| Id |
Subject |
Object |
Predicate |
Lexical cue |
| BEL:20003906 |
267-327 |
p(HGNC:TNF) increases bp(GOBP:"inflammatory response") |
denotes |
Tumor necrosis factor (TNF) alpha has defined proinflammator |
| BEL:20016824 |
1064-1262 |
p(MGI:Tnf) increases p(MGI:Mapk1,pmod(P)) |
denotes |
TNFalpha, but not IGF-I, induced tissue inhibitor of metalloproteinase-1 (TIMP-1) expression and reduced matrix metalloproteinases-2 activity and collagen degradation. TNFalpha also activated ERK1/2 |
| BEL:20063298 |
1064-1262 |
p(MGI:Tnf) decreases cat(p(MGI:Mmp2)) |
denotes |
TNFalpha, but not IGF-I, induced tissue inhibitor of metalloproteinase-1 (TIMP-1) expression and reduced matrix metalloproteinases-2 activity and collagen degradation. TNFalpha also activated ERK1/2 |
| BEL:20063676 |
1064-1262 |
p(MGI:Tnf) increases r(MGI:Timp1) |
denotes |
TNFalpha, but not IGF-I, induced tissue inhibitor of metalloproteinase-1 (TIMP-1) expression and reduced matrix metalloproteinases-2 activity and collagen degradation. TNFalpha also activated ERK1/2 |
| BEL:20033192 |
1264-1400 |
cat(p(MGI:Tnfrsf1b)) decreases cat(p(MGI:Mmp2)) |
denotes |
These responses to TNFalpha were absent in TNFR2-/- and TNFR1/2-/- myofibroblasts, whereas TNFR1-/- cells showed similar responses to WT |
| BEL:20033200 |
1264-1400 |
cat(p(MGI:Tnfrsf1b)) increases p(MGI:Mapk1,pmod(P)) |
denotes |
These responses to TNFalpha were absent in TNFR2-/- and TNFR1/2-/- myofibroblasts, whereas TNFR1-/- cells showed similar responses to WT |
| BEL:20033206 |
1264-1400 |
cat(p(MGI:Tnfrsf1b)) increases r(MGI:Timp1) |
denotes |
These responses to TNFalpha were absent in TNFR2-/- and TNFR1/2-/- myofibroblasts, whereas TNFR1-/- cells showed similar responses to WT |
| BEL:20002252 |
1761-2048 |
kin(p(HGNC:MAPK1)) increases bp(GOBP:"cell proliferation") |
denotes |
We conclude that TNFalpha and IGF-I may additively contribute to fibrosis during intestinal inflammation. TNFR2 is a primary mediator of fibrogenic actions of TNFalpha acting through ERK1/2 to stimulate proliferation and through STAT3 to stimulate TIMP-1 and inhibit collagen degradation |
| BEL:20038756 |
1761-2048 |
kin(p(MGI:Mapk1)) increases bp(GOBP:"cell proliferation") |
denotes |
We conclude that TNFalpha and IGF-I may additively contribute to fibrosis during intestinal inflammation. TNFR2 is a primary mediator of fibrogenic actions of TNFalpha acting through ERK1/2 to stimulate proliferation and through STAT3 to stimulate TIMP-1 and inhibit collagen degradation |
| BEL:20053876 |
1761-2048 |
p(MGI:Igf1) increases bp(GOBP:"inflammatory response") |
denotes |
We conclude that TNFalpha and IGF-I may additively contribute to fibrosis during intestinal inflammation. TNFR2 is a primary mediator of fibrogenic actions of TNFalpha acting through ERK1/2 to stimulate proliferation and through STAT3 to stimulate TIMP-1 and inhibit collagen degradation |
