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1 PPi is a linear uncompetitive inhibitor, suggesting that
2 PPi levels in the perfusates both in the liver and kidne
3 PPi triggers a series of reactions resulting in producti
4 PPi-mediated excision produces AZT-5'-triphosphate (AZTT
6 ristolochene synthase complexed with Mg(2+)3-PPi and ammonium or iminium analogues of bicyclic carboc
7 tics parameters for tryptophan-dependent (32)PPi exchange, specificity for tryptophan versus tyrosine
8 rcoal powder to separate it from excess [32P]PPi and then measuring [32P]ATP in a scintillation count
9 method follows the initial velocity of [32P]PPi incorporation into ATP by capturing the nucleotide o
10 ection of the enamel rods, were exposed to a PPi-stabilized supersaturated calcium phosphate (CaP) so
14 tension product is efficiently removed after PPi detection by either a chemical method or photolysis.
16 vessels in culture, suggesting that altered PPi metabolism could contribute to vascular calcificatio
19 disable the complexation between Cu(2+) and PPi, facilitating the formation of fluorescent CuNPs thr
24 The patient-derived cns increased ATP- and PPi-mediated AZTMP excision on an RNA template compared
27 zyme capacity was found for fructokinase and PPi-dependent phosphofructokinase during cell division a
30 corresponding nucleoside monophosphates and PPi and subsequently hydrolyzes the resultant PPi to Pi.
33 ntly, expression of alkaline phosphatase and PPi breakdown, further contributing to PPi accumulation.
34 ontrol pericellular concentrations of Pi and PPi include tissue-nonspecific alkaline phosphatase (TNA
35 inorganic pyrophosphate (PPi) production and PPi-generating nucleoside triphosphate pyrophosphohydrol
36 lowed by (2S,5S)-5-carboxymethyl proline and PPi is the last product released based on initial veloci
38 ion, appears to support matrix synthesis and PPi elaboration and to regulate MV composition and miner
39 rts the model for H(+)-PPases functioning as PPi synthases in the phloem by arguing that the increase
42 Both enzymes were functionally active in ATP-PPi exchange and aminoacylation assays, and showed simil
46 significantly reduced k(cat) values for ATP:PPi isotope exchange assays, suggesting that the Zn(2+)
50 's fluorescence; the recovery occurs because PPi complexes with Cu(2+), effectively sequestering the
51 hod relies on the strong interaction between PPi and Cu(2+), which would hamper the effective formati
53 e in response to inflammatory mediators, but PPi production fell, reflecting lower ectonucleotide pyr
57 amined whether reduced levels of circulating PPi, an antimineralization factor, is the sole mechanism
61 s and implements multiple enzymes to convert PPi to ATP that is, in turn, utilized to produce light a
63 first time analyzed the effect of decreased PPi on dental development in individuals with generalize
65 to measure the rate constant of diphosphate (PPi) dissociation during the prenyltransferase reaction
66 al studies demonstrate that the diphosphate (PPi) group of FPP resides in a binding pocket made up of
67 lribose 1-diphosphate) to yield diphosphate (PPi) and the nucleotide OMP (orotidine 5'-monophosphate)
77 e ability of IGF-1 to decrease extracellular PPi, an activity specific for the CILP-1 N-terminal doma
78 ess may be caused by decreased extracellular PPi levels and that the incisor phenotype is likely due
79 nction of ANKH causes elevated extracellular PPi levels, predisposing to CPPD crystal deposition.
80 ty and concordant increases in extracellular PPi, which are strongly associated with human aging-asso
81 ein variant promoted increased extracellular PPi in CH-8 cells, but unexpectedly, these ANKH mutants
82 t effects on the expression of extracellular PPi and the chondrocyte hypertrophy marker, type X colla
84 able to increase expression of extracellular PPi, with or without addition of TGFbeta (10 ng/ml) to t
85 isease by divergent effects on extracellular PPi and chondrocyte hypertrophy, which is likely to medi
87 e developed and evaluated two algorithms for PPi measurement from luminescence kinetics acquired from
90 tion, comparable only with the high K(m) for PPi (165.5 microM) in Tritrichomonas foetus HGXPRTase-ca
95 rophosphorylation occurs with a Kd value for PPi of 3.7 mm and a maximal rate constant of 11 s(-1).
98 y = polyP45 approximately = polyP25 > PPPi > PPi), with K(1/2) values ranging from 0.2 to 2.8 mM.
99 , utilized to produce light and to hydrolyze PPi for measurement of the steady state background lumin
100 n endomembranes, and rather than hydrolyzing PPi to create pmf, pmf is utilized to synthesize PPi.
