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1 r and collected into an aLkaline fluorescein mercuric acetate (FMA) solution flowing under a controll
2 zinc in the crystal structure, analysis of a mercuric acetate derivative suggests a total of four Zn2
3     Activation experiments with amino phenyl mercuric acetate suggested that the 52-54 kDa gelatin-de
4 t of the bacterial detoxification system for mercuric and organomercurial species.
5                                         From mercuric binding titrations monitored by UV-vis spectros
6 d under which the nonphysiological substrate mercuric bromide (HgBr2) is rapidly turned over, both by
7 s the catalytic reduction of nitrosothiol by mercuric cation (Hg2+).
8 the mercury within [(N-acryloylamino)phenyl] mercuric chloride (APM) polyacrylamide gels, whereas mil
9  with arylisothiocyanates in the presence of mercuric chloride (HgCl(2)) yielded the corresponding re
10             In susceptible mice treated with mercuric chloride (HgCl(2)), administration of a blockin
11 y astrocyte cultures were exposed to MeHg or mercuric chloride (HgCl2) for 1 or 6 h.
12 lly susceptible H-2s mice, subtoxic doses of mercuric chloride (HgCl2) induce a complex autoimmune sy
13 oablation could confer the ability to resist mercuric chloride (HgCl2)-induced autoimmunity.
14 cetylcysteine, and DMSO inhibit injury after mercuric chloride administration.
15                                              Mercuric chloride also suppressed hypoxia- and Co-induce
16 esicles was partially inhibited (30%-39%) by mercuric chloride and phloretin, a non-specific channel
17              A comparison of formalin, PVA, (mercuric chloride based), and STF was done by aliquoting
18 ies and are often presented as one-vial, non-mercuric chloride fixatives that aim at performing the s
19 eased from S-nitrosothiols by treatment with mercuric chloride in an acidic environment.
20 induced by 5 mg/kg subcutaneous injection of mercuric chloride in BALB/c mice.
21                                 In contrast, mercuric chloride induces anti-fibrillarin Abs only in S
22 jected intraperitoneally at 0 and 24 h after mercuric chloride injection, or DMSO treatment was delay
23 yvinyl alcohol (PVA) containing the fixative mercuric chloride is considered the "gold standard" for
24                                     However, mercuric chloride is potentially hazardous to laboratory
25                                      Neither mercuric chloride nor DMSO affected catalase activity si
26 ated products was optimized with a magnesium/mercuric chloride reagent system and afforded desulfonyl
27                                   Until now, mercuric chloride supported on carbon is used as the cat
28                                              Mercuric chloride treatment of the enzyme results in con
29                            The inhibition by mercuric chloride was readily reversible by 2-mercaptoet
30 ation agents (rho-hydroxymercuribenzoate and mercuric chloride) irreversibly inhibit the ROC1-CUL1 ub
31 eon Sulfolobus solfataricus was sensitive to mercuric chloride, and low-level adaptive resistance cou
32            This AqpB mutant was inhibited by mercuric chloride, confirming the presence of a cysteine
33 e to hydrogen peroxide or menadione, but not mercuric chloride, resulted in significantly greater lac
34 fers resistance to erythromycin, gentamicin, mercuric chloride, streptomycin, tetracycline-minocyclin
35 id and severe injury after administration of mercuric chloride, with increased serum creatinine, incr
36                                 Formalin and mercuric chloride-based low-viscosity polyvinyl alcohol
37 pounds, many laboratories have switched from mercuric chloride-based Schaudinn's and polyvinyl alcoho
38 SO acts in part as an antioxidant to inhibit mercuric chloride-induced acute renal injury.
39                   DMSO partially prevented a mercuric chloride-induced decrease in glutathione peroxi
40  impairment and reduced tubular apoptosis in mercuric chloride-induced injury.
41 ATc1 expression in a PTC subpopulation after mercuric chloride-induced injury.
42  and their resealed ghosts in the dark via a mercuric chloride-inhibitable mechanism and with a speed
43 -fold; this water transport was inhibited by mercuric chloride.
44  395 nm upon addition of the thiol chelator, mercuric chloride.
