Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1832526 (PCC)
 5,967 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

HlyU upregulates expression of the haemolysin, HlyA, of Vibrio cholerae. DNA sequence analysis indicates that HlyU is an 11.9 kDa protein containing a putative helix-turn-helix motif and belonging to a family of small regulatory proteins, including NoIR (Rhizobium meliloti), SmtB (Synechococcus PCC 7942) and ArsR (plasmids R773, Escherichia coli; pI258, Staphylococcus aureus; and pSX267, Staphylococcus xylosus). An hlyU mutant was constructed by insertional inactivation, and found to be deficient in the production of both the haemolysin and a 28 kDa secreted protein. The mutant was assessed for virulence in the infant mouse cholera model, revealing a 100-fold increase in the LD50. This suggests that HlyU promotes expression of virulence determinant(s) in vivo.
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PMID:The transcriptional activator HlyU of Vibrio cholerae: nucleotide sequence and role in virulence gene expression. 823 7

Mass occurrences of cyanobacteria, due to their inherent capacity for toxin production, specifically of microcystins (MC), have been associated with fish kills worldwide. The uptake of MC-LR and the sequence of pathological and associated biochemical changes was investigated in carp (Cyprinus carpio) in vivo over 72 h. Carp were gavaged with a single sublethal bolus dose of toxic Microcystis aeruginosa (PCC 7806) amounting to an equivalent of 400 microg MC-LR/kg body wt. Damage of renal proximal tubular cells and hepatocytes was observed as early as 1 h, followed by pathological changes in the intestinal mucosa at approximately 12 h postdosing. These alterations were characterized in hepatopancreas by a dissociation of hepatocytes, an early onset of apoptotic cell death, and delayed cell lysis. In the renal proximal tubules (P2) observations included increased vacuolation of individual tubular epithelial cells, apoptosis, cell shedding, and finally proteinaceous casts at the cortico-medullary junction. Concurrently with the pathological alterations, MC-immunopositive staining was observed in hepatocytes and the proximal tubular cells; the staining increasing in the hepatopancreas in intensity with increasing time postdosing. The presence of apoptotic cell death was determined using in situ fragment end labeling (ISEL) of the respective tissue sections and agarose gel electrophoresis for detection of DNA-laddering. The analysis of carp tissue extracts (hepatopancreas, kidney, GI tract, skeletal muscle, brain, heart, spleen, and gills) demonstrated MC-LR adducts having molecular weights of 38 kDa (putatively catalytic subunit of protein phosphatases-1 and -2A) and 28 kDa, respectively. An additional band was found to be present at 23 kDa in both hepatopancreas and kidney. The present data demonstrate that, in comparison to the pathological events in salmonids exposed to MC, where a slower development of pathology and primarily necrotic cell death prevails, the pathology in carp develops rapidly and at lower toxin concentrations. This is most likely due to a more efficient uptake of toxin, while the mechanism of cell death is primarily apoptosis.
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PMID:Pathological and biochemical characterization of microcystin-induced hepatopancreas and kidney damage in carp (Cyprinus carpio). 1073 46