Edward H. Kass Professor of Medicine, Brigham and Women's Hospital
Infectious Disease
Dr. Matthew K. Waldor, MD
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Matthew Waldor is an expert in the field of Infectious Disease. He attended Stanford University School of Medicine. Stanford University School of Medicine is a one of the best medicals schools. Stanford University School of Medicine has a rank of 2 in research and a 25 in primary care He received 1 awards: "Investigator". Matthew Waldor is a published doctor. He has 101 papers published. The most current publication "A Cytosine Methytransferase Modulates the Cell Envelope Stress Response in the Cholera Pathogen."
Publications
- A Cytosine Methytransferase Modulates the Cell Envelope Stress Response in the Cholera Pathogen.
- Sequence tag-based analysis of microbial population dynamics.
- A D, D-carboxypeptidase is required for Vibrio cholerae halotolerance.
- High-resolution genetic analysis of the requirements for horizontal transmission of the ESBL plasmid from Escherichia coli O104:H4.
- ARTIST: High-Resolution Genome-Wide Assessment of Fitness Using Transposon-Insertion Sequencing.
- Insights into Vibrio cholerae Intestinal Colonization from Monitoring Fluorescently Labeled Bacteria.
- Comparative RNA-Seq based dissection of the regulatory networks and environmental stimuli underlying Vibrio parahaemolyticus gene expression during infection.
- Cell separation in Vibrio cholerae is mediated by a single amidase whose action is modulated by two non-redundant activators.
- A Novel Peptidoglycan Binding Protein Crucial for PBP1A-Mediated Cell Wall Biogenesis in Vibrio cholerae.
- Reciprocal regulation of RND efflux systems and the Cpx two-component system in Vibrio cholerae.
- Differential requirement for PBP1a and PBP1b in the in vivo and in vitro fitness of Vibrio cholerae.
- Structural basis for the broad specificity of a new family of amino-acid racemases.
- PprA Contributes to Deinococcus radiodurans Resistance to Nalidixic Acid, Genome Maintenance after DNA Damage and Interacts with Deinococcal Topoisomerases.
- Tn-Seq Analysis of Vibrio cholerae Intestinal Colonization Reveals a Role for T6SS-Mediated Antibacterial Activity in the Host.
- ParP prevents dissociation of CheA from chemotactic signaling arrays and tethers them to a polar anchor.
- Substrate specificity of an elongation-specific peptidoglycan endopeptidase and its implications for cell wall architecture and growth of Vibrio cholerae.
- High-resolution definition of the Vibrio cholerae essential gene set with hidden Markov model-based analyses of transposon-insertion sequencing data.
- A Vibrio parahaemolyticus T3SS Effector Mediates Pathogenesis by Independently Enabling Intestinal Colonization and Inhibiting TAK1 Activation.
- Entering the era of bacterial epigenomics with single molecule real time DNA sequencing.
- Horizontal gene transfer: linking sex and cell fate.
- Comparative Genomics of Recent Shiga Toxin-Producing Escherichia coli O104:H4: Short-Term Evolution of an Emerging Pathogen.
- Studies of dynamic protein-protein interactions in bacteria using renilla luciferase complementation are undermined by nonspecific enzyme inhibition.
- The Hydrophilic Translocator for Vibrio parahaemolyticus, T3SS2, Is Also Translocated.
- Inflammation and Disintegration of Intestinal Villi in an Experimental Model for Vibrio parahaemolyticus-Induced Diarrhea.
- A double long polar fimbriae mutant of Escherichia coli O157:H7 expresses curli and exhibits reduced in vivo colonization.
- An Escherichia coli O157-specific engineered pyocin prevents and ameliorates infection by E. coli O157:H7 in an animal model of diarrheal disease.
- RNA-Seq-Based Monitoring of Infection-Linked Changes in Vibrio cholerae Gene Expression.
- Origins of the E. coli Strain Causing an Outbreak of Hemolytic-Uremic Syndrome in Germany.
- A family of ParA-like ATPases promotes cell pole maturation by facilitating polar localization of chemotaxis proteins.
- Regulatory Cross-Talk Links Vibrio cholerae Chromosome II Replication and Segregation.
- The three vibrio cholerae chromosome II-encoded ParE toxins degrade chromosome I following loss of chromosome II.
- The origin of the Haitian cholera outbreak strain.
- Meeting Cholera's Challenge to Haiti and the World: A Joint Statement on Cholera Prevention and Care.
- Type III Secretion Is Essential for the Rapidly Fatal Diarrheal Disease Caused by Non-O1, Non-O139 Vibrio cholerae.
- Vibrio cholerae ParE2 poisons DNA gyrase via a mechanism distinct from other gyrase inhibitors.
- A national cholera vaccine stockpile--a new humanitarian and diplomatic resource.
- Back to the future: studying cholera pathogenesis using infant rabbits.
- ParA2, a Vibrio cholerae chromosome partitioning protein, forms left-handed helical filaments on DNA.
- Reactogenicity of live-attenuated Vibrio cholerae vaccines is dependent on flagellins.
- Mobile antibiotic resistance encoding elements promote their own diversity.
- Comparative ICE genomics: insights into the evolution of the SXT/R391 family of ICEs.
- Vibrio cholerae LexA coordinates CTX prophage gene expression.
- Targeting the replication initiator of the second Vibrio chromosome: towards generation of vibrionaceae-specific antimicrobial agents.
- D-amino acids govern stationary phase cell wall remodeling in bacteria.
- Analysis of the genome of the Escherichia coli O157:H7 2006 spinach-associated outbreak isolate indicates candidate genes that may enhance virulence.
- Genetic analysis of activation of the Vibrio cholerae Cpx pathway.
