Grant List
Represents Grant table in the DB
GET /v1/grants?page%5Bnumber%5D=1384&sort=keywords
{ "links": { "first": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1&sort=keywords", "last": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1405&sort=keywords", "next": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1385&sort=keywords", "prev": "https://cic-apps.datascience.columbia.edu/v1/grants?page%5Bnumber%5D=1383&sort=keywords" }, "data": [ { "type": "Grant", "id": "6777", "attributes": { "award_id": "1U19AI171110-01", "title": "Developing Antivirals Targeting Proteases and Polymerases of Coronaviruses, Picornaviruses and Bunyavirales", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [], "start_date": "2022-05-16", "end_date": "2025-04-30", "award_amount": 5168269, "principal_investigator": { "id": 22581, "first_name": "CHARLES Scott", "last_name": "CRAIK", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 768, "ror": "https://ror.org/043mz5j54", "name": "University of California, San Francisco", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [], "awardee_organization": { "id": 768, "ror": "https://ror.org/043mz5j54", "name": "University of California, San Francisco", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true }, "abstract": null, "keywords": [ "Antiviral Agents", "Bunyavirales", "Coronavirus", "Family Picornaviridae", "Peptide Hydrolases", "Polymerase", "pandemic disease", "programs", "response" ], "approved": true } }, { "type": "Grant", "id": "9132", "attributes": { "award_id": "272201800008I-0-759302000002-1", "title": "Task C10: Chemical Synthesis and Process Optimization of an anti-viral for enteroviruses and coronaviruses", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [], "start_date": "2020-07-31", "end_date": "2021-05-30", "award_amount": 844080, "principal_investigator": { "id": 24910, "first_name": "GREG", "last_name": "MARTIN", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 1800, "ror": "", "name": "ALBANY MOLECULAR RESEARCH, INC.", "address": "", "city": "", "state": "NY", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [], "awardee_organization": { "id": 1800, "ror": "", "name": "ALBANY MOLECULAR RESEARCH, INC.", "address": "", "city": "", "state": "NY", "zip": "", "country": "United States", "approved": true }, "abstract": "The Non-clinical Services for Development of Interventional Agents for Infectious Diseases program provides services to facilitate preclinical product development of promising therapeutics for infectious disease-causing pathogens and/or toxins. Services include: preclinical product development planning and evaluation; lead identification and development; chemistry and GMP manufacturing; in vitro and in vivo preclinical microbiological, safety, toxicology and pharmacokinetics.", "keywords": [ "Antiviral Agents", "C10", "Chemistry", "Communicable Diseases", "Coronavirus", "Development", "Development Plans", "Drug Kinetics", "Enterovirus", "Evaluation", "In Vitro", "Interventional Agent Development", "Lead", "Microbiology", "Safety", "Services", "Support Contracts", "Therapeutic", "Toxicology", "Toxin", "chemical synthesis", "in vivo", "pathogen", "pre-clinical", "process optimization", "product development", "programs", "therapeutic development" ], "approved": true } }, { "type": "Grant", "id": "7301", "attributes": { "award_id": "3R01AI150698-01S1", "title": "Metabolic modulation by the HCMV UL38 gene", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 22533, "first_name": "Christopher E.", "last_name": "Beisel", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2020-07-21", "end_date": "2021-01-31", "award_amount": 23971, "principal_investigator": { "id": 23089, "first_name": "JOSHUA C", "last_name": "MUNGER", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 464, "ror": "https://ror.org/022kthw22", "name": "University of Rochester", "address": "", "city": "", "state": "NY", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [], "awardee_organization": { "id": 464, "ror": "https://ror.org/022kthw22", "name": "University of Rochester", "address": "", "city": "", "state": "NY", "zip": "", "country": "United States", "approved": true }, "abstract": "Human Cytomegalovirus (HCMV) is a major cause of congenital birth defects and causes severe disease in a wide variety of immunosuppressed patient populations, including hematological cancer patients and transplant recipients. We have found that HCMV institutes a pro-viral metabolic program that drives numerous cellular metabolic activities to support the production of viral progeny. More recently, we find that the HCMV UL38 protein is necessary and sufficient to drive many aspects of HCMV-induced metabolic remodeling, and we hypothesize that UL38 supports infection through its inhibition of the TSC2 tumor suppressor protein to induce metabolic modulation. We will test this hypothesis in Aim 1 by elucidating how