45 in strains of mice, subtoxic doses of HgCl2 (mercuric chloride; mercury) induce a complex autoimmune
46 ury in Balb/c mice and Nfatc1(+/-) mice with mercuric chloride; the PTCs of Nfatc1(+/-) mice demonstr
47             p-Aminophenylmercuric acetate, a mercuric compound that is known to activate matrix metal
48                                     However, mercuric compounds specifically induced a conformational
49 of hOAT1 gained the ability to transport the mercuric conjugate 2-amino-4-(3-amino-3-carboxy-propylsu
50            Recently, we established that the mercuric conjugate of cysteine [2-amino-3-(2-amino-2-car
51 greater when the mercury is in the form of a mercuric conjugate of cysteine than in the form of a mer
52  conjugate of cysteine than in the form of a mercuric conjugate of cysteinylglycine or GSH.
53                    As Cys-S-Hg-S-Cys and the mercuric conjugate of Hcy (2-amino-4-(3-amino-3-carboxy-
54 rganic anion transporters in the uptake of a mercuric conjugate of Hcy in a mammalian cell.
55  that at least some of the luminal uptake of mercuric conjugates of cysteine occurs at the site of on
56  the JD for mercury in tubules perfused with mercuric conjugates of cysteine was reduced by approxima
57 ot been defined, current evidence implicates mercuric conjugates of cysteine, primarily 2-amino-3-(2-
58 e uptake of mercury in tubules perfused with mercuric conjugates of cysteinylglycine.
59                                         When mercuric conjugates of glutathione (GSH), cysteinylglyci
60 f S2 segments after they had been exposed to mercuric conjugates of glutathione of the laminal membra
61 mount of the luminal uptake of mercury, when mercuric conjugates of GSH are present in the lumen, is
62 the J,, for mercury in tubules perfused with mercuric conjugates of GSH.
63                                        Thus, mercuric conjugates of Hcy are potential transportable s
64 a from our laboratory have demonstrated that mercuric conjugates of Hcy are transported into these ce
65 ne transporter in the uptake and toxicity of mercuric conjugates of Hcy in any epithelial cell.
66 T1), the hypothesis that hOAT1 can transport mercuric conjugates of homocysteine (Hcy) was tested.
67  mitochondrial dehydrogenase) confirmed that mercuric conjugates of the thiols N-acetylcysteine (NAC)
68 trosothiol (SNO)/mol Hb tetramer (P = 0.032, mercuric-displaced photolysis-chemiluminescence assay),
69 redox cycling of elemental mercury Hg(0) and mercuric Hg(II) is critically important in affecting ino
70                                              Mercuric Hg(II) species form complexes with natural diss
71 ommunication we report a sensor for divalent mercuric (Hg(2)(+)) ions that we constructed from a pery
72 effective trapping agents for the removal of mercuric(II) ions from water.
73 ased scanometric method for the detection of mercuric ion (Hg (2+)).
74 rapid, sensitive, and selective detection of mercuric ion (Hg(2+)) in aqueous solution.
75 uid crystal (LC) sensor system for detecting mercuric ion (Hg(2+)) in aqueous solutions.
76 ensor and DNA chemistry for the detection of mercuric ion (Hg(2+)).
77 ure was found to be 0.2 and 0.1 ng g(-1) for mercuric ion and methylmercury, respectively.
78  Hg(II) binding of a red-emitting sensor for mercuric ion are presented.
79                       This suggests that the mercuric ion can be transferred between the two enzymes
80 cted activity assuming free diffusion of the mercuric ion from MerB to MerA.
81 TPCAD) prior to addition of the inducer, the mercuric ion Hg(II).
82 T complex have shown that the ligands to the mercuric ion in the complex consist of both sulfurs from
83 e effect of DMSO is not related to chelating mercuric ion or inhibiting its uptake.
84                                    Wild-type mercuric ion reductase (CCCC enzyme) possesses four cyst
85 f the N-terminal HMA domain (NmerA) of Tn501 mercuric ion reductase (MerA) aimed at identifying struc
86 hout any codon modification), which code for mercuric ion reductase (merA) and organomercurial lyase
87 ial lyase (MerB), and the second enzyme is a mercuric ion reductase (MerA).
88 ial lyase (MerB: RHg(I) --> RH + Hg(II)) and mercuric ion reductase (MerA: Hg(II) --> Hg(0)) enzymes,
89 CCAA enzyme) leads to a loss of steady-state mercuric ion reductase activity using Hg(SR)2 substrates
90 ations of Hg2+ in liquid media only when the mercuric ion reductase function is artificially inactiva
91 ome, expressing organomercurial lyase and/or mercuric ion reductase in the cytoplasm, endoplasmic ret
92  operon-lacZ fusions, point mutations in the mercuric ion reductase merA gene, and transcomplementati
93                                   The enzyme mercuric ion reductase MerA is the central component of
94 tance enzymes organomercurial lyase MerB and mercuric ion reductase MerA.
