Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.1.1 (hexokinase)
 5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

By combining field and experimental investigations, we were able to study several new aspects of fundamental problems concerning human and animal schistosomiasis in Senegal. Because of the controversy about the identity of Schistosoma curassoni and the possibly connected zoonosis, this parasite has been described once more. A great variety of experimental techniques were used. The eggs of S. curassoni are significantly smaller than those of the two other African species of Schistosoma we know of in ruminants (S. bovis and S. mattheei). But eggs of S. curassoni cannot be distinguished from those of the human, pathogenic S. haematobium. The study of the tegument of adult male worms shows a clear difference between S. bovis on one hand, and S. curassoni and S. haematobium on the other hand. S. bovis' tubercles are well formed, but have no stings at all. The tubercles of S. haematobium and of S. curassoni definitely possess stings. S. curassoni, S. haematobium and S. bovis are also clearly different as to their development in hamsters (Mesocricetus auratus). S. curassoni develops more rapidly and gets bigger than S. bovis and S. haematobium. Finally, different enzymatic systems allow us to distinguish S. curassoni from other schistosoma's of the haematobium group. S. curassoni has a typical pattern for phosphoglucomutase and hexokinase, differing from S. haematobium's patterns. In S. bovis, it differs by the patterns of phosphoglucomutase, glucosephosphate-isomerase, hexokinase and acid phosphatase. Epidemiological studies proved that, in Senegal, Bulinus guernei is the main vector of S. bovis, Bulinus senegalensis of S. haematobium (Northern Senegal) and Bulinus umbilicatus of S. curassoni and S. haematobium (Southern Senegal). There is no indication to consider S. curassoni as a zoonosis. When ruminants are infested by S. curassoni, the symptoms are light and the most important lesions can be found in the liver, the intestines and, in a lesser degree, in the bladder. S. curassoni develops easily in laboratory animals, giving severe lesions in liver and bowels. That makes it an interesting new model for studying the pathogenesis of schistosomes of the haematobium group and the action of new anthelmintics to be used against them.
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PMID:[Schistosoma species in Senegal with special reference to the biology, epidemiology and pathology of Schistosoma curassoni Brumpt, 1931]. 219 9

DNA encoding a Schistosoma mansoni hexokinase (SHEX) was amplified from cDNA by the polymerase chain reaction using opposing oligonucleotide primers designed to hybridize with two short segments of hexokinase coding sequences that are well-conserved through evolution. The resulting DNA fragment was then used as a probe to identify a full-length hexokinase cDNA clone. SHEX cDNA encodes a 50-kDa protein that is approximately 46% homologous to rat hexokinase, 40% to rat glucokinase, and 34% to yeast hexokinase A. SHEX coding DNA was expressed within Escherichia coli cells and the 50-kDa recombinant product (rSHEX) was partially purified. Mice repeatedly immunized with rSHEX produced antibodies which recognize rSHEX but this offered no significant protection against subsequent cercarial challenge. On Western blots, rSHEX is weakly recognized by antisera against rat brain hexokinase but not by sera from three strains of mice experimentally infected with S. mansoni parasites or from numerous human schistosomiasis patients. Thus, unlike other reported S. mansoni glycolytic enzymes, hexokinase appears to be poorly immunogenic during schistosome infection and of limited potential as a vaccine candidate.
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PMID:Schistosoma mansoni hexokinase: cDNA cloning and immunogenicity studies. 782 9