wistar InstitutePhiladelphiaPA 19104USA Cell and Molecular Biology Program Perelman School of Medicine at the University of PennsylvaniaPhiladelphiaPA 19104USA

The TP53 gene is well known to be the most frequently mutated gene in human *** addition to mutations,there are > 20 different coding region single-nucleotide polymorphisms (SNPs) in the TP53 gene,as well as SNPs in MDM2,the negative regulator of *** of these SNPs are known to alter p53 pathway *** makes p53 rather unique among cancer-critical genes,*** coding regions of other cancer-critical genes like Ha-Ras,RB,and PI3KCA do not have non-synonymous coding region SNPs that alter their function in *** next frontier in p53 biology will consist of probing which of these coding region SNPs are moderately or strongly pathogenic and whether they influence cancer risk and the efficacy of cancer *** challenge after that will consist of determining whether we can tailor chemotherapy to correct the defects for each ofthese *** we review the SNPs in TP53 and MDM2 that show the most significant impact on cancer and other *** also propose avenues for how this information can be used to better inform personalized medicine approaches to cancer and other diseases.

关键词： p53 Pro47Ser Pro72Arg PAS MDM2 SNP309

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Author Correction: Mutated processes predict immune checkpoint inhibitor therapy benefit in metastatic melanoma

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Nature communications 2023年第1期14卷 5865页

作者： Andrew Patterson Noam Auslander Genomics and Computational Biology Graduate Group University of Pennsylvania - Perelman School of Medicine Philadelphia PA 19104 USA. Program in Molecular and Cellular Oncogenesis The Wistar Institute Philadelphia PA 19104 USA. Program in Molecular and Cellular Oncogenesis The Wistar Institute Philadelphia PA 19104 USA. nauslander@***.

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Microsecond electric pulses effects in spinal cord injuries: results from RISEUP project

Microsecond electric pulses effects in spinal cord injuries:...

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International Conference on Electromagnetics in Advanced Applications (ICEAA)

作者： Giorgia Innamorati Camilla Codazzi Giulia Bergafora Paola Giardullo Caterina Merla Francesca Camera Marina Sanchez Petidier Leslie Vallet Micol Colella Laura Caramazza Noemi Dolciotti Sara Fontana Maria Pedraza Paolo Marracino Claudia Consales Department of Biology PhD Program in Cellular and Molecular Biology University of Rome “Tor Vergata” Rome Italy Division of Health Protection Technologies ENEA-Italian National Agency for New Technologies Energy and Sustainable Economic Development Rome Italy Institut Gustave Roussy CNRS Metabolic and Systemic aspects of the oncogenesis (METSY) Université Paris-Saclay Villejuif France Department of Information Engineering Electronics and Telecommunications Sapienza BioEMLab Group DIET University of Rome Italy Neuronal and Tissue Regeneration Laboratory Centro de Investigación Príncipe Felipe Valencia Spain RISE TECHNOLOGY SRL Ostia (RM) Italy

Spinal Cord Injury (SCI), a major cause of paralysis, currently has no effective therapies. Every year almost 500.000 people are diagnosed with SCI worldwide. he difficulty on the neuronal restoration after SCI is based on the complex cascade of events that inexorably cause a degenerative chronic stage mainly favored by the non-permissive environment and limited capacity for axonal regrowth. RISEUP, an Europen project, proposes to attain neuronal functional regeneration after SCI by an unprecedented and unique bio-hybrid-compatible electro-activated and wireless rechargeable implantable technology. RISEUP introduces high voltage microsecond electric pulses stimulations and low amplitude direct currents on a combination of stem cells, induced neural stem cells (iNSCs) and multipotent stromal cells (MSCs), whose transplantation is facilitated by an innovative scaffold biomaterial (Fig.1).

