Group photo. From left to right: Roberto Balbontín, Andrea Bullones Bolaños, Paula Martín Muñoz, Claudia Vallejo Grijalba, Jesús Fernández García, Francisco Ramos Morales, Joaquín Bernal Bayard.
Many Gram-negative pathogenic bacteria possess type III secretion systems (T3SS) associated with virulence. These devices are evolutionarily related to the flagellum, similar to tiny syringes capable of injecting bacterial proteins into the cells of the eukaryotic organism they infect. These proteins, called effectors, often interfere with host cell signal transduction pathways to enable pathogen entry or survival. In many cases, the specific function performed by each effector is unknown. Salmonella enterica serovar Typhimurium is a bacterium capable of infecting numerous animal species. While in mice it produces a life-threatening systemic illness similar to typhoid fever, in humans it causes gastroenteritis. Its virulence largely depends on two T3SSs (T3SS1 and T3SS2) that are encoded in two pathogenicity islands called SPI1 and SPI2, respectively. Between the two they secrete more than 40 effectors (Ramos-Morales, 2012). Salmonella serovar Typhimurium is a bacterium capable of infecting numerous animal species. While in mice it produces a life-threatening systemic illness similar to typhoid fever, in humans it causes gastroenteritis. Its virulence largely depends on two T3SSs (T3SS1 and T3SS2) that are encoded in two pathogenicity islands called SPI1 and SPI2, respectively. Between the two they secrete more than 40 effectors (Ramos-Morales, 2012). Salmonella settles in a vacuole. The establishment of this survival and replication niche depends on effectors of T3SS2, although effectors of the system encoded in SPI1 also participate.
settles in a vacuole. The establishment of this survival and replication niche depends on effectors of T3SS2, although effectors of the system encoded in SPI1 also participate. Salmonella settles in a vacuole. The establishment of this survival and replication niche depends on effectors of T3SS2, although effectors of the system encoded in SPI1 also participate.
SlrP has a domain with several leucine-rich repeat (LRR) motifs that are often involved in protein-protein interactions. In the carboxyl terminal region it has another domain called NEL that is present in other effectors that are part of a new family of proteins with ubiquitin ligase activity. Our group demonstrated that SlrP possesses this activity and that it is capable of interacting with human thioredoxin (Trx), ubiquitylating it and causing a drop in its activity (Bernal-Bayard & Ramos-Morales, 2009). We solved the three-dimensional structure of the complex formed by SlrP and Trx in collaboration with the group of Dr. S. Nessler (Orsay, France). The two proteins form a heterotetramer in which the two SlrP molecules interact with the two Trx molecules, with one via the aforementioned LRR domain, the other via a linker region between the LRR domain and the NEL domain ( Zouhir et al.Ramos-Morales, 2009). We solved the three-dimensional structure of the complex formed by SlrP and Trx in collaboration with the group of Dr. S. Nessler (Orsay, France). The two proteins form a heterotetramer in which the two SlrP molecules interact with the two Trx molecules, with one via the aforementioned LRR domain, the other via a linker region between the LRR domain and the NEL domain ( Zouhir et al., 2010). The effect of both interactions could explain the increase in the rate of cell death that we have observed in HeLa cell cultures expressing SlrP. On the other hand, we also studied the conditions of expression and secretion of SlrP (Cordero-Alba & , 2010). The effect of both interactions could explain the increase in the rate of cell death that we have observed in HeLa cell cultures expressing SlrP. On the other hand, we also studied the conditions of expression and secretion of SlrP (Cordero-Alba
, 2010). The effect of both interactions could explain the increase in the rate of cell death that we have observed in HeLa cell cultures expressing SlrP. On the other hand, we also studied the conditions of expression and secretion of SlrP (Cordero-Alba star , 2010). The effect of both interactions could explain the increase in the rate of cell death that we have observed in HeLa cell cultures expressing SlrP. On the other hand, we also studied the conditions of expression and secretion of SlrP (Cordero-Alba & Ramos-Morales, 2013). In addition, transcriptomic analysis was performed on HeLa cells stably transfected with the SteA effector gene. The expression of SteA in these epithelial cells, through the modification of different signal transduction pathways, resulted in an alteration of cell morphology and a decrease in the rate of spontaneous cell death, intercellular junctions and migration speed. cell phone (Cardinal-Muñoz et al.Ramos-Morales, 2013). In addition, transcriptomic analysis was performed on HeLa cells stably transfected with the SteA effector gene. The expression of SteA in these epithelial cells, through the modification of different signal transduction pathways, resulted in an alteration of cell morphology and a decrease in the rate of spontaneous cell death, intercellular junctions and migration speed. cell phone (Cardinal-Muñoz
