Dataset Information

SEC16A forms a complex with PI31 and TBK1

ABSTRACT: To identify interaction partners of PI31, we immunoprecipitated PI31 from NOD2 and TLR2 stimulated DCs, followed by performing tryptic digestion and mass spectrometry analysis.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Dendritic Cell, Blood

SUBMITTER: Nicola Ternette

LAB HEAD: Nicola Ternette

PROVIDER: PXD013249 | Pride | 2026-05-28

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	20160324_Daniele_RUN2_Progenesis_Mascot.mgf	Mgf
	20160324_Daniele_RUN2_Progenesis_Mascot.pride.mgf.gz	Mgf
	F189845.mzid.gz	Mzid
	F189845.pride.mztab.gz	Mztab
	FL0111a_DC_NT_3_neg.raw	Raw

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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.