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RETRACTION: IspH inhibitors kill Gram-negative bacteria and mobilize immune clearance (Retraction of Vol 589, Pg 597, 2021)

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NATURE 2021年第7885期599卷 518-518页

作者： Singh, Kumar Sachin Sharma, Rishabh Reddy, Poli Adi Narayana Vonteddu, Prashanthi Good, Madeline Sundarrajan, Anjana Choi, Hyeree Muthumani, Kar Kossenkov, Andrew Goldman, Aaron R. Tang, Hsin-Yao Totrov, Maxim Cassel, Joel Murphy, Maureen E. Somasundaram, Rajasekharan Herlyn, Meenhard Salvino, Joseph M. Dotiwala, Farokh Vaccine and Immunotherapy Center The Wistar Institute Philadelphia PA USA Program in Molecular and Cellular Oncogenesis The Wistar Institute Philadelphia PA USA Molecular Screening and Protein Expression Facility The Wistar Institute Philadelphia PA USA Bioinformatics Facility The Wistar Institute Philadelphia PA USA Proteomics and Metabolomics Facility The Wistar Institute Philadelphia PA USA Molsoft San Diego CA USA

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Synthesis and characterization of I-BET151 derivatives for use in identifying protein targets in the African trypanosome

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Current research in chemical biology 2023年 3卷 100047页

作者： Adi Narayana Reddy Poli Rebecca C Blyn Gracyn Y Buenconsejo Melvin Hodanu Eric Tang Channy Danh Joel Cassel Erik W Debler Danae Schulz Joseph M Salvino Medicinal Chemistry Molecular and Cellular Oncogenesis (MCO) Program United States. Department of Biology Harvey Mudd College Claremont CA 91711 United States. Department of Biochemistry and Molecular Biology Thomas Jefferson University Philadelphia PA 19107 United States. The Wistar Cancer Center Molecular Screening The Wistar Institute Philadelphia PA 19104 United States.

, the causative agent of Human African Trypanosomiasis (HAT) and animal trypanosomiases, cycles between a bloodstream form in mammals and a procyclic form in the gut of its insect vector. We previously discovered that the human bromodomain inhibitor I-BET151 causes transcriptome changes that resemble the transition from the bloodstream to the procyclic form. In particular, I-BET151 induces replacement of variant surface glycoprotein (VSG) with procyclin protein. While modest binding of I-BET151 to Bdf2 and Bdf3 has been demonstrated, it is unknown whether I-BET151 binds to other identified bromodomain proteins and/or other targets. To identify target(s) in , we have synthesized I-BET151 derivatives maintaining the key pharmacophoric elements with functionality useful for chemoproteomic approaches. We identified compounds that are potent in inducing expression of procyclin, delineating a strategy towards the design of drugs against HAT and other trypanosomiases. Furthermore, these derivatives represent useful chemical probes to elucidate the molecular mechanism underlying I-BET151-induced differentiation.

关键词： Bromodomain Chemical probes Human African trypanosomiasis Inhibitor

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Kaposi's sarcoma-associated herpesvirus induces mitochondrial fission to evade host immune responses and promote viral production

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Nature microbiology 2025年 2025 May 22页

作者： Qing Zhu Robert McElroy Janvhi Suresh Machhar Joel Cassel Zihan Zheng Behzad Mansoori Hongrui Guo Sen Guo Christian Pangilinan Jinghui Liang Dongliang Shen Lu Zhang Qin Liu Andrew V Kossenkov Dario C Altieri Paul M Lieberman Shou-Jiang Gao Pinghui Feng Maureen E Murphy Jikui Song Joseph M Salvino Qiming Liang Jae U Jung Chengyu Liang Program in Molecular and Cellular Oncogenesis The Wistar Institute Philadelphia PA USA. Department of Molecular Microbiology and Immunology Keck School of Medicine University of Southern California Los Angeles CA USA. Program in Genome Regulation and Cell Signaling The Wistar Institute Philadelphia PA USA. Cancer Virology Program University of Pittsburgh Medical Center Hillman Cancer Center University of Pittsburgh School of Medicine Pittsburgh PA USA. Section of Infection and Immunity Herman Ostrow School of Dentistry Norris Comprehensive Cancer Center University of Southern California Los Angeles CA USA. Department of Biochemistry University of California Riverside CA USA. Center for Immune-Related Diseases at Shanghai Institute of Immunology Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai China. Department of Cancer Biology Department of Infection Biology and Global Center for Pathogen and Human Health Research Lerner Research Institute Cleveland Clinic Cleveland OH USA. Program in Molecular and Cellular Oncogenesis The Wistar Institute Philadelphia PA USA. cliang@***. Department of Molecular Microbiology and Immunology Keck School of Medicine University of Southern California Los Angeles CA USA. cliang@***.

