Proteomics

Dataset Information

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Inherited defect in ST6GalNAc1 reveals roles of sialylation in intestinal homeostasis


ABSTRACT: Chronic inflammatory bowel disease (IBD) causes disability, suffering and risk of colon cancer in over 30 million people globally. Here, we investigate 3 kindreds of IBD with mutations in the N-acetylgalactosamide alpha-2,6-sialyltransferase 1/ST6GALNAC1 (ST6) glycosyltransferase gene that is uniquely expressed in the goblet cells (GCs). These mutations cause defective sialic acid (SA) conjugation, elimination of the onco-antigen S-Tn (Sialyl-Tn), and altered glycosylation of the MUC2 protein, a key component of intestinal mucus. Decreased MUC2 sialylation increases susceptibility to bacterial proteolytic degradation and compromises the gastrointestinal (GI) mucus barrier. Mice harboring the patient ST6 mutations recapitulate human colitis and reveal that defective sialylation causes dysbiosis, butyrate overproduction, and impaired GI stem cell proliferation during injury. Thus, this new genetic disease illustrates how sialylation controls host-microbe homeostasis and reveals several new potential approaches to IBD treatment.

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (human) Mus Musculus (mouse)

TISSUE(S): Epithelial Cell, Colon

DISEASE(S): Colon Cancer

SUBMITTER: Yanlong Ji  

LAB HEAD: Kuan-Ting Pan

PROVIDER: PXD028239 | Pride | 2022-03-17

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
202010-uniprot-human-sp.fasta Fasta
All._raw_data_and_corresponding_experiment.xlsx Xlsx
Glycans-HT29.xlsx Xlsx
Glycans-LS180.xlsx Xlsx
Glycans-Mice_ICEs.xlsx Xlsx
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