Jason Crawford, PhD
Professor of Chemistry and of Microbial PathogenesisDownloadHi-Res Photo
Cards
Appointments
Chemistry
Primary
Microbial Pathogenesis
Secondary
Contact Info
Institute of Biomolecular Design and Discovery
Institute of Biomolecular Design & Discovery, PO Box 27392
West Haven, CT 06516-7392
United States
About
Titles
Professor of Chemistry and of Microbial Pathogenesis
Appointments
Chemistry
ProfessorPrimaryMicrobial Pathogenesis
Associate Professor on TermSecondary
Other Departments & Organizations
- Chemistry
- CPIRT - Center for Pulmonary Injury, Inflammation, Repair and Therapeutics
- Developmental Therapeutics
- Immunology
- Institute of Biomolecular Design and Discovery
- Microbial Pathogenesis
- Microbiology
- Yale Cancer Center
- Yale Combined Program in the Biological and Biomedical Sciences (BBS)
Education & Training
- Postdoctoral Fellowship & Pathway to Independence Fellowship
- Harvard Medical School (2012)
- PhD
- Johns Hopkins University (2007)
- MA
- Johns Hopkins University (2003)
Research
Overview
Medical Research Interests
Bacteria; Chemistry; Host-Pathogen Interactions
- View Lab Website
Crawford Lab
Research at a Glance
Yale Co-Authors
Frequent collaborators of Jason Crawford's published research.
Publications Timeline
A big-picture view of Jason Crawford's research output by year.
Research Interests
Research topics Jason Crawford is interested in exploring.
Richard Flavell, PhD, FRS
Noah Wolcott Palm, PhD
Vincent Pieribone, PhD, BA, MA
Weiwei (Wendy) Wang
Abhishek Jain, PhD, ME, BEngSci
Andrew Goodman, PhD
98Publications
4,707Citations
Bacteria
Host-Pathogen Interactions
Publications
2024
Mucosal sugars delineate pyrazine vs pyrazinone autoinducer signaling in Klebsiella oxytoca
Hamchand R, Wang K, Song D, Palm N, Crawford J. Mucosal sugars delineate pyrazine vs pyrazinone autoinducer signaling in Klebsiella oxytoca. Nature Communications 2024, 15: 8902. PMID: 39406708, PMCID: PMC11480411, DOI: 10.1038/s41467-024-53185-6.Peer-Reviewed Original ResearchAltmetricMeSH Keywords and ConceptsConceptsK. oxytocaGeneral carbohydrate metabolismVirulence factor productionPLP-dependent enzymesAssociated with gutEnterobactin biosynthesisAutoinducer signalBacterial virulenceKlebsiella oxytocaSpecific carbohydratesHost immune responseCarbohydrate metabolismAutoinducerMolecular signalsVirulenceHistamine receptor H4BiosynthesisHost signalAcquisition responsesProtease inhibitorsPathwayHostLung pathologyLung isolationImmune responseBacterial small molecule metabolites implicated in gastrointestinal cancer development
Turocy T, Crawford J. Bacterial small molecule metabolites implicated in gastrointestinal cancer development. Nature Reviews Microbiology 2024, 1-16. PMID: 39375475, DOI: 10.1038/s41579-024-01103-4.Peer-Reviewed Original ResearchAltmetricConceptsSmall molecule metabolitesGastrointestinal cancer developmentAssociated with cancer progressionHost–microorganism interactionsGastrointestinal cancerCancer riskCancer developmentCancer progressionCancerTherapeutic interventionsMicrobiome membersHuman microbiomeBacterial speciesGlobal causeMolecular mechanismsMetabolitesRiskHuman AKR1C3 binds agonists of GPR84 and participates in an expanded polyamine pathway
Dudkina N, Park H, Song D, Jain A, Khan S, Flavell R, Johnson C, Palm N, Crawford J. Human AKR1C3 binds agonists of GPR84 and participates in an expanded polyamine pathway. Cell Chemical Biology 2024 PMID: 39163853, DOI: 10.1016/j.chembiol.2024.07.011.Peer-Reviewed Original ResearchCitationsConceptsHuman aldo-keto reductase family 1 member C3Mammalian fatty acid synthaseDNA double-strand break responseDouble-strand break responseAldo-keto reductase family 1 member C3Associated with poor prognosisPolyamine pathwayFatty acid synthesisFatty acid synthaseAcid synthaseAKR1C3 activityPoor prognosisBiochemical roleAcid synthesisClinical significanceLigand screeningFerroptosis resistanceDNA damageAKR1C3Metabolic diseasesDiverse cancersDNANADPHAgonists of GPR84GPR84The Xenorhabdus nematophila LrhA transcriptional regulator modulates production of γ-keto-N-acyl amides with inhibitory activity against mutualistic host nematode egg hatching