Mitochondrial dynamics are pivotal for host immune responses upon infection, yet how viruses manipulate these processes to impair host defence and enhance viral fitness remains unclear. Here we show that Kaposi's sarcoma-associated herpesvirus (KSHV), an oncogenic virus also known as human herpesvirus 8, encodes Bcl-2 (vBcl-2), which reprogrammes mitochondrial architecture. It binds with NM23-H2, a host nucleoside diphosphate (NDP) kinase, to stimulate GTP loading of the dynamin-related protein (DRP1) GTPase, which triggers mitochondrial fission, inhibits mitochondrial antiviral signalling protein (MAVS) aggregation and impairs interferon responses in cell lines. An NM23-H2-binding-defective vBcl-2 mutant fails to evoke fission, leading to defective virion assembly due to activated MAVS-IFN signalling. Notably, we identify two key interferon-stimulated genes restricting vBcl-2-dependent virion morphogenesis. Using a high-throughput drug screening, we discover an inhibitor targeting vBcl-2-NM23-H2 interaction that blocks virion production in vitro. Our study identifies a mechanism in which KSHV manipulates mitochondrial dynamics to allow for virus assembly and shows that targeting the virus-mitochondria interface represents a potential therapeutic strategy.

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RETRACTED ARTICLE: IspH inhibitors kill Gram-negative bacteria and mobilize immune clearanceAssociated Content

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Nature 2021年第7843期589卷

作者： Kumar Sachin Singh Rishabh Sharma Prashanthi Vonteddu Anjana Sundarrajan Hyeree Choi Kar Muthumani Farokh Dotiwala Poli Adi Narayana Reddy Madeline Good Maureen E. Murphy Rajasekharan Somasundaram Meenhard Herlyn Joseph M. Salvino Andrew Kossenkov Aaron R. Goldman Hsin-Yao Tang Maxim Totrov Joel Cassel Vaccine and Immunotherapy Center The Wistar Institute Philadelphia PA USA Program in Molecular and Cellular Oncogenesis The Wistar Institute Philadelphia PA USA Molecular Screening and Protein Expression Facility The Wistar Institute Philadelphia PA USA Bioinformatics Facility The Wistar Institute Philadelphia PA USA Proteomics and Metabolomics Facility The Wistar Institute Philadelphia PA USA Molsoft San Diego CA USA

Isoprenoids are vital for all organisms, in which they maintain membrane stability and support core functions such as respiration1. IspH, an enzyme in the methyl erythritol phosphate pathway of isoprenoid synthesis, is essential for Gram-negative bacteria, mycobacteria and apicomplexans2,3. Its substrate, (E)-4-hydroxy-3-methyl-but-2-enyl pyrophosphate (HMBPP), is not produced in metazoans, and in humans and other primates it activates cytotoxic Vγ9Vδ2 T cells at extremely low concentrations4,5,6. Here we describe a class of IspH inhibitors and refine their potency to nanomolar levels through structure-guided analogue design. After modification of these compounds into prodrugs for delivery into bacteria, we show that they kill clinical isolates of several multidrug-resistant bacteria—including those from the generaAcinetobacter,Pseudomonas,Klebsiella,Enterobacter,Vibrio,Shigella,Salmonella,Yersinia,MycobacteriumandBacillus—yet are relatively non-toxic to mammalian cells. Proteomic analysis reveals that bacteria treated with these prodrugs resemble those after conditional IspH knockdown. Notably, these prodrugs also induce the expansion and activation of human Vγ9Vδ2 T cells in a humanized mouse model of bacterial infection. The prodrugs we describe here synergize the direct killing of bacteria with a simultaneous rapid immune response by cytotoxic γδ T cells, which may limit the increase of antibiotic-resistant bacterial populations.

