D M Monack

Summary

Affiliation: Stanford University
Country: USA

Publications

  1. pmc Yersinia virulence factor YopJ acts as a deubiquitinase to inhibit NF-kappa B activation
    Honglin Zhou
    Molecular Oncology Department, Genentech, Inc, San Francisco, CA 94080, USA
    J Exp Med 202:1327-32. 2005
  2. ncbi request reprint Persistent bacterial infections: the interface of the pathogen and the host immune system
    Denise M Monack
    Department of Microbiology and Immunology, Stanford School of Medicine, Stanford University, Stanford, California 94305, USA
    Nat Rev Microbiol 2:747-65. 2004
  3. pmc Yersinia-induced apoptosis in vivo aids in the establishment of a systemic infection of mice
    D M Monack
    Department of Microbiology and Immunology, Stanford School of Medicine, Stanford University, Stanford, California 94305, USA
    J Exp Med 188:2127-37. 1998
  4. pmc Salmonella exploits caspase-1 to colonize Peyer's patches in a murine typhoid model
    D M Monack
    Department of Microbiology and Immunology, Stanford School of Medicine, Stanford University, Stanford, California 94305, USA
    J Exp Med 192:249-58. 2000
  5. ncbi request reprint Salmonella-induced macrophage death: the role of caspase-1 in death and inflammation
    D M Monack
    Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Microbes Infect 3:1201-12. 2001
  6. pmc Salmonella typhimurium persists within macrophages in the mesenteric lymph nodes of chronically infected Nramp1+/+ mice and can be reactivated by IFNgamma neutralization
    Denise M Monack
    Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford University, Stanford, CA 94305, USA
    J Exp Med 199:231-41. 2004
  7. ncbi request reprint Salmonella pathogenicity island 2-dependent macrophage death is mediated in part by the host cysteine protease caspase-1
    D M Monack
    Department of Microbiology and Immunology, Stanford University School of Medicine, 299 Campus Drive, Stanford, CA 94305, USA
    Cell Microbiol 3:825-37. 2001
  8. ncbi request reprint Macrophage-dependent induction of the Salmonella pathogenicity island 2 type III secretion system and its role in intracellular survival
    D M Cirillo
    Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305, USA
    Mol Microbiol 30:175-88. 1998
  9. ncbi request reprint Actin-based motility is sufficient for bacterial membrane protrusion formation and host cell uptake
    D M Monack
    Department of Microbiology and Immunology, Stanford University School of Medicine, 279 West Campus Drive, Stanford, CA 94305-5307, USA
    Cell Microbiol 3:633-47. 2001
  10. ncbi request reprint virK, somA and rcsC are important for systemic Salmonella enterica serovar Typhimurium infection and cationic peptide resistance
    Corrella S Detweiler
    Department of Microbiology and Immunology, Stanford School of Medicine, Stanford University, Stanford, CA 94305 5124, USA
    Mol Microbiol 48:385-400. 2003

