In particular, CJ conducted Van-Alexa568 staining and localization of Wag31 in cells expressing
different Alvespimycin solubility dmso mutant form of Wag31. HE conducted the enzymatic assay of Mur proteins. JJL performed the yeast two-hybrid experiments and Van-Alexa568 and localization of wild-type Wag31 in the presence of kinase overexpression. KH and MBS participated in culture and isolation of P60 samples for Mur enzyme assays and Raman spectrometry. JSH, SN and JYL constructed plasmids for localization and yeast two-hybrid assay. JWS, SHL, and SJR participated in the data analysis, and drafting and revision of the manuscript. DCC participated in the conception and design of the study, general supervision of the Mur enzyme assays. CMK participated in the design of the study, general supervision of the research, and critical revision of the manuscript. All authors read and approved the final version of the manuscript.”
“Background The capacity of pathogenic Salmonella to infect their hosts is often dependent on the ability of Salmonella to inject virulent factors directly into the host
cell cytosol through the type-three secretion system (TTSS). These injected bacterial proteins, called effectors, are of special interest in studies of 4SC-202 cell line host-pathogen interactions because effectors can manipulate host cell function [1, 2]. The effectors often have unique functions suited to a particular pathogen’s infection strategy. AvrA is a Salmonella effector that is translocated into host Enzalutamide clinical trial cells . The AvrA gene is present in 80% of Salmonella enterica serovar Typhimurium strains . Previous studies show that AvrA related family members include Yersinia virulence factor, YopJ, and
the Xanthomonas campestris pv.vesicatoria protein, AvrBsT . Analysis with MEROPS database shows that AvrA belongs to YopJ-like proteins and genes (family C55) in bacterial species (see details in http://merops.sanger.ac.uk). Many studies highlight the remarkable complexity of the TTSS system and AvrA’s function. Studies show that AvrA possesses enzyme activities to remove the ubiquitins from IκBα and β-catenin, to transfer acetyl to inhibit JNK activity and to bind with Erk2 and MKK7 [6–9]. Although AvrA is known to regulate diverse bacterial-host interactions, the eukaryotic Baricitinib targets of AvrA are still not completely identified. Gene expression array technology is a powerful tool that has been used to expand the understanding of host-pathogen interactions. A number of reports have described host transcriptional responses to bacterial infection using microarrays [9–14], but the global physiological function of Salmonella effector protein AvrA in vivo is unclear. A whole genome approach, combined with bioinformatics assays, is needed to elucidate the in vivo genetic responses of the mouse colon to Salmonella, and particularly to effector protein AvrA.