95 ctivated in cells, whereas cells with active mercuric ion reductase require micromolar concentrations
96                                              Mercuric ion reductase, MerA, converts toxic Hg2+ to the
97 he well characterized metal handling enzyme, mercuric ion reductase.
98                                 In bacterial mercuric ion reductases (MerA), which catalyze reduction
99  prepared either by electrodeposition from a mercuric ion solution or by simple contact of the Pt dis
100 igating possible effects of DMSO on cellular mercuric ion uptake, MDCK cells that were transfected wi
101 sting of the organomercurial lyase (MerB), a mercuric ion, and a molecule of the MerB inhibitor dithi
102                                              Mercuric ion, Hg(2+), forms strong complexes with thiola
103                                              Mercuric ion, Hg(II), inactivates generalized transcript
104 has been suggested that DMSO may chelate the mercuric ion, more recent studies suggest that it has an
105 w sensitivity to block of the conductance by mercuric ion.
106 ximal tubules, are the primary targets where mercuric ions accumulate and exert their toxic effects.
107 tual mechanisms involved in the transport of mercuric ions along the proximal tubule have not been de
108                                              Mercuric ions are highly reactive and form a variety of
109 own to be the primary cellular targets where mercuric ions gain entry, accumulate, and induce patholo
110 uence the magnitude and/or site of uptake of mercuric ions in the kidney.
111                                              Mercuric ions, which antagonize the copper-deficiency re
112   Treating the C. reinhardtii wild type with mercuric ions, which were shown to inhibit the binding o
113 y controlled by the methylation of inorganic mercuric mercury (Hg(II)) to MeHg in water, sediments, a
114 ltammetric stripping analysis of 20-120 pmol mercuric nitrate samples was performed with a calibratio
115 ly disposed alkene, when treated with either mercuric perchlorate or mercuric trifluoromethanesulfona
116  and were different from those of the simple mercuric perchlorate.
117                                 The use of a mercuric precursor favors a kit formulation since the me
118  simultaneously derepresses transcription of mercuric reductase (merA) by interacting with the archae
119  of volatilized metallic mercury produced by mercuric reductase (MerA) extracted from an Hg-resistant
120 e cultures and plantlets to express modified mercuric reductase (merA) gene constructs.
121               Mercury resistance mediated by mercuric reductase (MerA) is widespread among bacteria a
122  structure, E3 shares a common ancestor with mercuric reductase (merA), whereas goR is more related t
123 tive elemental mercury [Hg(0)] by a specific mercuric reductase (MerA).
124                                      GCR and mercuric reductase activities were assayed using enzyme
125    The enzyme had robust GCR activity but no mercuric reductase activity.
126 s transformed with bacterial genes (merA for mercuric reductase and merB for organomercurial lyase) f
127 r to that documented for the related enzymes mercuric reductase and NADH oxidase; only 1 FAD is reduc
128 nd by an active site double mutant (CCAA) of mercuric reductase in which the C-terminal cysteines 557
129 in contrast to the soil enzyme, the ATII-LCL mercuric reductase is functional in high salt, stable at
130 B/Hg/DTT complex acts as a substrate for the mercuric reductase MerA.
131 LCL, and here we describe a gene for a novel mercuric reductase, a key component of the bacterial det
132 ide dehydrogenase, glutathione reductase and mercuric reductase, thioredoxin reductase contains a red
133 ooperativity model such as that proposed for mercuric reductase.
134 Halobacterium sp. NRC-1 that is annotated as mercuric reductase.
135 thione reductase, thioredoxin reductase, and mercuric reductase.
136 Studies of natural water samples spiked with mercuric salts indicate that MS5 can rapidly detect Hg(I
137 ial of mercury decreased during the aging of mercuric sulfides (from dissolved to nanoparticulate and
138 nd were each amended with different forms of mercuric sulfides: dissolved Hg and sulfide, nanoparticu
139 tritional copper signaling nor the effect of mercuric supplementation, but rendered CRR1 insensitive
140 esis directly, the transport and toxicity of mercuric-thiol conjugates were characterized in a Madin-
141  treated with either mercuric perchlorate or mercuric trifluoromethanesulfonate, produce bicyclic imi

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