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1 ctive groups that covalently bind amines and phenylhydrazine.
2 phenylacetylene, styrene, ethylbenzene, and phenylhydrazine.
3 II with either t-[(14)C]butylamine or [(14)C]phenylhydrazine.
4 ormation reaction between 5-methylisatin and phenylhydrazine.
5 including acetophenone, pyrazole amine, and phenylhydrazine.
8 ed BLO reacts in an irreversible manner with phenylhydrazine, an amine substrate analog, and catalyze
11 tion catalysed by HRP-C during turnover with phenylhydrazine and its vulnerability towards inactivati
12 ehyde endured a unique cascade reaction with phenylhydrazine and propargyl tosylate, yielding synthet
14 and glyoxylate, reaction of glyoxylate with phenylhydrazine, and oxidative conversion of phenylhydra
15 ing of CP47, D2, and D1 with methylamine and phenylhydrazine approached a one-to-one stoichiometry, a
17 aining intact LTQ in the apoBLO reacted with phenylhydrazine, both in the presence and absence of the
18 )-4,5,6-trihydroxyhexane-1,2-diylidene)bis(N-phenylhydrazine carbothioamide), was used to make a comp
20 alphaF55A MADH has also been determined with phenylhydrazine covalently bound to TTQ in the active si
23 ation of the cells with hydrogen peroxide or phenylhydrazine did not affect A23187-induced uptake of
24 from classical spot tests using aniline and phenylhydrazine dyes that enable molecular recognition o
27 reatment of a sulfidodiiron(II) complex with phenylhydrazine gave an isolable mixed-valence FeII-Fe(I
28 as the result of oxidative stress induced by phenylhydrazine, hydrogen peroxide, tert-butyl hydropero
29 interaction with nine fSWNTs, n-propylamine, phenylhydrazine, hydroxyl, phenydicarboxy, phenyl, sulfo
33 high bacterial load, features reproduced by phenylhydrazine-induced hemolysis or hemin administratio
34 were analyzed under basal conditions, after phenylhydrazine-induced hemolysis, and after induction o
35 eficient mice, we show that lack of ROCK1 in phenylhydrazine-induced oxidative stress model results i
41 l of beta-conditionally deficient mice after phenylhydrazine is severely compromised because of their
43 resonance Raman spectra of this adduct and a phenylhydrazine-labeled model compound of lysine tyrosyl
45 n inactivators of monoamine oxidase, namely, phenylhydrazine, N-cyclopropyl-alpha-methylbenzylamine,
47 mic iron availability (e.g., iron dextran or phenylhydrazine) on the induction, kinetics, and size of
48 layed during stress hematopoiesis induced by phenylhydrazine or by 5-fluorouracil, suggesting impairm
50 me by [1-14C]beta-aminopropionitrile, [U-14C]phenylhydrazine, or [35S]homocysteine thiolactone was ob
53 In this study, we present the advantage of phenylhydrazine (PHN) labeling for the detection and eff
54 displays intravascular hemolysis induced by phenylhydrazine (PHZ), as well as the role of intravascu
55 rence from wild-type mice in both normal and phenylhydrazine (PHZ)-induced stress erythropoiesis, PPA
57 w cells obtained from mice that had received phenylhydrazine plus control IgG or with marrow cells ob
58 ge and an accompanying spreading lesion with phenylhydrazine pretreatment (e.g., increases in circula
60 avascular hemolysis, induced by injection of phenylhydrazine, resulted in increased alanine aminotran
61 s study, stress induced by 5-fluorouracil or phenylhydrazine revealed a delay in the recovery of eryt
62 e and comparison to the oxidants diamide and phenylhydrazine revealed that oxidation does not partici
63 is in the adult, we compared the response to phenylhydrazine stress in 3 genetically deficient models
64 r, under extreme demand for porphyrins (e.g. phenylhydrazine stress), these adaptations appear inadeq
66 ve reagents (diamide, hydrogen peroxide, and phenylhydrazine) to cross-link sulfhydryl groups and wit
68 U-GM content to less than half that found in phenylhydrazine-treated control mice and nearly totally
70 throblasts were isolated from the spleens of phenylhydrazine-treated mice, and Epo stimulation result
71 revious studies using bone marrow cells from phenylhydrazine-treated, anemic mice, we find that both
73 o monitor thiol redox status during in vitro phenylhydrazine treatment and over the course of in vivo
76 wild-type and C30A mutant enzymes, although phenylhydrazine was 10 times more potent than N-cyclopro
79 ion of ferric APX with the suicide substrate phenylhydrazine yields predominantly (60%) a covalent ha