Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The oral cephalosporins: cefatrizine and cephaloglycine inhibit the L-leucine absorption in vivo on rat jejunum. 2. This inhibition is dose and time dependent and the effect is irreversible. 3. These antibiotics have a systemic effect on L-leucine absorption. 4. The inhibition of these antibiotics affect only leucine transport, without affecting the diffusion. 5. Cefatrizine and cephaloglycine inhibit the basolateral (Na(+)-K+) ATPase activity in rat jejunum.
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PMID:Effect of cefatrizine and cephaloglycine on L-leucine absorption in rat jejunum. 198 Apr 43

(1) The serological diagnosis of PBC is possible in almost 100% of cases when appropriate methods and specific antigen preparations are used such as the purified ATPase fraction by ELISA for the detection of anti-M2, sonicated mitochondria by immunodiffusion for the demonstration of precipitating antibodies against M-A or M-B, and cell cultures by immunofluorescence for the detection of antibodies against nuclear dots. (2) The establishment of AMA profiles obtained by ELISA and CFT seems to be a sensitive approach to a better definition of the natural course of PBC. A distinction between a rather benign and a more progressive course seems especially possible in the presence of the AMA profiles A and B (anti-M9 and/or anti-M2-positive only by ELISA) versus D (anti-M2-, anti-M4-, anti-M8-positive in the CFT). (3) The analysis of cellular immune reactions in vitro and in vivo suggests an activation of cytotoxic T cells as well as a defect in the function of T suppressor cells. (4) Although the aetiology of PBC is unknown, the detection of MHC Class II antigens on bile duct epithelial cells in liver biopsies of patients with PBC but not of normal individuals may imply that an infectious agent being exposed in association with these MHC structures may trigger the disease. The inability of the immune system in controlling this infectious process would then lead to an ongoing inflammatory reaction which is responsible for the continuous destruction of bile ducts within portal triads.
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PMID:Immunology of primary biliary cirrhosis. 332 37

Staphylococcus aureus is frequently the initial bacterium isolated from young cystic fibrosis (CF) patients, and yet its role in CF disease progression has not been determined. Recent data from our lab demonstrates that S. aureus can invade and replicate within the CF tracheal epithelial cell line (CFT-1). Here we describe the finding that the fate of internalized S. aureus in CFT-1 cells differs from its complemented counterpart (LCFSN). S. aureus strain RN6390 was able to replicate within the mutant CFT-1 cells after invasion but not in the complemented LCFSN cells. At 1 h postinvasion, S. aureus containing vesicles within both cell lines acquired vacuolar-ATPase, lysosomal markers LAMP 1 and 2, and the lysomotrophic dye LysoTracker to a similar degree. However, at 4 h postinvasion, the percentage of S. aureus within CFT-1 cells associated with these markers decreased significantly compared to LCFSN, where the association approached 100%. Transmission electron microscopic analysis revealed that the majority of bacteria within CFT-1 cells were free in the cytosol at 4 h after invasion, whereas most S. aureus bacteria internalized by LCFSN cells remained within vesicles. These results demonstrate a fundamental difference in the fate of live S. aureus after invasion of CFT-1 versus LCFSN cell lines and may explain the propensity of S. aureus to cause chronic lung infection in CF patients.
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PMID:Staphylococcus aureus escapes more efficiently from the phagosome of a cystic fibrosis bronchial epithelial cell line than from its normal counterpart. 1662 92

Staphylococcus aureus colonizes the lungs of cystic fibrosis patients and treatment with antibiotics usually results in recurrent and relapsing infections. We have shown that S. aureus can invade and replicate within a cystic fibrosis epithelial cell line (CFT-1), and that these internalized bacteria subsequently escape from the endocytic vesicle. The accessory gene regulator, agr, in S. aureus has been shown to control the expression of a large number of secreted toxins involved in virulence. Here we show that an agr mutant of S. aureus strain RN6390 was unable to escape from the endocytic vesicle after invasion of the CFT-1 cells using markers of vesicular trafficking (LAMP-1 and 2, LysoTracker and Vacuolar-ATPase). Trafficking analysis of live S. aureus which did not express alpha-haemolysin, a specific agr regulated toxin, revealed a defect in vesicular escape that was undistinguishable from the trafficking defect exhibited by the agr mutant. Furthermore, overexpression of alpha-haemolysin under an inducible promoter in an agr mutant of S. aureus partially restored the phagosome-escaping phenotype of an agr mutant. These results demonstrate that the expression of agr is required for vesicular escape, and that biologically active alpha-haemolysin is required for S. aureus escape from the endocytic vesicle into the cytosol of CFT-1 cells.
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PMID:The expression of alpha-haemolysin is required for Staphylococcus aureus phagosomal escape after internalization in CFT-1 cells. 1846 45