Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using isolated cells and subcellular fractions from pig gastric mucosa, antigenic structures with specific binding of IgG from sera of patients with auto-immune atrophic gastritis were characterized by means of immunoblotting and enzyme-linked immunosorbent assay. In immunoblotting experiments using mucosal cells as the antigen source, two dominating bands of 94 and 41 kDa were found. The two major antigens were identified as the H,K-ATPase (94 kDa), which constitutes the parietal cell acid pump, and pepsinogen (41 kDa) located in the chief cells. There was also a small but significant binding of antibodies to a preparation of Na,K-ATPase, an enzyme which is about 60% homologous to H,K-ATPase. Commercial preparations of hog gastric pepsinogen and pepsin bound pernicious anaemia IgG with equal efficacy. When sera from seven patients with the diagnosis pernicious anaemia were tested, all were found to contain auto-antibodies against H,K-ATPase as well as pepsinogen. In intact, isolated H,K-ATPase-containing vesicles the cytosolic part of the ATPase molecule is facing the outside of the vesicles. Both intact and trypsinized vesicles were incubated with patient sera and with a monoclonal antibody against H,K-ATPase. Pernicious anaemia IgG was found to bind to a cytosolic, trypsin-resistant structure, but the binding of the monoclonal antibody was lost upon trypsinization. The present results indicate that intracellular structures of the gastric mucosa, due to cell damage, may be exposed to immune-competent cells, which do not recognize these structures as 'self'.
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PMID:Characterization of antigenic structures in auto-immune atrophic gastritis with pernicious anaemia. The parietal cell H,K-ATPase and the chief cell pepsinogen are the two major antigens. 252 90

Using radioimmunoassays specific for essential processing sites of human progastrin in combination with chromatography before and after cleavage with trypsin and carboxypeptidase B, we have examined antral biopsy specimens and serum from 10 hypergastrinemic patients with fundic atrophic gastritis and 7 normal control subjects. Four types of processing were studied: N-terminal proteolysis (at the N-terminus of component I, gastrin 34, and gastrin 17); C-terminal proteolysis (at the C-terminus of the amide donor, glycine93 in preprogastrin); alpha-carboxyamidation (of phenylalanine92); and O-sulfation (of tyrosine87). The results show that progastrin during permanent G-cell hypersecretion is less completely processed with respect to C-terminal proteolysis, alpha-amidation, and tyrosine-sulfation. In contrast, the degree of N-terminal proteolysis is normal. Thus, the processing of progastrin adjacent to the active site of gastrin is more restrictively controlled than N-terminal processing during G-cell hypersecretion associated with pernicious anemia.
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PMID:Progastrin processing during antral G-cell hypersecretion in humans. 292 53

We found in four of five pernicious anemia gastric juices a partly degraded R binder which was cobalamin specific and has an apparent molecular weight of 60-70,000 daltons. Twenty-nine to 74% (4.8-27.0 ng/ml) of the corrinoid binding capacity could not be blocked by cobinamide (a noncobalamin corrinoid). The fifth pernicious anemia gastric juice and five nonpernicious anemia gastric juices had minimal amounts of this binder (2.5 and 2.2 +/- 1.4 ng/ml). Scatchard analysis revealed that cobalamin-specific R binder has 1000-fold lower affinity for cobinamide than cobalamin. Increasing quantities of trypsin and/or chymotrypsin digested increasing amounts of saliva R binder and an increasing percentage of the remaining digest-resistant R binder acquired cobalamin specificity. Partly degraded R binder in pernicious anemia gastric juice was resistant to further proteolysis. Cobalamin-specific R binder, perhaps produced in vivo by the action of refluxed pancreatic enzymes on swallowed R would preferentially bind ingested and/or biliary cobalamin rather than analogue and thereby could play a role in hastening the development of cobalamin deficiency in pernicious anemia.
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PMID:Cobalamin-specific R binder in pernicious anemia gastric juice: production by digestive enzyme action on saliva R binder. 299 28

The function of human purified colostral and gastrointestinal IgA has been studied by its ability to agglutinate common gastrointestinal organisms. Agglutinating activity was unaffected by trypsin or acid but it was abolished rapidly by pepsin. Both colostral and gastrointestinal IgA agglutinated a wide range of enteric organisms. Variations in this activity occurred between different individuals, and between different gastrointestinal sites in the same individual. In preliminary studies, saliva and IgA prepared from gastric and jejunal secretions in patients with pernicious anaemia showed a more uniform agglutination pattern than IgA prepared from the same sites in other patients. The agglutinin activity of IgA prepared from a particular site may be determined by the bacterial flora at that site. Agglutination methods for assessing the function of gastrointestinal antibody may be of value in the study of the possible roles of antibodies in inflammatory bowel disease.
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PMID:Bacterial agglutination studies with secretory IgA prepared from human gastrointestinal secretions and colostrum. 455 7

The apparent molecular size and charge of immunoreactive gastrin components were studied in sera from patients with pernicious anaemia or gastrinomas (the Zollinger-Ellison syndrome) by Sephadex gel filtration and aminoethylcellulose chromatography. The following serum components were distinguished: (1) a monophasic component I similar in size to proinsulin which was converted into ;little' gastrin I by trypsin digestion; (2) a biphasic component II, corresponding to ;big' gastrins I and II (Gregory and Tracy); (3) a biphasic component III corresponding to ;little' gastrins I and II (Gregory and Tracy); and (4) a biphasic component IV, corresponding to ;minigastrins' I and II (Gregory and Tracy). ;Big, big' gastrin, a plasma component found in the void volume of the Sephadex G-50 column by Yalow and Berson (1972) was undetectable in the sera investigated. A component in gastrinoma and antral mucosa extracts corresponding in size to ;big big' gastrin was detectable by the assay; the ;big big' gastrin fraction from gastrinoma tissue was heterogenous, with components of apparent MW 30 000-100 000. It is concluded that serum gastrin circulates in the form of at least four components, of which the three smaller ones are in pairs.
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PMID:Immunoreactive gastrin components in human serum. 482 Jun 33