about
Guidelines for the use and interpretation of assays for monitoring autophagySalmonella effectors within a single pathogenicity island are differentially expressed and translocated by separate type III secretion systemsStructure-Function Analysis of DipA, a Francisella tularensis Virulence Factor Required for Intracellular ReplicationThe Francisella tularensis pathogenicity island encodes a secretion system that is required for phagosome escape and virulence.Dissemination of invasive Salmonella via bacterial-induced extrusion of mucosal epithelia.A Legionella pneumophila effector protein encoded in a region of genomic plasticity binds to Dot/Icm-modified vacuolesAcid phosphatases do not contribute to the pathogenesis of type A Francisella tularensis.The Francisella O-antigen mediates survival in the macrophage cytosol via autophagy avoidance.Host-microbe interaction systems biology: lifecycle transcriptomics and comparative genomics.Brucella coopts the small GTPase Sar1 for intracellular replicationFTT0831c/FTL_0325 contributes to Francisella tularensis cell division, maintenance of cell shape, and structural integrity.Bacterial avoidance of phagocytosis.Noncanonical inflammasome activation of caspase-4/caspase-11 mediates epithelial defenses against enteric bacterial pathogensEnteropathogenic Escherichia coli (EPEC) attachment to epithelial cells: exploiting the host cell cytoskeleton from the outside.Low dose vaccination with attenuated Francisella tularensis strain SchuS4 mutants protects against tularemia independent of the route of vaccination.Virulence factors of the human opportunistic pathogen Serratia marcescens identified by in vivo screeningBrucella modulates secretory trafficking via multiple type IV secretion effector proteins.Phagocytic receptors dictate phagosomal escape and intracellular proliferation of Francisella tularensis.Selective subversion of autophagy complexes facilitates completion of the Brucella intracellular cycle.Cytosolic clearance of replication-deficient mutants reveals Francisella tularensis interactions with the autophagic pathwaySurviving inside a macrophage: the many ways of Brucella.LRSAM1, an E3 Ubiquitin ligase with a sense for bacteria.The early phagosomal stage of Francisella tularensis determines optimal phagosomal escape and Francisella pathogenicity island protein expression.Direct and indirect impairment of human dendritic cell function by virulent Francisella tularensis Schu S4.Postreplication Roles of the Brucella VirB Type IV Secretion System Uncovered via Conditional Expression of the VirB11 ATPase.Bacteria, the endoplasmic reticulum and the unfolded protein response: friends or foes?The changing nature of the Brucella-containing vacuole.Avoidance and Subversion of Eukaryotic Homeostatic Autophagy Mechanisms by Bacterial Pathogens.Secreted Effectors Encoded within and outside of the Francisella Pathogenicity Island Promote Intramacrophage Growth.Objections to the transfer of Francisella novicida to the subspecies rank of Francisella tularensisA Brucella Type IV Effector Targets the COG Tethering Complex to Remodel Host Secretory Traffic and Promote Intracellular Replication.Brucella Intracellular Replication Requires Trafficking Through the Late Endosomal/Lysosomal CompartmentOf Microbes and Membranes: Pathogenic Subversion of Host Cell ProcessesEpistatic Interplay between Type IV Secretion Effectors Engages the Small GTPase Rab2 in the Brucella Intracellular CycleSopF, a phosphoinositide binding effector, promotes the stability of the nascent Salmonella-containing vacuole
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P50
description
researcher
@en
wetenschapper
@nl
հետազոտող
@hy
name
Jean Celli
@ast
Jean Celli
@en
Jean Celli
@es
Jean Celli
@nl
Jean Celli
@sl
type
label
Jean Celli
@ast
Jean Celli
@en
Jean Celli
@es
Jean Celli
@nl
Jean Celli
@sl
prefLabel
Jean Celli
@ast
Jean Celli
@en
Jean Celli
@es
Jean Celli
@nl
Jean Celli
@sl
P106
P1153
6701919408
P31
P496
0000-0002-6793-1788