Advanced search
Combine gene, variant, phenotype, region and year filters
Every result shows the extracted entities next to the sentences that support them; rows for the searched entities come first.
Transparent by designEvery result links extracted entities to its source sentence and publication identifier.
Knowledge-base search
About your search
IRF3 and inflammatory bowel disease are reported together in 1 article.
Gene
IRF3
- HGNC
- HGNC:6118
10articles
10mentions
0variants with confirmed gene link
Most co-reported phenotypes (articles)
Phenotype
Inflammatory bowel disease
693articles
693mentions
12co-reported genes shown
Most co-reported genes (articles)
Counts are literature co-mentions in SaudiVarKB, not clinical or causal assertions. Gene details: HGNC; variant status: ClinVar via dbSNP.
Publications
1 records shown · first 60Canagliflozin ameliorates ulcerative colitis via regulation of TLR4/MAPK/NF-κB and Nrf2/PPAR-γ/SIRT1 signaling pathways.
PMID 37898288 | DOI 10.1016/j.ejphar.2023.176166 · European journal of pharmacology · 2023 · 5 validated mentions
Evidence preview
| Type | Entity | Source evidence | Confidence | Extractor |
|---|---|---|---|---|
| gene | IRF3 | “Canagliflozin attenuates inflammation in AA-induced colitis, evidenced by significant and dose-dependently downregulation of p38 MAPK, NF-κB-p65, IKK, IRF3, and NADPH-oxidase as well as colonic levels of IL-6 and IL-1β and MPO enzymatic activity.” | 0.98 | hgnc_dict_v1 |
| phenotype | inflammatory bowel disease | “Ulcerative colitis (UC) is one of the most common subtypes of inflammatory bowel disease (IBD) that affects the colon and is characterized by severe intestinal inflammation.” | 0.98 | phenotype_alias_lexicon_v2 |
| gene | TLR4 | “Canagliflozin ameliorates ulcerative colitis via regulation of TLR4/MAPK/NF-κB and Nrf2/PPAR-γ/SIRT1 signaling pathways.” | 0.98 | hgnc_dict_v1 |
| gene | SIRT1 | “Canagliflozin ameliorates ulcerative colitis via regulation of TLR4/MAPK/NF-κB and Nrf2/PPAR-γ/SIRT1 signaling pathways.” | 0.98 | hgnc_dict_v1 |