Dataset Information

TBK1 mediates NOD2 and TLR2 mediated PI31 phosphorylation

ABSTRACT: We sought to identify the residue on which PI31 is phosphorylated following NOD2 and TLR2 activation. We immunoprecipitated endogenous PI31 from cellular extracts of THP1 cells stimulated with MDP and PAM3CSK4, and then conducted LC-MS/MS analysis on the immunoprecipitated material.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Macrophage

SUBMITTER: Nicola Ternette

LAB HEAD: Nicola Ternette

PROVIDER: PXD013248 | Pride | 2026-05-28

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	FL0385_MSQ892_20161212_DanieleCorridoni_MP.mgf	Mgf
	FL0385_MSQ892_20161212_DanieleCorridoni_MP.pride.mgf.gz	Mgf
	FL0385_MSQ892_20161212_DanieleCorridoni_MP.raw	Raw
	FL0385_MSQ892_20161212_DanieleCorridoni_US.mgf	Mgf
	FL0385_MSQ892_20161212_DanieleCorridoni_US.pride.mgf.gz	Mgf

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Publications

NOD2 and TLR2 Signal via TBK1 and PI31 to Direct Cross-Presentation and CD8 T Cell Responses.

Corridoni Daniele D Shiraishi Seiji S Chapman Thomas T Steevels Tessa T Muraro Daniele D Thézénas Marie-Laëtitia ML Prota Gennaro G Chen Ji-Li JL Gileadi Uzi U Ternette Nicola N Cerundolo Vincenzo V Simmons Alison A

Frontiers in immunology 20190430

NOD2 and TLR2 recognize components of bacterial cell wall peptidoglycan and direct defense against enteric pathogens. CD8<sup>+</sup> T cells are important for immunity to such pathogens but how NOD2 and TLR2 induce antigen specific CD8<sup>+</sup> T cell responses is unknown. Here, we define how these pattern recognition receptors (PRRs) signal in primary dendritic cells (DCs) to influence MHC class I antigen presentation. We show NOD2 and TLR2 phosphorylate PI31 via TBK1 following activation i ...[more]

PMID: 31114588

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Project description:Instability in the composition of gut bacterial communities, referred as dysbiosis, has been associated with important human intestinal disorders such as CrohnM-bM-^@M-^Ys disease and colorectal cancer. Here, we show that dysbiosis coupled to Nod2 or Rip2 deficiency suffices to cause an increased risk for intestinal inflammation and colitis-associated carcinogenesis in mice. Aggravated epithelial lesions and dysplasia upon chemical-induced injury associated with loss of Nod2 or Rip2 can be prevented by antibiotics or anti-IL6R treatment. Nod2-mediated risk for intestinal inflammation and colitis-associated tumorigenesis is communicable through maternally-transmitted microbiota even to wild-type hosts. Disease progression was identified to drive complex NOD2-dependent changes of the colonic-associated microbiota. Reciprocal microbiota transplantation rescues the vulnerability of Nod2-deficient mice to colonic injury. Altogether, our results unveil an unexpected function for NOD2 in shaping a protective assembly of gut microbial communities, providing a rationale for intentional manipulation of genotype-dependent dysbiosis as a causative therapeutic principle in chronic intestinal inflammation. Analysis used RNA extracted from colonic mucosa of untreated, antibiotics-treated or metronidazole-treated C57Bl/6J and Nod2-deficient mice in CAC model. Direct comparisons were performed as follow: C57Bl/6J untreated mice vs Nod2-deficient untreated mice, C57Bl/6J antibiotics-treated mice vs Nod2-deficient antibiotics-treated mice, C57Bl/6J metronidazole-treated mice vs Nod2-deficient metronidazole-treated mice, C57Bl/6J untreated mice vs C57Bl/6J antibiotics-treated mice, C57Bl/6J untreated mice vs C57Bl/6J metronidazole-treated mice, Nod2-deficient untreated mice vs Nod2-deficient antibiotics-treated mice, Nod2-deficient untreated mice vs Nod2-deficient metronidazole-treated mice. Indirect comparisons with control data were made across multiple arrays with raw data pulled from different channels for data analysis.