- A toxin-antitoxin system promotes the maintenance of an integrative conjugative element.
- CadA negatively regulates Escherichia coli O157:H7 adherence and intestinal colonization.
- Targeting QseC signaling and virulence for antibiotic development.
- ATP negatively regulates the initiator protein of Vibrio cholerae chromosome II replication.
- Transient shielding of intimin and the type III secretion system of enterohemorrhagic and enteropathogenic Escherichia coli by a group 4 capsule.
- Type 2 secretion promotes enterohemorrhagic Escherichia coli adherence and intestinal colonization.
- Genomic and functional analysis of ICEPdaSpa1, a fish-pathogen-derived SXT-related integrating conjugative element that can mobilize a virulence plasmid.
- Dam methyltransferase is required for stable lysogeny of the Shiga toxin (Stx2)-encoding bacteriophage 933W of enterohemorrhagic Escherichia coli O157:H7.
- High-throughput, kingdom-wide prediction and annotation of bacterial non-coding RNAs.
- Distribution of centromere-like parS sites in bacteria: insights from comparative genomics.
- Determinants of entry exclusion within Eex and TraG are cytoplasmic.
- Distinct centromere-like parS sites on the two chromosomes of Vibrio spp.
- Adrenergic regulation of bacterial virulence.
- Enterohemorrhagic Escherichia coli O157:H7 gal mutants are sensitive to bacteriophage P1 and defective in intestinal colonization.
- The SXT/R391 family of integrative conjugative elements is composed of two exclusion groups.
- par genes and the pathology of chromosome loss in Vibrio cholerae.
- Characterization of a higBA toxin-antitoxin locus in Vibrio cholerae.
- Global gene expression and phenotypic analysis of a Vibrio cholerae rpoH deletion mutant.
- LexA represses CTXphi transcription by blocking access of the alpha C-terminal domain of RNA polymerase to promoter DNA.
- A dynamic, mitotic-like mechanism for bacterial chromosome segregation.
- Independent control of replication initiation of the two Vibrio cholerae chromosomes by DnaA and RctB.
- Requirement for Vibrio cholerae integration host factor in conjugative DNA transfer.
- The current ICE age: biology and evolution of SXT-related integrating conjugative elements.
- SXT-related integrating conjugative element in New World Vibrio cholerae.
- Activation of the Vibrio cholerae SOS response is not required for intestinal cholera toxin production or colonization.
- Disarming pathogens--a new approach for antibiotic development.
- Autorepression of RctB, an initiator of Vibrio cholerae chromosome II replication.
- Characterization of the small untranslated RNA RyhB and its regulon in Vibrio cholerae.
- Interactions between inner membrane proteins in donor and recipient cells limit conjugal DNA transfer.
- The locus of enterocyte effacement-encoded effector proteins all promote enterohemorrhagic Escherichia coli pathogenicity in infant rabbits.
- LexA cleavage is required for CTX prophage induction.
- Identification of operators and promoters that control SXT conjugative transfer.
- The Vibrio cholerae ToxR-regulated porin OmpU confers resistance to antimicrobial peptides.
- Formation of SXT tandem arrays and SXT-R391 hybrids.
- The CTXphi repressor RstR binds DNA cooperatively to form tetrameric repressor-operator complexes.
- Transcription of the toxin genes present within the Staphylococcal phage phiSa3ms is intimately linked with the phage's life cycle.
- Critical roles for stx2, eae, and tir in enterohemorrhagic Escherichia coli-induced diarrhea and intestinal inflammation in infant rabbits.
- Control of SXT integration and excision.
- Distinct replication requirements for the two Vibrio cholerae chromosomes.
- Deletion of a Vibrio cholerae ClC channel results in acid sensitivity and enhanced intestinal colonization.
- pIIICTX, a predicted CTXphi minor coat protein, can expand the host range of coliphage fd to include Vibrio cholerae.
- Comparison of Shiga toxin production by hemolytic-uremic syndrome-associated and bovine-associated Shiga toxin-producing Escherichia coli isolates.
- Genomic and functional analyses of SXT, an integrating antibiotic resistance gene transfer element derived from Vibrio cholerae.
- Bacteriophage control of bacterial virulence.
- Autotransporters but not pAA are critical for rabbit colonization by Shiga toxin-producing Escherichia coli O104:H4.
- Deciphering the origins and tracking the evolution of cholera epidemics with whole-genome-based molecular epidemiology.
- Evolutionary and functional analyses of variants of the toxin-coregulated pilus protein TcpA from toxigenic Vibrio cholerae non-O1/non-O139 serogroup isolates.
- Filamentous phage integration requires the host recombinases XerC and XerD.
- Bacteriophage control of Shiga toxin 1 production and release by Escherichia coli.
- Molecular analysis of antibiotic resistance gene clusters in vibrio cholerae O139 and O1 SXT constins.
- Evidence for a rolling-circle mechanism of phage DNA synthesis from both replicative and integrated forms of CTXphi.
- Role for a phage promoter in Shiga toxin 2 expression from a pathogenic Escherichia coli strain.
- Human neutrophils and their products induce Shiga toxin production by enterohemorrhagic Escherichia coli.
- Formation of chromosomal tandem arrays of the SXT element and R391, two conjugative chromosomally integrating elements that share an attachment site.
Schools
Stanford University
Brigham Womens Hospital
Massachusetts General Hospital
Doctors Specialties
- Infectious Disease Medicine
- Infectious Disease
Accepted Insurances
Awards
- Investigator
Education
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Massachusetts General Hospital -
Brigham and Women's Hospital -
Stanford University School of Medicine
Hospital
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Brigham and Women's Hospital
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