Collaborators

Detail Information

Publications24

  1. pmc Yersinia virulence factor YopJ acts as a deubiquitinase to inhibit NF-kappa B activation
    Honglin Zhou
    Molecular Oncology Department, Genentech, Inc, San Francisco, CA 94080, USA
    J Exp Med 202:1327-32. 2005
    ..Moreover, an in vitro assay was established to demonstrate directly the deubiquitinating activity of purified YopJ...
  2. ncbi request reprint Persistent bacterial infections: the interface of the pathogen and the host immune system
    Denise M Monack
    Department of Microbiology and Immunology, Stanford School of Medicine, Stanford University, Stanford, California 94305, USA
    Nat Rev Microbiol 2:747-65. 2004
    ..The nature of the host immune response to this type of infection and the balance between clearance of the pathogen and avoidance of damage to host tissues are also discussed...
  3. pmc Yersinia-induced apoptosis in vivo aids in the establishment of a systemic infection of mice
    D M Monack
    Department of Microbiology and Immunology, Stanford School of Medicine, Stanford University, Stanford, California 94305, USA
    J Exp Med 188:2127-37. 1998
    ....
  4. pmc Salmonella exploits caspase-1 to colonize Peyer's patches in a murine typhoid model
    D M Monack
    Department of Microbiology and Immunology, Stanford School of Medicine, Stanford University, Stanford, California 94305, USA
    J Exp Med 192:249-58. 2000
    ..These results show that Casp-1, which is both proapoptotic and proinflammatory, is essential for S. typhimurium to efficiently colonize the cecum and PP and subsequently cause systemic typhoid-like disease in mice...
  5. ncbi request reprint Salmonella-induced macrophage death: the role of caspase-1 in death and inflammation
    D M Monack
    Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Microbes Infect 3:1201-12. 2001
    ..Salmonella that reside in the phagocytic vacuole do not cause this early cell death and can trigger a macrophage death at a much later time point. This late-phase cell death is dependent on SPI2-encoded genes and ompR...
  6. pmc Salmonella typhimurium persists within macrophages in the mesenteric lymph nodes of chronically infected Nramp1+/+ mice and can be reactivated by IFNgamma neutralization
    Denise M Monack
    Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford University, Stanford, CA 94305, USA
    J Exp Med 199:231-41. 2004
    ..Thus, interferon-gamma, which may affect the level of macrophage activation, plays an essential role in the control of the persistent S. typhimurium infection in mice...
  7. ncbi request reprint Salmonella pathogenicity island 2-dependent macrophage death is mediated in part by the host cysteine protease caspase-1
    D M Monack
    Department of Microbiology and Immunology, Stanford University School of Medicine, 299 Campus Drive, Stanford, CA 94305, USA
    Cell Microbiol 3:825-37. 2001
    ....
  8. ncbi request reprint Macrophage-dependent induction of the Salmonella pathogenicity island 2 type III secretion system and its role in intracellular survival
    D M Cirillo
    Department of Microbiology and Immunology, Stanford University School of Medicine, CA 94305, USA
    Mol Microbiol 30:175-88. 1998
    ..We conclude that SPI-2 genes are specifically expressed upon entry into mammalian cells and are required for intracellular growth in host cells in vivo and in vitro...
  9. ncbi request reprint Actin-based motility is sufficient for bacterial membrane protrusion formation and host cell uptake
    D M Monack
    Department of Microbiology and Immunology, Stanford University School of Medicine, 279 West Campus Drive, Stanford, CA 94305-5307, USA
    Cell Microbiol 3:633-47. 2001
    ..The frequency of membrane protrusion formation across all strains tested correlates with the efficiency of unidirectional actin-based movement, but not with bacterial speed...
  10. ncbi request reprint virK, somA and rcsC are important for systemic Salmonella enterica serovar Typhimurium infection and cationic peptide resistance
    Corrella S Detweiler
    Department of Microbiology and Immunology, Stanford School of Medicine, Stanford University, Stanford, CA 94305 5124, USA
    Mol Microbiol 48:385-400. 2003
    ..We conclude that virK, somA and rcsC are important for late stages of Salmonella enteric fever, and that they probably contribute to the remodelling of the bacterial outer membrane in response to the host environment...
  11. pmc Host transmission of Salmonella enterica serovar Typhimurium is controlled by virulence factors and indigenous intestinal microbiota
    Trevor D Lawley
    Department of Microbiology and Immunology, 299 Campus Drive, Stanford University, Stanford, CA 94305, USA
    Infect Immun 76:403-16. 2008
    ..This novel model should facilitate the study of host, pathogen, and intestinal microbiota factors that contribute to infectious disease transmission...
  12. pmc In vivo negative selection screen identifies genes required for Francisella virulence
    David S Weiss
    Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA
    Proc Natl Acad Sci U S A 104:6037-42. 2007
