Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.26.9 (
ribonuclease
)
6,589
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Although the AE1 chloride/bicarbonate exchanger of the red blood cell is among the most thoroughly investigated of membrane transport proteins, less is known about the related
AE2
polypeptide of parietal cells. We have studied enzymatic deglycosylation of native
AE2
polypeptide in gastric mucosal membranes from pig and rabbit. Deglycosylation of
AE2
was maximal at low ionic strength. Deglycosylation of
AE2
in membranes was preferentially inhibited by bicarbonate compared with other anions. This inhibition was maximal at alkaline pH and was not evident after detergent solubilization of
AE2
. Deglycosylation of
AE2
increased its susceptibility to proteolytic degradation, but the presence of bicarbonate protected against this degradation. Bicarbonate failed to inhibit deglycosylation of the membrane glycoproteins AE1 and gastric H(+)-K(+)-adenosinetriphosphatase beta-subunit or deglycosylation of the soluble glycoproteins fetuin and
ribonuclease
B. These data suggest that bicarbonate induces a conformational change in
AE2
that can protect the polypeptide from deglycosylation and proteolysis. Pig
AE2
was purified in sodium dodecyl sulfate, and its monosaccharide composition was determined after blotting onto polyvinylidene fluoride membrane.
AE2
was found to be devoid of sialic acid, with a composition suggestive of the presence of lactosamine-type chains.
...
PMID:HCO3(-)-dependent conformational change in gastric parietal cell AE2, a glycoprotein naturally lacking sialic acid. 877 47
