Any feedback?
Please rate this page
(literature.php)
(0/150)

BRENDA support

Literature summary for 3.4.24.86 extracted from

  • Saha, A.; Backert, S.; Hammond, C.E.; Gooz, M.; Smolka, A.J.
    Helicobacter pylori CagL activates ADAM17 to induce repression of the gastric H, K-ATPase alpha subunit (2010), Gastroenterology, 139, 239-248.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.4.24.86

Application

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

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Source Tissue

Source Tissue Comment Organism Textmining
AGS cell
-
 Homo sapiens
-

Expression

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

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