Lam Y, Hamchand R, Mucci N, Kauffman S, Dudkina N, Reagle E, Casanova-Torres Á, DeCuyper J, Chen H, Song D, Thomas M, Palm N, Goodrich-Blair H, Crawford J. The Xenorhabdus nematophila LrhA transcriptional regulator modulates production of γ-keto-N-acyl amides with inhibitory activity against mutualistic host nematode egg hatching. Applied And Environmental Microbiology 2024, 90: e00528-24. PMID: 38916293, PMCID: PMC11267870, DOI: 10.1128/aem.00528-24.Peer-Reviewed Original ResearchConceptsRegulatory hierarchyG protein-coupled receptorsSmall molecule signalsHost-bacteria interactionsSymbiotic relationshipNatural productsHuman G protein-coupled receptorsAmino acid metabolismRegulating amino acid metabolismNull mutantsDiverse natural productsSecondary metabolismNematode progeny productionPathogen interactionsGlobal regulatorNematode egg hatchingWild typeInsect hostsSecondary metabolitesHatching rateLrhAAcylated appendagesMolecular networksMolecule signalsAmide signalsIL-10 constrains sphingolipid metabolism to limit inflammation
York A, Skadow M, Oh J, Qu R, Zhou Q, Hsieh W, Mowel W, Brewer J, Kaffe E, Williams K, Kluger Y, Smale S, Crawford J, Bensinger S, Flavell R. IL-10 constrains sphingolipid metabolism to limit inflammation. Nature 2024, 627: 628-635. PMID: 38383790, PMCID: PMC10954550, DOI: 10.1038/s41586-024-07098-5.Peer-Reviewed Original ResearchCitationsAltmetricConceptsActivity of RelCeramide productionVery long chainFatty acid synthesis pathwayCeramide synthase 2Fatty acid homeostasisMetabolic fluxAvailable to cellsRegulatory nodesTranscription factorsCeramide accumulationSynthesis pathwayVLC ceramidesIL-10 deficiencyGene expressionSphingolipid metabolismAcid homeostasisAberrant activationIL-10Cell types1Innate immune cellsInflammatory gene expressionCeramideSignaling resultsGenetic deletion
2023
Gut microbes modulate (p)ppGpp during a time-restricted feeding regimen
Ontai-Brenning A, Hamchand R, Crawford J, Goodman A. Gut microbes modulate (p)ppGpp during a time-restricted feeding regimen. MBio 2023, 14: e01907-23. PMID: 37971266, PMCID: PMC10746209, DOI: 10.1128/mbio.01907-23.Peer-Reviewed Original ResearchCitationsAltmetricAuthor Correction: LACC1 bridges NOS2 and polyamine metabolism in inflammatory macrophages
Wei Z, Oh J, Flavell R, Crawford J. Author Correction: LACC1 bridges NOS2 and polyamine metabolism in inflammatory macrophages. Nature 2023, 618: e21-e21. PMID: 37231312, DOI: 10.1038/s41586-023-06244-9.Peer-Reviewed Original ResearchAltmetricIdentification of Efflux Substrates Using a Riboswitch-Based Reporter in Pseudomonas aeruginosa
Urdaneta-Páez V, Hamchand R, Anthony K, Crawford J, Sutherland A, Kazmierczak B. Identification of Efflux Substrates Using a Riboswitch-Based Reporter in Pseudomonas aeruginosa. MSphere 2023, 8: e00069-23. PMID: 36946743, PMCID: PMC10117056, DOI: 10.1128/msphere.00069-23.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLiquid chromatography-mass spectrometryCompound uptakeHigh-resolution liquid chromatography-mass spectrometryChromatography-mass spectrometryNovel antibioticsHigh-throughput screeningRational designMore rational designChemical librariesDiverse compoundsInitial hitsSelect compoundsPermeable compoundsDrug candidatesCompoundsStructural propertiesBacterial cellsPowerful methodAntifolate drugsSubstrateSpectrometrySynthesisPseudomonas aeruginosaClasses of antibioticsMembrane
2022
Cellular Stress-Induced Metabolites in Escherichia coli
Gatsios A, Kim C, York A, Flavell R, Crawford J. Cellular Stress-Induced Metabolites in Escherichia coli. Journal Of Natural Products 2022, 85: 2626-2640. PMID: 36346625, PMCID: PMC9949963, DOI: 10.1021/acs.jnatprod.2c00706.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsCommensal microbiota from patients with inflammatory bowel disease produce genotoxic metabolites
Cao Y, Oh J, Xue M, Huh WJ, Wang J, Gonzalez-Hernandez JA, Rice TA, Martin AL, Song D, Crawford JM, Herzon SB, Palm NW. Commensal microbiota from patients with inflammatory bowel disease produce genotoxic metabolites. Science 2022, 378: eabm3233. PMID: 36302024, PMCID: PMC9993714, DOI: 10.1126/science.abm3233.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsColorectal cancerInflammatory bowel disease patientsBowel disease patientsInflammatory bowel diseaseIndigenous gut microbesBowel diseaseDisease patientsCommensal microbiotaDNA damageColon tumorigenesisElicit DNA damageGut microbesGenotoxic metabolitesGut commensalsMorganella morganiiPatientsGenotoxic chemicalsDiseaseMicrobiotaMetabolitesGenotoxicityCancerMiceFull spectrumDamage
News
News
- July 11, 2024
Protein Detects and Responds to Changes in Blood Flow
- April 04, 2022Source: YaleNews
Synthetic Key Unlocks a Hidden Biology Treasure Chest
- April 01, 2022
Synthetic Key Unlocks a Hidden Biology Treasure Chest
- June 07, 2021Source: Yale West Campus
$8.5M Federal Grant Aims for Big Impact from Small Molecules in the Gut
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Contacts
Mailing Address
Institute of Biomolecular Design and Discovery
Institute of Biomolecular Design & Discovery, PO Box 27392
West Haven, CT 06516-7392
United States