Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.3.1 (Mg2+-ATPase)
 1,484 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Escherichia coli O11 belongs to Shiga toxin-producing Escherichia coli (STEC), which can cause food-borne disease, hemorrhagic colitis, and hemolytic-uremic syndrome (HUS) in humans. Because of its character of specificity, the O-antigen gene cluster provides the best material for the selection of molecular markers which can be used for rapid genotyping of bacterial strain. In this study, the E.coli O11 O-antigen gene cluster was amplified by Long-range PCR and was sequenced using Shotgun-sequencing approach. Twelve open reading frames were assigned functions on the basis of homology in the E. coli O11 O-antigen gene cluster, including UDP-N-acetyl glucosamine-4-epimerase gene (gne), genes responsible for the biosynthesis of GDP-L-fucose (gmd, fcl, gmm, manC, manB), glycosyl transferase genes, O-unit flippase gene (wzx) and O-antigen polymerase gene (wzy). By polymerase chain reaction against representative stains for all the 166 E. coli and 43 Shigella O serotypes, two genes and four pairs of primers were identified to be specific to E. coli O11. Further PCR was done to detect E. coli O11 from the environmental specimens, and the sensitivities for detecting E.coli O11 from the pork and dejecta specimens were 0.25 cfu/g and 2.5 x 10(3) cfu/g, respectively. Moreover, eight probes were designed and proved to be unique to E. coli O11, which provides the basis for a sensitive test of the rapid detection of E. coli O11 by DNA microarray method.
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PMID:[Sequence of Escherichia coli O11 O-antigen gene cluster and identification of molecular markers specific to O11]. 1693 98

Shiga toxin-producing Escherichia coli (STEC) strains belonging to serogroup O145 are an important cause of hemorrhagic colitis and hemolytic uremic syndrome worldwide. Cattle and other animals are potential reservoirs for this pathogen. To develop PCR assays for detection and identification of E. coli O145, the wzx (O-antigen flippase) and wzy (O-antigen polymerase) genes in the O145 O-antigen gene cluster that are specific for this serogroup were selected as targets. Oligonucleotide primers complementary to regions in the E. coli O145 wzx and wzy genes were designed to perform PCR assays with DNA from strains of E. coli O145, non-O145 E. coli serogroups, and other bacterial genera. The assays were highly specific for E. coli O145. A multiplex PCR assay targeting the E. coli O145 wzx and wzy genes and the Shiga toxin 1 (stx(1)) and Shiga toxin 2 (stx(2)) genes and a real-time multiplex PCR assay targeting the O145 wzy, stx(1), and stx(2) genes were developed for detection of STEC O145. The assays were used for detecting STEC O145 in seeded ground beef, lettuce, and raw milk initially inoculated with ca. 2, 20, or 200 CFU/25 g or 25 mL after 8 or 20 h of enrichment at 42 degrees C in modified EC broth containing 20 mg/L of novobiocin. STEC O145 was detected in all samples inoculated with 2 CFU/25 g or 25 mL. The detection limit of the multiplex PCR assays was <or=7.9 x 10(4) CFU/mL, which corresponded to <or=400 CFU/PCR reaction. The PCR assays can be employed to identify enterohemorrhagic E. coli serogroup O145 and to detect low levels of the pathogen in food.
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PMID:PCR detection of enterohemorrhagic Escherichia coli O145 in food by targeting genes in the E. coli O145 O-antigen gene cluster and the shiga toxin 1 and shiga toxin 2 genes. 1943 8

Improving our understanding of the pathogenesis of chronic immune-mediated cholangiopathies such as primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC), as well as the development of novel diagnostic, prognostic and therapeutic tools for these disorders critically depends on easily reproducible animal models. Recently, several spontaneous mouse models for PBC (not requiring previous manipulations for breakdown of immunotolerance) have been reported, including NOD.c3c4 and NOD.c3c4-derived mice, IL-2Ralpha(-/-) mice, dominant negative TGF-beta receptor II mice and Ae2(a,b)(-/-) mice. To date, no animal model exhibits all of the attributes of PSC. Rodent models induced by bacterial cell components or colitis may help to explain the strong association between PSC and inflammatory bowel disease. Other models include direct injury to biliary epithelia, peribiliary vascular endothelia or portal venous endothelia. Mice with targeted disruption of the Mdr2 (Abcb4) gene encoding a canalicular phospholipid flippase (Mdr2(-/-) mice) spontaneously develop sclerosing cholangitis with macroscopic and microscopic features of human PSC. Another example for a transporter involved in the pathogenesis of sclerosing cholangitis is the cystic fibrosis transmembrane conductance regulator (CFTR/ABCC7). Xenobiotics and drugs may also lead to bile duct injury and biliary fibrosis via direct toxic and indirect immune-mediated injury. Hydrophobic bile acids, such as lithocholic acid, cause bile duct injury and destructive cholangitis with periductal fibrosis resembling sclerosing cholangitis. These models have enhanced our understanding of the pathogenesis of PBC and PSC and will hopefully result in improved treatment of these disorders.
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PMID:New insights into autoimmune cholangitis through animal models. 2046 Aug 97