107 g time-dependent fluorescence intensity into PPi (substrate) concentration, thus allowing calculation
108 ene mutation results in higher intracellular PPi concentration and lower extracellular concentration.
109 xpression caused elevations in intracellular PPi, the major effects of PC-1 and B10 were exerted in d
110 Interestingly, detection of intracellular PPi ions in model human cells could also be possible by
111 nd B10 increased the levels of intracellular PPi, but PC-1 and B10 appeared to act principally in dif
114 hat the factor that normally prevents PXE is PPi, which is provided to the circulation in the form of
118 e known role mineralization inhibitors, like PPi, play in the regulation of mineralized tissue format
122 ulose acetate dialyzer was 36%, and the mean PPi removal in five patients was 43 +/- 5 micromol, cons
123 ociated with the growing DNA strands and Mg2 PPi crystals during the rolling circle process, ultimate
124 nteractions among the activator (AMP or Mg2+.PPi), the enzyme, and GTP), to affect the energetic coup
127 gether with the crystal structure of the NMN.PPi.Mg2.enzyme complex, the reaction coordinate is defin
128 efficacy of bisphosphonates, nonhydrolyzable PPi analogs, in preventing ectopic mineralization in the
130 e bound to the active site in the absence of PPi, suggests that nucleotide binding stimulates PPi dis
131 inc complex and the complex upon addition of PPi have been demonstrated through atomic force microsco
132 in, we determined that the administration of PPi and the bisphosphonate etidronate to Abcc6(-/-) mice
133 atophore membranes as well as the amounts of PPi and polyP increased when bacteria were grown in the
134 , we show that non-hydrolyzable analogues of PPi, bisphosphonates, are potent inhibitors of T. cruzi
137 al is generated upon enzymatic conversion of PPi to ATP and ATP levels subsequently detected with fir
138 d the practical utility for the detection of PPi anions by "off-on" response rapidly in a label free
139 ue platform for the fluorogenic detection of PPi having a very low limit of detection (LOD) of 0.60x1
140 GO proved very valuable for the detection of PPi in unprecedented sensitivity over other competing io
142 reasing intracellular ATP and elaboration of PPi, a critical inhibitor of hydroxyapatite deposition.
143 r or plasmid transfection, and expression of PPi was assessed in cultured articular chondrocytes and
147 x found by NMR, but it decreased the K(I) of PPi 12-fold, suggesting direct coordination of the PPi p
148 ve, as yet unknown mechanism, independent of PPi, by which ABCC6 prevents ectopic mineralization unde
155 the side chain in S2, but in the presence of PPi and Mg(2+), the quinuclidine's cationic center inter
157 rated recently that endogenous production of PPi prevents calcification of rat aorta that are culture
159 d (250 versus 24 s(-1)), whereas the rate of PPi release decreased to approximately 58 s(-1) so that
161 ing followed by cysteine binding, release of PPi, binding of GlcN-Ins, followed by the release of Cys
162 ed during the experiment; the sensitivity of PPi detection is about 7 pg/ml or 15 pM of PPi in ATP-co
164 redispose to chondrocalcinosis by effects on PPi transport, but may also influence chondrocyte matura
165 ing through each pathway depends strongly on PPi concentration, with ligand binding redistributing th
166 alyze the hydrolysis of inorganic phosphate (PPi) to inorganic phosphate Pi, driving biosynthetic rea
171 , resulting in only a 27% increase in plasma PPi levels, led to a major reduction in acute and chroni
173 n ENPP1 in Enpp1(asj) mice normalized plasma PPi levels to that of wild-type mice and, consequently,
175 e of hepatic ABCC6 in contributing to plasma PPi levels, identifying liver as a target of molecular c
182 could be used as an analytical tool to probe PPi generation in a prototype polymerase chain reaction
183 propose that the dissociation of the product PPi after nucleotide addition produces the protein confo
186 nt increase in expression of genes promoting PPi synthesis and extracellular transport, namely Enpp1
189 e natural substrates, NMN and pyrophosphate (PPi), the intrinsic KIEs of [1'-(14)C], [1-(15)N], [1'-(
190 bean (Vigna radiata L.), and pyrophosphate (PPi)- or ATP-dependent acidification was monitored using
194 ith Ufm1 and ATP, and its ATP-pyrophosphate (PPi) exchange activity was inhibited by both AMP and PPi
195 at Ras was capable of binding pyrophosphate (PPi) with a dissociation constant of 26 microM and that
197 pper nanoparticles (CuNPs) by pyrophosphate (PPi), a novel label-free turn-on fluorescent strategy to
198 e locked-open time induced by pyrophosphate (PPi), which reflects the stability of the full NBD dimer