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Protein Detection in Gels Using Fixation

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Current Protocols in Protein Science 2018年第1期91卷 10-10页

作者： Beer, Lynn A. Speicher, David W. Molecular and Cellular Oncogenesis Program The Wistar Institute Pennsylvania United States

The most commonly used types of gels for separating proteins are SDS gels, either in a 1-D format or as the second dimension of various 2-D separations, and the most common methods of visualizing proteins in these gels use protein binding dyes after fixing the proteins in the gel matrix. In recent years, there has been a continuing trend away from preparing staining solutions in the laboratory to using commercially available kits, which are convenient, save time, have defined shelf lives, and may provide greater reproducibility than stains formulated in research laboratories. In general, when using commercial kits, satisfactory results can be readily obtained by following the manufacturer's protocols. This unit reviews commonly used fixation-based stains and provides a number of manual formulations with staining protocols for those who prefer such staining methods. © 2018 by John Wiley & Sons, Inc. Copyright © 2018 John Wiley & Sons, Inc.

关键词： Coomassie stains MS compatible stains SDS gel stains silver stains SYPRO Ruby

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IRE1α governs cytoskeleton remodeling and cell migration through a direct interaction with filamin A (vol 20, pg 942, 2018)

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NATURE CELL BIOLOGY 2021年第5期23卷 577-577页

作者： Urra, Hery Henriquez, Daniel R. Canovas, Jose Villarroel-Campos, David Carreras-Sureda, Amado Pulgar, Eduardo Molina, Emiliano Hazari, Younis M. Limia, Celia M. Alvarez-Rojas, Sebastian Figueroa, Ricardo Vidal, Rene L. Rodriguez, Diego A. Rivera, Claudia A. Court, Felipe A. Couve, Andres Qi, Ling Chevet, Eric Akai, Ryoko Iwawaki, Takao Concha, Miguel L. Glavic, Alvaro Gonzalez-Billault, Christian Hetz, Claudio Biomedical Neuroscience Institute Faculty of Medicine University of Chile Santiago Chile Center for Geroscience Brain Health and Metabolism (GERO) Santiago Chile Program of Cellular and Molecular Biology Institute of Biomedical Sciences University of Chile Santiago Chile Program of Anatomy and Developmental Biology Institute of Biomedical Sciences University of Chile Santiago Chile Center for Integrative Biology Faculty of Sciences Universidad Mayor Santiago Chile Department of Neuroscience Faculty of Medicine University of Chile Santiago Chile The Buck Institute for Research in Aging Novato CA USA Department of Immunology and Infectious Diseases Harvard School of Public Health Boston MA USA Department of Biology Faculty of Sciences University of Chile Santiago Chile Center for Genome Regulation Faculty of Sciences University of Chile Santiago Chile Department of Molecular and Integrative Physiology Division of Metabolism Endocrinology and Diabetes The University of Michigan Medical School Ann Arbor MI USA INSERM U1242 Chemistry Oncogenesis Stress and Signaling University of Rennes 1 Rennes France Centre de Lutte contre le Cancer Eugène Marquis Rennes France Division of Cell Medicine Department of Life Science Medical Research Institute Kanazawa Medical University Uchinada Japan

A Correction to this paper has been published: https://***/10.1038/s41556-021-00673-2.

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