Department of Infection Biology
London School of Hygiene and Tropical Medicine
Damian Lobato Marquez
Department of Infection Biology, London School of Hygiene and Tropical Medicine
Department of Infection Biology, London School of Hygiene and Tropical Medicine
A group of pathogenic bacteria that includes Shigella ., 2016), so they can be prescribed as an alternative or complementary treatment of infections by Listeria monocytogenes O Rickettsia spp., replicate in the cytosol of the infected host cell where they polymerize cellular actin and form “actin tails”, which propel the pathogen allowing it to invade adjacent cells (Goldberg, 2001). To counter infection, the host has not only innate and adaptive immune responses mediated by specialized cells, but also more immediate responses at the host cell level. In the case of infection by Shigella flexneriDepartment of Infection Biology, London School of Hygiene and Tropical Medicine
Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as et alAutophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as et al., 2011). The autophagy system then encompasses Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as ., 2011). The autophagy system then encompasses et al., 2011). The autophagy system then encompasses
GBPs block actin polymerization during infection by Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as., 2011). The autophagy system then encompasses Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as ., 2011). The autophagy system then encompasses et al., 2011). The autophagy system then encompasses et al., 2011). The autophagy system then encompasses et al., 2011). The autophagy system then encompasses ., 2011). The autophagy system then encompasses it loses its ability to efficiently polymerize actin tails, thus allowing the host cell to restrict the spread of the pathogen. Septins make up the cell cytoskeleton together with actin, intermediate filaments and microtubules (Mostowy & it loses its ability to efficiently polymerize actin tails, thus allowing the host cell to restrict the spread of the pathogen. Septins make up the cell cytoskeleton together with actin, intermediate filaments and microtubules (Mostowy et alit loses its ability to efficiently polymerize actin tails, thus allowing the host cell to restrict the spread of the pathogen. Septins make up the cell cytoskeleton together with actin, intermediate filaments and microtubules (Mostowy & it loses its ability to efficiently polymerize actin tails, thus allowing the host cell to restrict the spread of the pathogen. Septins make up the cell cytoskeleton together with actin, intermediate filaments and microtubules (Mostowy Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as, Mycobacterium marinum O Pseudomonas aeruginosa it loses its ability to efficiently polymerize actin tails, thus allowing the host cell to restrict the spread of the pathogen. Septins make up the cell cytoskeleton together with actin, intermediate filaments and microtubules (Mostowy & it loses its ability to efficiently polymerize actin tails, thus allowing the host cell to restrict the spread of the pathogen. Septins make up the cell cytoskeleton together with actin, intermediate filaments and microtubules (Mostowy et alit loses its ability to efficiently polymerize actin tails, thus allowing the host cell to restrict the spread of the pathogen. Septins make up the cell cytoskeleton together with actin, intermediate filaments and microtubules (Mostowy et alit loses its ability to efficiently polymerize actin tails, thus allowing the host cell to restrict the spread of the pathogen. Septins make up the cell cytoskeleton together with actin, intermediate filaments and microtubules (Mostowy Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such asAutophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as et al., 2010). Septin cages have a dual antimicrobial role: (1) they block actin polymerization, thus preventing bacteria from infecting adjacent cells (Figure 1); and (2) bacteria trapped in these structures are marked for degradation by autophagy (Sirianni et al., 2010). Septin cages have a dual antimicrobial role: (1) they block actin polymerization, thus preventing bacteria from infecting adjacent cells (Figure 1); and (2) bacteria trapped in these structures are marked for degradation by autophagy (Sirianni et al., 2018b). Therefore, these structures can be considered as "antimicrobial cages". To understand how septin boxes fuse with autophagosomes/lysosomes in the cytosol of the infected cell, we are investigating this process using low-energy X-ray cryo-tomography. We carried out this pioneering study in collaboration with José Javier Conesa (CNB-CSIC, Madrid) and the ALBA synchrotron (Barcelona).