200 processive primer extension, pyrophosphate (PPi) release was rate-limiting so that the average rate
201 to an unusually high K(m) for pyrophosphate (PPi) (323.9 microM) in the reverse reaction, comparable
202 ocumented role in hydrolyzing pyrophosphate (PPi) and capturing the released energy to pump H(+) acro
205 ATP synthesis, and inorganic pyrophosphate (PPi) generation, and the mineralizing potential of relea
206 for measurement of inorganic pyrophosphate (PPi) in adenosine 5'-triphosphate (ATP)-contaminated sam
207 t and metabolism of inorganic pyrophosphate (PPi) in control of mineralization, and as the likely exp
211 Elevated cartilage inorganic pyrophosphate (PPi) production and PPi-generating nucleoside triphospha
212 anced extracellular inorganic pyrophosphate (PPi) that promotes the deposition of calcium pyrophospha
213 combines the use of inorganic pyrophosphate (PPi) to control the onset and rate of enamel regeneratio
215 tein that regulates inorganic pyrophosphate (PPi) transport, are linked to autosomal-dominant familia
217 monophosphates and inorganic pyrophosphate (PPi), a strong inhibitor of mineralization that plays a
218 In the presence of inorganic pyrophosphate (PPi), the elongation complex catalyzes the reverse pyrop
225 ignificantly higher levels of pyrophosphate (PPi ) and short-chain polyphosphate (polyP), suggesting
226 possesses cellular levels of pyrophosphate (PPi ) at least 10 times higher than those of ATP and mol
228 te probe for the detection of pyrophosphate (PPi) in physiological conditions and in in vitro live me
233 s thought that the release of pyrophosphate (PPi) triggers reverse conformational changes in a polyme
234 raphysiologic accumulation of pyrophosphate (PPi), a strong inhibitor of hydroxyapatite formation, an
237 ith DNA templates showed that pyrophosphate (PPi) dissociation was fast after nucleotide incorporatio
238 sequence DNA by detecting the pyrophosphate (PPi) group that is generated when a nucleotide is incorp
239 2)) deletion in exon 9 of the pyrophosphate (PPi) transporter ANK leads to CMD-like features in an An
241 lytica ACK (EhACK) which uses pyrophosphate (PPi)/inorganic phosphate (Pi) (acetyl phosphate + Pi [Fo
242 zation of the H(+)-PPase with pyrophosphate (PPi) and short and long chain polyphosphates (polyPs) bu
247 imino) methyl)-4 methyl phenol]) could sense PPi anion through "turn-on" colorimetric and fluorimetri
248 1.2Zn can selectively and specifically sense PPi among all the other biologically important anions in
254 suggests that nucleotide binding stimulates PPi dissociation and occurs before polymerase translocat
257 dissociation constant of 26 microM and that PPi and GMP, but neither alone, synergistically potentia
262 sistence in tissues of mice, suggesting that PPi and polyP are essential for the parasite to resist t
265 rs to be a universal module that assists the PPi release even in multi-subunit RNAPs with charge faci
267 /-) rats were significantly reduced, but the PPi levels in the liver perfusates of wild-type rats wer
268 e PPi release in T7 RNAP is initiated by the PPi dissociation from two catalytic aspartic acids, foll
270 We have thus tentatively identified the PPi-binding loop in G. lamblia GPRTase, and attributed t
274 king them highly sensitive regulators of the PPi level in response to the changes in cell energy stat
275 from this first mutagenic exploration of the PPi motif in any adenylyltransferase is that the residue
278 ere we investigated detailed dynamics of the PPi release process in a single-subunit RNA polymerase (
279 ined a jump-from-cavity kinetic model of the PPi release utilizing extensive nanosecond MD simulation
283 nd that it exhibits weak binding affinity to PPi relative to NTP, suggesting a mechanism in which PPi
284 s three cns showed a higher ratio of ATP- to PPi-mediated excision, indicating that some cn mutations
285 he reaction, the cleavage of the P-O bond to PPi, corresponds to the highest point on the free energy
290 ates the extent of fluorescence recovery to [PPi], making the PPECO2-Cu(2+) system a sensitive and se
291 The motif appears to be unique to the N-type PPi synthetase family, and mutations in it are linked, i
294 st to MSCs treated with dexamethasone, where PPi levels did not fall and mineralization was fuelled b
296 tive to NTP, suggesting a mechanism in which PPi is rapidly released after each nucleotide addition a
298 reveal hPolbeta in an open conformation with PPi bound in the active site, thereby strongly suggestin
299 rted to chromatographically fractionate with PPi-generating nucleotide pyrophosphatase phosphodiester
300 uinuclidine's cationic center interacts with PPi and three Mg(2+), mimicking a transition state invol
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