UL38-TSC2-mediated metabolic remodeling contributes to HCMV infection. In addition, we find that HCMV-induces the expression of neuronal enolase 2 (ENO2), which we find is important for robust HCMV infection. We hypothesize that ENO2 induction is critical for HCMV-mediated metabolic modulation, which we will test in Aim 2. Lastly, we find that both HCMV infection and UL38 expression sensitizes cells to metabolic perturbations, revealing vulnerabilities that could potentially be targeted therapeutically. We hypothesize that HCMV infection and UL38 expression induces a metabolically rigid state that sensitizes cells to metabolic challenges, a hypothesis we will test in Aim 3. The proposed work will broaden our understanding of an important host pathogen interaction, and given that these processes are essential for productive infection, the proposed experiments will highlight novel targets for therapeutic intervention.", "keywords": [ "Antiviral Agents", "Cancer Patient", "Cells", "Cessation of life", "Congenital Abnormality", "Cytomegalovirus", "Cytomegalovirus Infections", "Disease", "Ensure", "Genes", "Goals", "Hematologic Neoplasms", "Human", "Immune system", "Immunocompromised Host", "Individual", "Infant", "Infection", "Institutes", "Knowledge", "Mediating", "Metabolic", "Neurons", "Process", "Production", "Proteins", "Research", "Resources", "TSC2 gene", "Testing", "Therapeutic Intervention", "Transplant Recipients", "Tumor Suppressor Proteins", "United States", "Viral", "Work", "cancer transplantation", "enolase", "experimental study", "new therapeutic target", "novel", "novel therapeutics", "pathogen", "patient population", "programs", "targeted treatment" ], "approved": true } }, { "type": "Grant", "id": "9023", "attributes": { "award_id": "75N91019D00024-P00004-759102000010-1", "title": "The Adaptive COVID-19 Treatment Trial (ACTT)", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [], "start_date": "2020-04-03", "end_date": "2025-04-02", "award_amount": 25075500, "principal_investigator": { "id": 23486, "first_name": "BETH", "last_name": "BASELER", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 1610, "ror": "", "name": "LEIDOS BIOMEDICAL RESEARCH, INC.", "address": "", "city": "", "state": "MD", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [], "awardee_organization": { "id": 1610, "ror": "", "name": "LEIDOS BIOMEDICAL RESEARCH, INC.", "address": "", "city": "", "state": "MD", "zip": "", "country": "United States", "approved": true }, "abstract": "To support randomized, controlled clinical trials to evaluate the safety and efficacy of investigational antiviral drugs against COVID-19.", "keywords": [ "Antiviral Agents", "COVID-19", "COVID-19 therapeutics", "COVID-19 treatment", "Investigation", "Randomized Controlled Clinical Trials", "Safety", "therapeutic evaluation", "treatment trial" ], "approved": true } }, { "type": "Grant", "id": "7684", "attributes": { "award_id": "75N91019D00024-0-759102000010-1", "title": "The Adaptive COVID-19 Treatment Trial (ACTT)", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [], "start_date": "2020-04-03", "end_date": "2025-04-02", "award_amount": 40199082, "principal_investigator": { "id": 23486, "first_name": "BETH", "last_name": "BASELER", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 1610, "ror": "", "name": "LEIDOS BIOMEDICAL RESEARCH, INC.", "address": "", "city": "", "state": "MD", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [], "awardee_organization": { "id": 1610, "ror": "", "name": "LEIDOS BIOMEDICAL RESEARCH, INC.", "address": "", "city": "", "state": "MD", "zip": "", "country": "United States", "approved": true }, "abstract": "To support randomized, controlled clinical trials to evaluate the safety and efficacy of investigational antiviral drugs against COVID-19.", "keywords": [ "Antiviral Agents", "COVID-19", "Investigation", "Randomized Controlled Clinical Trials", "Safety", "therapeutic evaluation", "treatment trial" ], "approved": true } }, { "type": "Grant", "id": "7685", "attributes": { "award_id": "75N91019D00024-0-759102000010-2", "title": "The Adaptive COVID-19 Treatment Trial (ACTT)", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [], "start_date": "2020-04-03", "end_date": "2025-04-02", "award_amount": 18166213, "principal_investigator": { "id": 23486, "first_name": "BETH", "last_name": "BASELER", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 1610, "ror": "", "name": "LEIDOS BIOMEDICAL RESEARCH, INC.", "address": "", "city": "", "state": "MD", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [], "awardee_organization": { "id": 1610, "ror": "", "name": "LEIDOS BIOMEDICAL RESEARCH, INC.", "address": "", "city": "", "state": "MD", "zip": "", "country": "United States", "approved": true }, "abstract": "To support randomized, controlled clinical trials to evaluate the safety and efficacy of investigational antiviral drugs against COVID-19.", "keywords": [ "Antiviral Agents", "COVID-19", "Investigation", "Randomized Controlled Clinical Trials", "Safety", "therapeutic evaluation", "treatment trial" ], "approved": true } }, { "type": "Grant", "id": "7550", "attributes": { "award_id": "3U19AI100627-09S1", "title": "Systems Approach to Immunity and Inflammation", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 6173, "first_name": "QIAN", "last_name": "Liu", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2020-06-11", "end_date": "2022-08-31", "award_amount": 838582, "principal_investigator": { "id": 20889, "first_name": "Richard J", "last_name": "Ulevitch", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 745, "ror": "", "name": "SCRIPPS RESEARCH INSTITUTE, THE", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [], "awardee_organization": { "id": 745, "ror": "", "name": "SCRIPPS RESEARCH INSTITUTE, THE", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true }, "abstract": "The innate immune response is a double-edged sword; it is absolutely required for host defense, but unregulated, causes inflammatory disease. Diverse and potent mechanisms have evolved to recognize and counter invading microorganisms. These include a variety of pattern recognition receptors, including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), Nod-like receptors (NLRs) and C-type lectin like receptors (CLRs) that recognize conserved molecular motifs on pathogens. While significant progress has been made in identifying the ligands detected by these receptors and the signaling cascades that they activate, a number of critical questions regarding the mechanisms that appropriately tailor the outputs of these pathways remain unanswered. Furthermore, the immune response to live pathogens is shaped by the interaction of multiple receptors and their cognate signaling pathways. The aggregate response is complex and cannot be predicted from analysis of each pathway in isolation; however, it is tractable using the tools of systems biology and forward genetics. Over the past 15 years members of this U19 consortium have collaborated using cross-disciplinary approaches to define the molecular mechanisms underlying the regulation of immune receptors and pathways. Their genetic approaches have also linked the pathways to pathogenesis and to immunity in vivo. These studies have also generated a significant body of work demonstrating cross-regulation between innate immune receptors. This U19 consists of two interrelated Projects that probe the innate immune response to infection. In Project 1, the Beutler laboratory will work in close collaboration with the Aderem, Nolan, and Ulevitch laboratories, taking a highly automated forward genetic approach to the analysis of innate immune signaling. In Project 2, the Aderem laboratory will determine mechanisms by which the TLR and type I interferon pathways cross-regulate each other. The Projects will be supported by three scientific Cores: The Signaling Core, will bring to bear several novel technologies for highly multiplexed molecular phenotyping of immune cells. The Data Management and Bioinformatics Core will support the individual Projects as well as the overall goals of the program through integrated computational analysis of all large-scale datasets. The Human Correlation Core will examine the relevance of mouse genes, demonstrated in Projects 1 and 2 to mediate innate immune functions, in the analogous human pathways.", "keywords": [ "Antiviral Response", "Architecture", "Bioinformatics", "C-Type Lectins", "Cells", "Collaborations", "Communicable Diseases", "Communities", "Complex", "Computer Analysis", "Data", "Disease", "Gene Proteins", "Genes", "Genomics", "Goals", "Host Defense", "Human", "Immune", "Immune response", "Immune signaling", "Immune system", "Immunity", "Immunologic Receptors", "Individual", "Infection", "Inflammation", "Inflammatory", "Influenza", "Informatics", "Innate Immune Response", "Interferon Type I", "Interferons", "Invaded", "Knowledge", "Laboratories", "Ligands", "Link", "Mediating", "Molecular", "Multiplexed Ion Beam Imaging", "Mus", "Mutant Strains Mice", "Orthologous Gene", "Output", "Pathogenesis", "Pathway interactions", "Pattern recognition receptor", "Pharmaceutical Preparations", "Proteomics", "Reagent", "Receptor Signaling", "Regulation", "Regulator Genes", "Resources", "Role", "Signal Pathway", "Signal Transduction", "Streptococcus pneumoniae", "System", "Systems Biology", "Toll-like receptors", "Ursidae Family", "Vaccine Design", "Work", "combat", "data management", "epigenomics", "forward genetics", "genetic approach", "human disease", "immunoregulation", "in vivo", "innate immune function", "large scale data", "macrophage", "member", "microorganism", "molecular phenotype", "new technology", "novel strategies", "pathogen", "phenotypic data", "program dissemination", "programs", "receptor", "response", "single cell