Search Results - "Scolnick, Laura R"

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    Probing the role of the hyper-reactive histidine residue of arginase by Colleluori, Diana M., Reczkowski, Robert S., Emig, Frances A., Cama, Evis, Cox, J. David, Scolnick, Laura R., Compher, Kevin, Jude, Kevin, Han, Shoufa, Viola, Ronald E., Christianson, David W., Ash, David E.

    Published in Archives of biochemistry and biophysics (01-12-2005)
    “…Rat liver arginase (arginase I) is potently inactivated by diethyl pyrocarbonate, with a second-order rate constant of 113 M −1s −1 for the inactivation…”
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    Altering the Binuclear Manganese Cluster of Arginase Diminishes Thermostability and Catalytic Function by Scolnick, Laura R, Kanyo, Zoltan F, Cavalli, R. Christopher, Ash, David E, Christianson, David W

    Published in Biochemistry (Easton) (26-08-1997)
    “…Arginase is a thermostable (T m = 75 °C) binuclear manganese metalloenzyme which hydrolyzes l-arginine to form l-ornithine and urea. The three-dimensional…”
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    X-ray Crystallographic Studies of Alanine-65 Variants of Carbonic Anhydrase II Reveal the Structural Basis of Compromised Proton Transfer in Catalysis by Scolnick, Laura R, Christianson, David W

    Published in Biochemistry (Easton) (24-12-1996)
    “…The three-dimensional structures of A65F, A65L, A65H, A65T, A65S, and A65G human carbonic anhydrase II (CAII) variants have been solved by X-ray…”
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    Structure of a unique binuclear manganese cluster in arginase by Kanyo, Z F, Scolnick, L R, Ash, D E, Christianson, D W

    Published in Nature (London) (10-10-1996)
    “…Each individual excretes roughly 10 kg of urea per year, as a result of the hydrolysis of arginine in the final cytosolic step of the urea cycle. This reaction…”
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    Molecular Basis of Hyperargininemia: Structure-Function Consequences of Mutations in Human Liver Arginase by Ash, David E., Scolnick, Laura R., Kanyo, Zoltan F., Vockley, Joseph G., Cederbaum, Stephen D., Christianson, David W.

    Published in Molecular genetics and metabolism (01-08-1998)
    “…Hyperargininemia is a rare autosomal recessive disorder that results from a deficiency of hepatic type I arginase. At the genetic level, this deficiency in…”
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