Ramos-Morales, 2013). In addition, transcriptomic analysis was performed on HeLa cells stably transfected with the SteA effector gene. The expression of SteA in these epithelial cells, through the modification of different signal transduction pathways, resulted in an alteration of cell morphology and a decrease in the rate of spontaneous cell death, intercellular junctions and migration speed. cell phone (Cardinal-Muñoz Salmonella Ramos-Morales, 2013). In addition, transcriptomic analysis was performed on HeLa cells stably transfected with the SteA effector gene. The expression of SteA in these epithelial cells, through the modification of different signal transduction pathways, resulted in an alteration of cell morphology and a decrease in the rate of spontaneous cell death, intercellular junctions and migration speed. cell phone (Cardinal-Muñoz srfJ is positively regulated by PhoP through the SsrA/SsrB two-component system and negatively by IolR, the repressor of genes involved in the use of myo-inositol as a carbon source (Cordero-Alba et al.is positively regulated by PhoP through the SsrA/SsrB two-component system and negatively by IolR, the repressor of genes involved in the use of myo-inositol as a carbon source (Cordero-Alba srfJ is positively regulated by PhoP through the SsrA/SsrB two-component system and negatively by IolR, the repressor of genes involved in the use of myo-inositol as a carbon source (Cordero-Alba Salmonella is positively regulated by PhoP through the SsrA/SsrB two-component system and negatively by IolR, the repressor of genes involved in the use of myo-inositol as a carbon source (Cordero-Alba Salmonella is positively regulated by PhoP through the SsrA/SsrB two-component system and negatively by IolR, the repressor of genes involved in the use of myo-inositol as a carbon source (Cordero-Alba et al.is positively regulated by PhoP through the SsrA/SsrB two-component system and negatively by IolR, the repressor of genes involved in the use of myo-inositol as a carbon source (Cordero-Alba
SseK1 is part of a family of effectors that catalyze the transfer of N-acetylglucosamine to arginine residues of certain host proteins. Our group has shown that SseK1 has a role in the virulence of Salmonella SseK1 is part of a family of effectors that catalyze the transfer of N-acetylglucosamine to arginine residues of certain host proteins. Our group has shown that SseK1 has a role in the virulence of sseK1 SseK1 is part of a family of effectors that catalyze the transfer of N-acetylglucosamine to arginine residues of certain host proteins. Our group has shown that SseK1 has a role in the virulence of et al.SseK1 is part of a family of effectors that catalyze the transfer of N-acetylglucosamine to arginine residues of certain host proteins. Our group has shown that SseK1 has a role in the virulence of
SseK1 is part of a family of effectors that catalyze the transfer of N-acetylglucosamine to arginine residues of certain host proteins. Our group has shown that SseK1 has a role in the virulence of Pseudomonas aeruginosaSseK1 is part of a family of effectors that catalyze the transfer of N-acetylglucosamine to arginine residues of certain host proteins. Our group has shown that SseK1 has a role in the virulence of S. enterica serovar Typhimurium in which we have expressed the PcrV antigen from P. aeruginosa in fusion with the SseJ effector of Salmonella. Mice immunized with this vaccine that were later infected with P. aeruginosa . Mice immunized with this vaccine that were later infected with et al.. Mice immunized with this vaccine that were later infected with
. Mice immunized with this vaccine that were later infected with
Representative bibliography
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(2019). A Live & . Mice immunized with this vaccine that were later infected with (2019). A Live Salmonella enterica. Front Microbiol 6(2019). A Live
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(2019). A Live & . Mice immunized with this vaccine that were later infected with (2019). A Live Salmonella (2019). A Live Salmonella (2019). A Live J Biol Chem (2019). A Live(2019). A Live
(2019). A Live & . Mice immunized with this vaccine that were later infected with (2019). A Live Salmonella enterica. J Bacteriol (2009). Relevant role of fibronectin-binding proteins in(2019). A Live
(2019). A Live & . Mice immunized with this vaccine that were later infected with (2019). A Live Salmonella (2019). A Live Biochem Biophys Res Commun (2019). A Live(2019). A Live
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(2014). Patterns of expression and translocation of the ubiquitin ligase SlrP in & . Mice immunized with this vaccine that were later infected with (2014). Patterns of expression and translocation of the ubiquitin ligase SlrP in Salmonella (2014). Patterns of expression and translocation of the ubiquitin ligase SlrP in J Bacteriol (2014). Patterns of expression and translocation of the ubiquitin ligase SlrP in(2014). Patterns of expression and translocation of the ubiquitin ligase SlrP in
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(2014). Patterns of expression and translocation of the ubiquitin ligase SlrP in & (2014). Patterns of expression and translocation of the ubiquitin ligase SlrP in (2014). Patterns of expression and translocation of the ubiquitin ligase SlrP in Biochem J (2014). Patterns of expression and translocation of the ubiquitin ligase SlrP in(2014). Patterns of expression and translocation of the ubiquitin ligase SlrP in