Application | Comment | Organism |
---|---|---|
medicine | during acute H pylori infection, CagL dissociates ADAM17 from the integrin alpha(5)beta1 and activates ADAM17-dependent, nuclear factor-kappaB-mediated repression of HKalpha, i.e. gastric H, K-adenosine triphosphatase alpha-subunit. This might contribute to transient hypochlorhydria in patients with H pylori infection | Homo sapiens |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
AGS cell | - |
Homo sapiens | - |
Organism | Comment | Expression |
---|---|---|
Homo sapiens | infection of AGS cells with wild-type H pylori or an H pylori cagL-deficient isogenic mutant that also contains a wild-type version of cagL, P12DeltacagL/cagL, represses HKalpha promoter-Luc reporter activity and stimulates ADAM17 activity. Both responses are inhibited by point mutations in the nuclear factor-kappaB binding site of HKalpha or by infection with P12DeltacagL | up |
General Information | Comment | Organism |
---|---|---|
physiological function | small interfering RNA-mediated silencing of ADAM17 in AGS cells inhibits the repression of wild-type HKalpha promoter, i.e. gastric H, K-adenosine triphosphatase alpha-subunit promoter, and reduces ADAM17 activity and heparin-binding epidermal growth factor production, compared to controls | Homo sapiens |