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1 ese altered enzymes were also insensitive to phenylglyoxal.
2 espectively, may explain their resistance to phenylglyoxal.
3 100, and sensitivity to N-ethylmaleimide and phenylglyoxal.
5 nophenyl)pyrimidin-2-amine (3) and 4-methoxy-phenylglyoxal (4), while eudistidine B (2) was synthesiz
9 ondrial GPAT with arginine-modifying agents, phenylglyoxal and cyclohexanedione, inactivated the enzy
10 odification of arginines and histidines with phenylglyoxal and diethyl pyrocarbonate, respectively, r
11 hly purified enzyme to N-ethylmaleimide, F-, phenylglyoxal, and diethylpyrocarbonate, both substrates
13 ATP and CTP), N-ethylmaleimide, propranolol, phenylglyoxal, and divalent cations (Ca(2+), Mn(2+), and
15 date, sodium fluoride, N-ethylmaleimide, and phenylglyoxal but was not significantly affected by lipi
16 ics in presence of alpha,beta-diones such as phenylglyoxal, cyclohaxanedione, and 2,3-butadione sugge
17 ous substitutions in both pyrazole amine and phenylglyoxal derivatives, enabling the synthesis of var
19 inactivation of the tritrichomonal enzyme by phenylglyoxal follows time-dependent and concentration-d
21 astinal, iodoacetamide, iodoacetic acid, and phenylglyoxal gave substantial inhibition, and methyl bo
23 ted alpha-ketoesters and cyclic ketones with phenylglyoxal hydrates were realized with cinchona alkal
24 om the cyanobacterium Anabaena PCC 7120 with phenylglyoxal in 50 mM Hepes, pH 8.0, at 25 degrees C re
28 total homocitrulline, and biotin-conjugated phenylglyoxal labeling and Western blot to detect carbam
30 ctrometry (MS/MS) was used to identify three phenylglyoxal-modified Arg residues in monomeric rabbit
31 ospray ionizaton Fourier-transform MS of the phenylglyoxal-modified CK that had lost approximately 80
33 room temperature between pyrazole amine and phenylglyoxal monohydrate in the presence of Na(2)-eosin
34 synthetase by the arginine-specific reagents phenylglyoxal or p-hydroxyphenylglyoxal inactivates the
36 was reductive cross-coupling with methyl- or phenylglyoxal promoted by SmI(2), resulting in either 5-
37 e pyrophosphorylase with the arginyl reagent phenylglyoxal resulted in complete desensitization to fr
38 itrulline-specific chemical probe, rhodamine-phenylglyoxal (Rh-PG), which we show can be used to inve
42 inine-specific modifiers 2,3-butanedione and phenylglyoxal were found to be inactivators, and inactiv
43 e sulfite oxidase was rapidly inactivated by phenylglyoxal, yielding a modified protein with kinetic