., 2018b). Therefore, these structures can be considered as "antimicrobial cages". To understand how septin boxes fuse with autophagosomes/lysosomes in the cytosol of the infected cell, we are investigating this process using low-energy X-ray cryo-tomography. We carried out this pioneering study in collaboration with José Javier Conesa (CNB-CSIC, Madrid) and the ALBA synchrotron (Barcelona). Autophagy is a cell recycling system (evolutionarily conserved from yeast to mammals) that plays a crucial role in the elimination of damaged cell organelles, and in the response against infection by bacterial pathogens such as., 2018b). Therefore, these structures can be considered as "antimicrobial cages". To understand how septin boxes fuse with autophagosomes/lysosomes in the cytosol of the infected cell, we are investigating this process using low-energy X-ray cryo-tomography. We carried out this pioneering study in collaboration with José Javier Conesa (CNB-CSIC, Madrid) and the ALBA synchrotron (Barcelona).Shigella. This is a question that, given the complexity of the intracellular environment, has been impossible to answer using cells in culture. Synthetic biology makes it possible to study in a simplified way biological processes that take place in biochemically complex environments. The essays in vitro (bottom-up. This is a question that, given the complexity of the intracellular environment, has been impossible to answer using cells in culture. Synthetic biology makes it possible to study in a simplified way biological processes that take place in biochemically complex environments. The essays et al.. This is a question that, given the complexity of the intracellular environment, has been impossible to answer using cells in culture. Synthetic biology makes it possible to study in a simplified way biological processes that take place in biochemically complex environments. The essays in vitro . This is a question that, given the complexity of the intracellular environment, has been impossible to answer using cells in culture. Synthetic biology makes it possible to study in a simplified way biological processes that take place in biochemically complex environments. The essays Shigella Depends on bacterial growth. In collaboration with the group of Prof. Martin Pilhofer (ETH, Zurich) we are combining our essay in vitro Depends on bacterial growth. In collaboration with the group of Prof. Martin Pilhofer (ETH, Zurich) we are combining our essay in vitroDepends on bacterial growth. In collaboration with the group of Prof. Martin Pilhofer (ETH, Zurich) we are combining our essay ShigellaDepends on bacterial growth. In collaboration with the group of Prof. Martin Pilhofer (ETH, Zurich) we are combining our essay Listeria is not trapped in septin boxes, and nothing is known about Rickettsiais not trapped in septin boxes, and nothing is known about in vitrois not trapped in septin boxes, and nothing is known about Listeria escapes from this immune mechanism and if Rickettsia is not trapped in septin boxes, and nothing is known about
CONTRIBUTION AND SELECTED PUBLICATIONS
- is not trapped in septin boxes, and nothing is known about & is not trapped in septin boxes, and nothing is known about is not trapped in septin boxes, and nothing is known about
- is not trapped in septin boxes, and nothing is known about & is not trapped in septin boxes, and nothing is known about is not trapped in septin boxes, and nothing is known about Shigella flexneri is not trapped in septin boxes, and nothing is known about
- is not trapped in septin boxes, and nothing is known about & Klionsky D.J. Klionsky D.J.
- Klionsky D.J. Klionsky D.J.
- Kornberg AKlionsky D.J.
- Klionsky D.J. & Mostowy S. Klionsky D.J.
- Klionsky D.J. Klionsky D.J. Shigella Klionsky D.J.
- Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C. & Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C. Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C.
- Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C. Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C. Shigella Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C.
- Lobato-Márquez D. & Mostowy S. Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C.
- Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C. & Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C. Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C.
- Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C. & Kutsch M., Sistemich L., Lesser C. F., Goldberg M.B., Herrmann C. (2011) p62 and NDP52 Proteins Target intracytosolic Shigella and Listeria (2011) p62 and NDP52 Proteins Target intracytosolic
- (2011) p62 and NDP52 Proteins Target intracytosolic & (2011) p62 and NDP52 Proteins Target intracytosolic (2011) p62 and NDP52 Proteins Target intracytosolic Shigella (2011) p62 and NDP52 Proteins Target intracytosolic
- (2011) p62 and NDP52 Proteins Target intracytosolic & (2011) p62 and NDP52 Proteins Target intracytosolic (2011) p62 and NDP52 Proteins Target intracytosolic Shigella flexneri(2011) p62 and NDP52 Proteins Target intracytosolic
- (2011) p62 and NDP52 Proteins Target intracytosolic & Mostowy S. (2011) p62 and NDP52 Proteins Target intracytosolic
- (2011) p62 and NDP52 Proteins Target intracytosolic & (2011) p62 and NDP52 Proteins Target intracytosolic (1997) Actin polymerization is induced by Arp2/3 protein complex at the surface of Listeria monocytogenes(1997) Actin polymerization is induced by Arp2/3 protein complex at the surface of