A surprising sweetener from enteropathogenic<i>Escherichia coli</i>

Pearson, Jaclyn S.; Hartland, Elizabeth L.

doi:10.4161/19490976.2014.983762

Cited by 6 publications

(4 citation statements)

References 28 publications

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“…The best-characterized function of effectors of the NleB/SseK family is the inhibition of NF-κB signaling and of host cell death through the modification of death domain-containing proteins [9][10][11]14,23,24]. However, other ligands of NleB/SseK effectors have been reported [8].…”

Section: Discussionmentioning

confidence: 99%

Tubulin Folding Cofactor TBCB is a Target of the Salmonella Effector Protein SseK1

Araujo-Garrido

Baisón-Olmo

Bernal-Bayard

et al. 2020

IJMS

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Salmonella enterica serovar Typhimurium is a human and animal pathogen that uses type III secretion system effectors to manipulate the host cell and fulfill infection. SseK1 is a Salmonella effector with glycosyltransferase activity. We carried out a yeast two-hybrid screen and have identified tubulin-binding cofactor B (TBCB) as a new binding partner for this effector. SseK1 catalyzed the addition of N-acetylglucosamine to arginine on TBCB, and its expression promoted the stabilization of the microtubule cytoskeleton of HEK293T cells. The conserved Asp-x-Asp (DxD) motif that is essential for the activity of SseK1 was required for the binding and modification of TBCB and for the effect on the cytoskeleton. Our study has identified a novel target for SseK1 and suggests that this effector may have a role in the manipulation of the host cell microtubule network to provide a safe niche for this pathogen.

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Section: Discussionmentioning

confidence: 99%

Tubulin Folding Cofactor TBCB is a Target of the Salmonella Effector Protein SseK1

Araujo-Garrido

Baisón-Olmo

Bernal-Bayard

et al. 2020

IJMS

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“…This inhibition depended on the N-GlcNAc transferase activity of NleB1, which specifically modified Arg 235 and Arg 117 in the death domains of TRADD and FADD, respectively. These modifications blocked interactions between death domains, thereby disrupting inflammatory NF-κB signaling, caspase 8-dependent apoptosis, and necroptosis [173]. NleB from C. rodentium showed the same activity, and the mouse model of infection with this A/E pathogen demonstrated that the GlcNAc transferase activity was crucial for virulence [140,141].…”

Section: Targets Of Nleb/ssek Effectorsmentioning

confidence: 99%

Type III Secretion Effectors with Arginine N-Glycosyltransferase Activity

2020

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Type III secretion systems are used by many Gram-negative bacterial pathogens to inject proteins, known as effectors, into the cytosol of host cells. These virulence factors interfere with a diverse array of host signal transduction pathways and cellular processes. Many effectors have catalytic activities to promote post-translational modifications of host proteins. This review focuses on a family of effectors with glycosyltransferase activity that catalyze addition of N-acetyl-d-glucosamine to specific arginine residues in target proteins, leading to reduced NF-κB pathway activation and impaired host cell death. This family includes NleB from Citrobacter rodentium, NleB1 and NleB2 from enteropathogenic and enterohemorrhagic Escherichia coli, and SseK1, SseK2, and SseK3 from Salmonella enterica. First, we place these effectors in the general framework of the glycosyltransferase superfamily and in the particular context of the role of glycosylation in bacterial pathogenesis. Then, we provide detailed information about currently known members of this family, their role in virulence, and their targets.

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“… 52 NleB1 Effector NleB1 directly inactivates the death domains in several proteins (including TRADD, FADD, RIPK1, and TNFR1), and disrupts inflammatory NF-κB signaling, caspase 8-dependent apoptosis, and necroptosis. 53 , 54 NleE Effector NleE inhibits the activation of NF-κB by preventing the activation of IKKβ and consequently the degradation of the IκB NF-kB inhibitor. NleE also inhibits the nuclear translocation of NF-κB subunit p65, thereby reducing the IL-8 response during bacterial infection.…”

Section: Ois Encoding Virulence Factorsmentioning

confidence: 99%

“… 53 These modifications blocked the interactions between the death domains, thereby disrupting the inflammatory NF-κB signaling, caspase 8-dependent apoptosis, and necroptosis. 54 NleE is a highly conserved T3SS effector protein of A/E pathogens that is encoded in the same operon containing NleB1. NleE inhibits the activation of NF-κB by preventing the activation of IKKβ and consequently the degradation of the IκB NF-kB inhibitor.…”

Section: Ois Encoding Effectorsmentioning

confidence: 99%