Project: Taking IBD Genes from GWAS to Function to Drug Target
2022-01-01 – 2025-12-31
- Abstract
Inflammatory bowel disease (IBD), mainly represented by Crohn’s disease and ulcerative colitis, affects ~1/300 people in Western societies and is increasing all over the world. The risk to develop IBD varies between individuals and is in part determined by genetics. Genome Wide Association Studies (GWAS) have revealed specific risk loci in our genome and indicated many candidate causative genes for IBD. Moreover, they have potential to reveal hitherto uncharted functional territories and therapeutic targets. However, pinpointing the causative genes remains to be done for >95% of risk loci and requires post-GWAS studies that combine genomic and functional approaches. A major problem is that for most genomicists, identifying the candidaterisk genes is the end of the road as further prioritization requires expertise in the cellular, molecular and immunological changes that cause disease, and specialized techniques and models for their evaluation. The aim of the BRIDGE project is to assemble a team of top-notch Belgian laboratories with complementary expertise in genomics, immunology and cell biology to jointly develop a pipeline to systematically interrogate IBD-relevant functions of GWAS-identified candidate genes in order to select promising new therapeutic drug targets.
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Interleukin-33-activated basophils promote asthma by regulating Th2 cell entry into lung tissue
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- Journal Article
- A1
- open access
CARD14 signalosome formation is associated with its endosomal relocation and mTORC1-induced keratinocyte proliferation
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- Journal Article
- A1
- open access
Polo-like kinase 1 (PLK1) is a novel CARD14-binding protein in keratinocytes
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- Journal Article
- A1
- open access
Chimeric and mutant CARD9 constructs enable analyses of conserved and diverged autoinhibition mechanisms in the CARD-CC protein family
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- Miscellaneous
- open access
Novel role for linear ubiquitination in regulating NFAT1 stability
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- Journal Article
- A1
- open access
A20 is a master switch of IL-33 signalling in macrophages and determines IL-33-induced lung immunity
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- Journal Article
- A1
- open access
Normal lymphocyte homeostasis and function in MALT1 protease-resistant HOIL-1 knock-in mice
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- Journal Article
- A1
- open access
GTF3A mutations predispose to herpes simplex encephalitis by disrupting biogenesis of the host-derived RIG-I ligand RNA5SP141
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- Journal Article
- A1
- open access
CARD14 signalling ensures cell survival and cancer associated gene expression in prostate cancer cells