Showing papers by "Jiri Stulik published in 2012"
TL;DR: It is proved that iTRAQ quantitation is fully compatible with cysteinyl peptide enrichment and is not influenced by the fractionation process, and CysTRAQ is a robust and straightforward method with potential application in quantitative proteomics experiments, i.e. as an alternative to the ICAT reagent approach.
40 citations
TL;DR: In this paper, the glycan structure modifying two C-terminal peptides of FTH_0069 was identified utilizing high resolution, high mass accuracy mass spectrometry, combined with in-source CID tandem MS experiments.
39 citations
TL;DR: A multi-stage study suggests cathelicidin as a candidate marker that should be considered for a panel of amniotic fluid proteins permitting identification of PPROM women with MIAC leading to HCA.
Abstract: Background
Preterm prelabor rupture of membranes (PPROM) complicated by microbial invasion of the amniotic cavity (MIAC) leading to histological chorioamnionitis (HCA) significantly impacts perinatal morbidity. Unfortunately, no well-established tool for identifying PPROM patients threatened by these disorders is available.
39 citations
TL;DR: It is shown that the iglH gene is necessary for intracellular growth and escape of F. tularensis from phagosomes and is avirulent in a mouse model of infection and persists in the organs for about three weeks after infection.
22 citations
TL;DR: It is demonstrated that B cell- mediated effector responses together with the induction of T cell-mediated immunity both play an important role in naïve and also in immunocompromised mice and this fact it would be appropriate to take into the account in the design of new vaccines.
14 citations
09 Mar 2012
TL;DR: This review will discuss aspects of F. tularensis intracellular fate within host macrophages, modulate host signaling pathways to benefit Francisella infection and summarize bacterial determinats involved in the process of phagosomal escape and intrACEllular replication.
Abstract: Summary Intracellular pathogen F. tularensis is a causative agent of tularemia disease and belongs to the most hazardeous pathogen worldwide, categorized by the Center for Disease Control and Prevention, USA (CDC) as a category A agent. However, no safe and licensed vaccine for prevention a F. tularensis infection is available for vaccination. Tularemia is manifested by several forms depending on a route of infection and virulence of a F. tularensis strain. Essential to a development of the disease is the ability to infect, survive and proliferate inside the mononuclear phagocytes, such as macrophages or dendritic cells. Therefore, this review will discuss aspects of F. tularensis intracellular fate within host macrophages, modulate host signaling pathways to benefit Francisella infection and finally, summarize bacterial determinats involved in the process of phagosomal escape and intracellular replication.
4 citations
01 Jan 2012
3 citations