analysis", "superinfection", "tool", "transcriptomics" ], "approved": true } }, { "type": "Grant", "id": "6148", "attributes": { "award_id": "3U19AI100627-10S2", "title": "Systems Approach to Immunity and Inflammation", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 20888, "first_name": "QIAN", "last_name": "Liu", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2012-09-01", "end_date": "2022-08-31", "award_amount": 302893, "principal_investigator": { "id": 20889, "first_name": "Richard J", "last_name": "Ulevitch", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [ { "id": 745, "ror": "", "name": "SCRIPPS RESEARCH INSTITUTE, THE", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true } ] }, "other_investigators": [], "awardee_organization": { "id": 745, "ror": "", "name": "SCRIPPS RESEARCH INSTITUTE, THE", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true }, "abstract": "The innate immune response is a double-edged sword; it is absolutely required for host defense, but unregulated, causes inflammatory disease. Diverse and potent mechanisms have evolved to recognize and counter invading microorganisms. These include a variety of pattern recognition receptors, including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), Nod-like receptors (NLRs) and C-type lectin like receptors (CLRs) that recognize conserved molecular motifs on pathogens. While significant progress has been made in identifying the ligands detected by these receptors and the signaling cascades that they activate, a number of critical questions regarding the mechanisms that appropriately tailor the outputs of these pathways remain unanswered. Furthermore, the immune response to live pathogens is shaped by the interaction of multiple receptors and their cognate signaling pathways. The aggregate response is complex and cannot be predicted from analysis of each pathway in isolation; however, it is tractable using the tools of systems biology and forward genetics. Over the past 15 years members of this U19 consortium have collaborated using cross-disciplinary approaches to define the molecular mechanisms underlying the regulation of immune receptors and pathways. Their genetic approaches have also linked the pathways to pathogenesis and to immunity in vivo. These studies have also generated a significant body of work demonstrating cross-regulation between innate immune receptors. This U19 consists of two interrelated Projects that probe the innate immune response to infection. In Project 1, the Beutler laboratory will work in close collaboration with the Aderem, Nolan, and Ulevitch laboratories, taking a highly automated forward genetic approach to the analysis of innate immune signaling. In Project 2, the Aderem laboratory will determine mechanisms by which the TLR and type I interferon pathways cross-regulate each other. The Projects will be supported by three scientific Cores: The Signaling Core, will bring to bear several novel technologies for highly multiplexed molecular phenotyping of immune cells. The Data Management and Bioinformatics Core will support the individual Projects as well as the overall goals of the program through integrated computational analysis of all large-scale datasets. The Human Correlation Core will examine the relevance of mouse genes, demonstrated in Projects 1 and 2 to mediate innate immune functions, in the analogous human pathways.", "keywords": [ "Antiviral Response", "Architecture", "Bioinformatics", "C-Type Lectins", "Cells", "Collaborations", "Communicable Diseases", "Communities", "Complex", "Computer Analysis", "Data", "Disease", "Gene Proteins", "Genes", "Genomics", "Goals", "Host Defense", "Human", "Immune", "Immune response", "Immune signaling", "Immune system", "Immunity", "Immunologic Receptors", "Individual", "Infection", "Inflammation", "Inflammatory", "Influenza", "Informatics", "Innate Immune Response", "Interferon Type I", "Interferons", "Invaded", "Knowledge", "Laboratories", "Ligands", "Link", "Mediating", "Molecular", "Multiplexed Ion Beam Imaging", "Mus", "Mutant Strains Mice", "Orthologous Gene", "Output", "Pathogenesis", "Pathway interactions", "Pattern recognition receptor", "Pharmaceutical Preparations", "Proteomics", "Reagent", "Receptor Signaling", "Regulation", "Regulator Genes", "Resources", "Role", "Signal Pathway", "Signal Transduction", "Streptococcus pneumoniae", "System", "Systems Biology", "Toll-like receptors", "Ursidae Family", "Vaccine Design", "Work", "combat", "data management", "epigenomics", "forward genetics", "genetic approach", "human disease", "immunoregulation", "in vivo", "innate immune function", "large scale data", "macrophage", "member", "microorganism", "molecular phenotype", "new technology", "novel strategies", "pathogen", "phenotypic data", "program dissemination", "programs", "receptor", "response", "single cell analysis", "superinfection", "tool", "transcriptomics" ], "approved": true } }, { "type": "Grant", "id": "6149", "attributes": { "award_id": "3U19AI100627-10S1", "title": "Systems Approach to Immunity and Inflammation", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 20890, "first_name": "QIAN", "last_name": "Liu", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2020-06-11", "end_date": "2022-08-31", "award_amount": 471985, "principal_investigator": { "id": 20891, "first_name": "Richard J", "last_name": "Ulevitch", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 745, "ror": "", "name": "SCRIPPS RESEARCH INSTITUTE, THE", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true }, "abstract": "The innate immune response is a double-edged sword; it is absolutely required for host defense, but unregulated, causes inflammatory disease. Diverse and potent mechanisms have evolved to recognize and counter invading microorganisms. These include a variety of pattern recognition receptors, including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), Nod-like receptors (NLRs) and C-type lectin like receptors (CLRs) that recognize conserved molecular motifs on pathogens. While significant progress has been made in identifying the ligands detected by these receptors and the signaling cascades that they activate, a number of critical questions regarding the mechanisms that appropriately tailor the outputs of these pathways remain unanswered. Furthermore, the immune response to live pathogens is shaped by the interaction of multiple receptors and their cognate signaling pathways. The aggregate response is complex and cannot be predicted from analysis of each pathway in isolation; however, it is tractable using the tools of systems biology and forward genetics. Over the past 15 years members of this U19 consortium have collaborated using cross-disciplinary approaches to define the molecular mechanisms underlying the regulation of immune receptors and pathways. Their genetic approaches have also linked the pathways to pathogenesis and to immunity in vivo. These studies have also generated a significant body of work demonstrating cross-regulation between innate immune receptors. This U19 consists of two interrelated Projects that probe the innate immune response to infection. In Project 1, the Beutler laboratory will work in close collaboration with the Aderem, Nolan, and Ulevitch laboratories, taking a highly automated forward genetic approach to the analysis of innate immune signaling. In Project 2, the Aderem laboratory will determine mechanisms by which the TLR and type I interferon pathways cross-regulate each other. The Projects will be supported by three scientific Cores: The Signaling Core, will bring to bear several novel technologies for highly multiplexed molecular phenotyping of immune cells. The Data Management and Bioinformatics Core will support the individual Projects as well as the overall goals of the program through integrated computational analysis of all large-scale datasets. The Human Correlation Core will examine the relevance of mouse genes, demonstrated in Projects 1 and 2 to mediate innate immune functions, in the analogous human pathways.", "keywords": [ "Antiviral Response", "Architecture", "Bioinformatics", "C-Type Lectins", "Cells", "Collaborations", "Communicable Diseases", "Communities", "Complex", "Computer Analysis", "Data", "Disease", "Gene Proteins", "Genes", "Genomics", "Goals", "Host Defense", "Human", "Immune", "Immune response", "Immune signaling", "Immune system", "Immunity", "Immunologic Receptors", "Individual", "Infection", "Inflammation", "Inflammatory", "Influenza", "Informatics", "Innate Immune Response", "Interferon Type I", "Interferons", "Invaded", "Knowledge", "Laboratories", "Ligands", "Link", "Mediating", "Molecular", "Multiplexed Ion Beam Imaging", "Mus", "Mutant Strains Mice", "Orthologous Gene", "Output", "Pathogenesis", "Pathway interactions", "Pattern recognition receptor", "Pharmaceutical Preparations", "Proteomics", "Reagent", "Receptor Signaling", "Regulation", "Regulator Genes", "Resources", "Role", "Signal Pathway", "Signal Transduction", "Streptococcus pneumoniae", "System", "Systems Biology", "Toll-like receptors", "Ursidae Family", "Vaccine Design", "Work", "combat", "data management", "epigenomics", "forward genetics", "genetic approach", "human disease", "immunoregulation", "in vivo", "innate immune function", "large scale data", "macrophage", "member", "microorganism", "molecular phenotype", "new technology", "novel strategies", "pathogen", "phenotypic data", "program dissemination", "programs", "receptor", "response", "single cell analysis", "superinfection", "tool", "transcriptomics" ], "approved": true } }, { "type": "Grant", "id": "6150", "attributes": { "award_id": "3U19AI100627-09S2", "title": "Systems Approach to Immunity and Inflammation", "funder": { "id": 4, "ror": "https://ror.org/01cwqze88", "name": "National Institutes of Health", "approved": true }, "funder_divisions": [ "National Institute of Allergy and Infectious Diseases (NIAID)" ], "program_reference_codes": [], "program_officials": [ { "id": 20892, "first_name": "QIAN", "last_name": "Liu", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] } ], "start_date": "2020-11-24", "end_date": "2022-08-31", "award_amount": 1887341, "principal_investigator": { "id": 20893, "first_name": "Richard J", "last_name": "Ulevitch", "orcid": null, "emails": "", "private_emails": "", "keywords": null, "approved": true, "websites": null, "desired_collaboration": null, "comments": null, "affiliations": [] }, "other_investigators": [], "awardee_organization": { "id": 745, "ror": "", "name": "SCRIPPS RESEARCH INSTITUTE, THE", "address": "", "city": "", "state": "CA", "zip": "", "country": "United States", "approved": true }, "abstract": "The innate immune response is a double-edged sword; it is absolutely required for host defense, but unregulated, causes inflammatory disease. Diverse and potent mechanisms have evolved to recognize and counter invading microorganisms. These include a variety of pattern recognition receptors, including Toll-like receptors (TLRs), RIG-I-like receptors (RLRs), Nod-like receptors (NLRs) and C-type lectin like receptors (CLRs) that recognize conserved molecular motifs on pathogens. While significant progress has been made in identifying the ligands detected by these receptors and the signaling cascades that they activate, a number of critical questions regarding the mechanisms that appropriately tailor the outputs of these pathways remain unanswered. Furthermore, the immune response to live pathogens is shaped by the interaction of multiple receptors and their cognate signaling pathways. The aggregate response is complex and cannot be predicted from analysis of each pathway in isolation; however, it is tractable using the tools of systems biology and forward genetics. Over the past 15 years members of this U19 consortium have collaborated using cross-disciplinary approaches to define the molecular mechanisms underlying the regulation of immune receptors and pathways. Their genetic approaches have also linked the pathways to pathogenesis and to immunity in vivo. These studies have also generated a significant body of work demonstrating cross-regulation between innate immune receptors. This U19 consists of two interrelated Projects that probe the innate immune response to infection. In Project 1, the Beutler laboratory will work in close collaboration with the Aderem, Nolan, and Ulevitch laboratories, taking a highly automated forward genetic approach to the analysis of innate immune signaling. In Project 2, the Aderem laboratory will determine mechanisms by which the TLR and type I interferon pathways cross-regulate each other. The Projects will be supported by three scientific Cores: The Signaling Core, will bring to bear several novel technologies for highly multiplexed molecular phenotyping of immune cells. The Data Management and Bioinformatics Core will support the individual Projects as well as the overall goals of the program through integrated computational analysis of all large-scale datasets. The Human Correlation Core will examine the relevance of mouse genes, demonstrated in Projects 1 and 2 to mediate innate immune functions, in the analogous human pathways.", "keywords": [ "Antiviral Response", "Architecture", "Bioinformatics", "C-Type Lectins", "Cells", "Collaborations", "Communicable Diseases", "Communities", "Complex", "Computer Analysis", "Data", "Disease", "Gene Proteins", "Genes", "Genomics", "Goals", "Host Defense", "Human", "Immune", "Immune response", "Immune signaling", "Immune system", "Immunity", "Immunologic Receptors", "Individual", "Infection", "Inflammation", "Inflammatory", "Influenza", "Informatics", "Innate Immune Response", "Interferon Type I", "Interferons", "Invaded", "Knowledge", "Laboratories", "Ligands", "Link", "Mediating", "Molecular", "Multiplexed Ion Beam Imaging", "Mus", "Mutant Strains Mice", "Orthologous Gene", "Output", "Pathogenesis", "Pathway interactions", "Pattern recognition receptor", "Pharmaceutical Preparations", "Proteomics", "Reagent", "Receptor Signaling", "Regulation", "Regulator Genes", "Resources", "Role", "Signal Pathway", "Signal Transduction", "Streptococcus pneumoniae", "System", "Systems Biology", "Toll-like receptors", "Ursidae Family", "Vaccine Design", "Work", "combat", "data management", "epigenomics", "forward genetics", "genetic approach", "human disease", "immunoregulation", "in vivo", "innate immune function", "large scale data", "macrophage", "member", "microorganism", "molecular phenotype", "new technology", "novel strategies", "pathogen", "phenotypic data", "program dissemination", "programs", "receptor", "response", "single cell analysis", "superinfection", "tool", "transcriptomics" ], "approved": true } } ], "meta": { "pagination": { "page": 1384, "pages": 1405, "count": 14046 } } }