    ..This finding indicates that the elucidation of the molecular mechanisms used by other uncharacterized genes identified in our screen will increase our understanding of the ways in which bacterial pathogens subvert the immune system...
  13. pmc Identification of MglA-regulated genes reveals novel virulence factors in Francisella tularensis
    Anna Brotcke
    Department of Microbiology and Immunology, Stanford University School of Medicine, 299 Campus Drive, Fairchild Bldg D041, Stanford, CA 94305, USA
    Infect Immun 74:6642-55. 2006
    ..We have identified five new Francisella virulence genes, and our results suggest that characterizations of additional MglA-regulated genes will yield further insights into the pathogenesis of this bacterium...
  14. pmc Caspase-1-mediated activation of interleukin-1beta (IL-1beta) and IL-18 contributes to innate immune defenses against Salmonella enterica serovar Typhimurium infection
    Barbel Raupach
    Department of Cellular Microbiology, Max Planck Institut für Infektionsbiologie, Schumannstrasse 21 22, 10117 Berlin, Germany
    Infect Immun 74:4922-6. 2006
    ..Thus, we show that Casp-1 is essential for host innate immune defense against S. enterica serovar Typhimurium and that Casp-1 substrates are required at distinct times and anatomical sites...
  15. pmc Genome-wide screen for Salmonella genes required for long-term systemic infection of the mouse
    Trevor D Lawley
    Department of Microbiology and Immunology, Stanford University, Stanford, California, USA
    PLoS Pathog 2:e11. 2006
    ....
  16. ncbi request reprint Cryopyrin activates the inflammasome in response to toxins and ATP
    Sanjeev Mariathasan
    Molecular Oncology Department, Genentech Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 440:228-32. 2006
    ..Therefore, cryopyrin is essential for inflammasome activation in response to signalling pathways triggered specifically by ATP, nigericin, maitotoxin, S. aureus or L. monocytogenes...
  17. pmc Innate immunity against Francisella tularensis is dependent on the ASC/caspase-1 axis
    Sanjeev Mariathasan
    Molecular Oncology Department, Genentech Inc, South San Francisco, CA 94080, USA
    J Exp Med 202:1043-9. 2005
    ....
  18. ncbi request reprint Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf
    Sanjeev Mariathasan
    Molecular Oncology Department, Genentech, Inc, 1 DNA Way, South San Francisco, California 94080, USA
    Nature 430:213-8. 2004
    ..Notably, cell death triggered by stimuli that engage caspase-1 was ablated in macrophages lacking either ASC or Ipaf, suggesting a coupling between the inflammatory and cell death pathways...
  19. pmc Identification of fevR, a novel regulator of virulence gene expression in Francisella novicida
    Anna Brotcke
    Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305, USA
    Infect Immun 76:3473-80. 2008
    ..Thus, fevR is a crucial virulence gene in Francisella, required for the expression of virulence factors known to be essential for this pathogen's subversion of host defenses and pathogenesis in vivo...
  20. pmc Type I interferon signaling is required for activation of the inflammasome during Francisella infection
    Thomas Henry
    Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305, USA
    J Exp Med 204:987-94. 2007
    ..This connection underscores the importance of the cytosolic recognition of pathogens and highlights how multiple innate immunity pathways interact before commitment to critical host responses...
  21. doi request reprint The inflammasome: a key player in the inflammation triggered in response to bacterial pathogens
    Denise M Monack
    Stanford University, Stanford, CA, USA
    J Pediatr Gastroenterol Nutr 46:E14. 2008
  22. ncbi request reprint Francisella tularensis: activation of the inflammasome
    David S Weiss
    Department of Microbiology and Immunology, Stanford University School of Medicine, 299 Campus Drive, Fairchild Building, Room D041, Stanford, CA 94305, USA
    Ann N Y Acad Sci 1105:219-37. 2007
    ..These results highlight the role that the inflammasome plays in the tug-of-war between Francisella and the immune system...
  23. ncbi request reprint The Salmonella-containing vacuole is a major site of intracellular cholesterol accumulation and recruits the GPI-anchored protein CD55
    Drew M Catron
    Departments of Pathology and Microbiology Immunology, Northwestern University Medical School, 303 E Chicago Avenue, Chicago, IL 60611, USA
    Cell Microbiol 4:315-28. 2002
    ..These data suggest that, in contrast to prevailing models, the SCV accumulates components of cholesterol-rich early endocytic pathways during intracellular bacterial replication...
  24. pmc Critical function for Naip5 in inflammasome activation by a conserved carboxy-terminal domain of flagellin
    Karla L Lightfield
    School of Public Health, University of California, Berkeley, CA 94720, USA
    Nat Immunol 9:1171-8. 2008
    ..These mice failed to activate the inflammasome in response to the 35 amino acids of flagellin or in response to Legionella pneumophila infection. Our data clarify the molecular basis for the cytosolic response to flagellin...