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1 nsation of pantoate and beta-alanine to form pantothenate.
2 location, and kinetic constants for ATP and pantothenate.
3 competitively inhibit the phosphorylation of pantothenate.
4 e medium) in the absence of thiamine excrete pantothenate.
5 ate to D-(-)-pantoate in the biosynthesis of pantothenate.
6 ad a conditional requirement for thiamine or pantothenate.
7 cofactors including biotin, riboflavin, and pantothenate.
8 rds from labeled essential nutrients such as pantothenate.
9 of CoA) was replaced with [(13)C(3)(15)N(1)]-pantothenate.
10 between PanK-III and its substrates ATP and pantothenate.
11 evels of leaf Beta-alanine (1.2- to 4-fold), pantothenate (3.2- to 4.1-fold) and total free amino aci
13 ctive with an apparent K(m) of 28 microM for pantothenate-7-amino-4-methylcoumarin (pantothenate-AMC)
14 e hepatocytes (Hepa 1c1c7) in media in which pantothenate (a precursor of CoA) was replaced with [(13
15 uman malaria parasites rely on the uptake of pantothenate across the parasite plasma membrane for sur
17 dodiphosphate (AMPPNP).Mg(2+), AMPPNP.Mg(2+).pantothenate, ADP.Mg(2+).phosphopantothenate, and AMP ph
18 ies was optimized to >99% [(13)C(3)(15)N(1)]-pantothenate after three passages of the murine cells in
19 M for pantothenate-7-amino-4-methylcoumarin (pantothenate-AMC), which was converted to pantothenic ac
20 te kinase that showed evidence of binding to pantothenate, an essential nutrient Mtb synthesizes, but
21 ement of genes required for the synthesis of pantothenate, an essential vitamin deficient in the lous
22 rolling intracellular coenzyme A levels, and pantothenate analogs are growth-inhibiting antimetabolit
23 rasite Plasmodium falciparum have shown that pantothenate analogs interfere with pantothenate phospho
26 utilize the N-alkylpantothenamide family of pantothenate analogues as alternative substrates, thus m
29 the transplacental transfer of the vitamins pantothenate and biotin and the essential metabolite lip
30 is-Menten constant (Kt) for the transport of pantothenate and biotin in cDNA-transfected cells is 4.9
32 mation phase: the pentose phosphate pathway, pantothenate and CoA biosynthesis and ascorbate and alda
33 le, gluconeogenesis, glutathione metabolism, pantothenate and CoA biosynthesis, and butanoate metabol
34 ion of PfPAT and its ability to deliver both pantothenate and fenpropimorph makes it an attractive ta
37 the adenosine moieties are buried while the pantothenate and pyrophosphate groups of the coenzyme ar
39 ing phagosome is limiting for riboflavin and pantothenate and that Histoplasma virulence requires de
41 A Cryptococcus yeast produces the B-vitamin pantothenate, and co-culturing with Variovorax leads to
42 mine HCl, riboflavin, niacinamide, d-calcium pantothenate, and pyridoxine HCl; 50 microg each of d-bi
43 ated forms of pyridoxine, vitamin D, niacin, pantothenate, and riboflavin exist in nature, whereas gl
47 ty and immunogenicity of a double lysine and pantothenate auxotroph of Mycobacterium tuberculosis in
49 has been known that E. coli yhhK strains are pantothenate auxotrophs, but the role of YhhK in pantoth
51 terium glutamicum panD(+) gene corrected the pantothenate auxotrophy of a S. enterica yhhK strain, su
55 psis encoded homologues of the remaining two pantothenate biosynthesis enzymes from E. coli, l-aspart
56 findings highlight the importance of de novo pantothenate biosynthesis in limiting the intracellular
64 e reductase (EC 1.1.1.169), an enzyme in the pantothenate biosynthetic pathway, catalyzes the NADPH-d
66 , induces inward currents in the presence of pantothenate, biotin, and lipoate in a Na+-, concentrati
67 which transports the water-soluble vitamins pantothenate, biotin, and lipoate, from a placental chor
69 acterial pathogen that is able to synthesize pantothenate but is lacking the known ketopantoate reduc
70 children below the EAR for vitamins A and E, pantothenate, calcium, and fiber; 2) >10% above the ULs
72 , metal acquisition, and the biosynthesis of pantothenate, coenzyme A, thiamine, menaquinone, siderop
75 fPAT mediated survival of yeast cells in low pantothenate concentrations and restored sensitivity of
77 several proteins essential for the canonical pantothenate-cysteine-dependent CoA biosynthesis pathway
78 ts receiving 13.5 mmol choline plus 1.4 mmol pantothenate/d had a significant decline in urinary carn
81 ignificantly higher levels of phosphorylated pantothenate-derived metabolites and CoA in vivo and exc
82 ECF transporters for folate (ECF-FolT2) and pantothenate (ECF-PanT) into proteoliposomes, and assaye
84 intermediates, TCA cycle intermediates, and pantothenate expand dramatically in both mitochondrial d
85 olutely dependent on the acquisition of host pantothenate for its development within human erythrocyt
86 ives of purF mutants that no longer required pantothenate for thiamine-independent growth were isolat
88 tase (EC 6.3.2.1) catalyzes the formation of pantothenate from ATP, D-pantoate, and beta-alanine in b
89 rium tuberculosis catalyzes the formation of pantothenate from ATP, D-pantoate, and beta-alanine.
91 sotope exchange of [(14)C]-beta-alanine into pantothenate in the presence of AMP was observed, indica
94 hia coli incorporated pyridoxal, niacin, and pantothenate into pyridoxal 5'-phosphate, NAD, and coenz
97 ement of panE mutants for either thiamine or pantothenate is manifest only when flux through the puri
102 K-III in complex with one of its substrates (pantothenate), its product (phosphopantothenate) as well
105 CoA biosynthesis in bacteria and mammals is pantothenate kinase (CoaA), which governs the intracellu
106 In Bacillus anthracis, the novel type III pantothenate kinase (PanK(Ba); encoded by coaX) catalyze
107 al and animal coenzyme A (CoA) biosynthesis, pantothenate kinase (PANK) activity is critical in regul
124 disease have mutations in the gene encoding pantothenate kinase 2 (PANK2); these patients are said t
130 gulator, and antimetabolite binding sites on pantothenate kinase and provide a framework for studies
131 e structural information on Escherichia coli pantothenate kinase by determining the structure of the
138 of two new classes of compounds that inhibit pantothenate kinase from M. tuberculosis are described,
139 s, including the finding of mutations in the pantothenate kinase gene and ferritin light chain gene,
140 ow that HSS is caused by a defect in a novel pantothenate kinase gene and propose a mechanism for oxi
142 , especially given the existence of multiple pantothenate kinase genes in humans and multiple PanK2 t
143 spatial and chemical distribution of evolved pantothenate kinase immobilized onto two diverse, microp
146 trate the key role of feedback regulation of pantothenate kinase in the control of intracellular CoA
147 ns indicate that this type of "bifunctional" pantothenate kinase is conserved in other higher eukaryo
150 report here the characterization of a second pantothenate kinase of Arabidopsis, AtPANK2, as well as
151 The absence of feedback regulation at the pantothenate kinase step allows the accumulation of high
155 ate specificities associated with endogenous pantothenate kinase, the first enzyme in the CoA biosynt
156 icated in neurodegenerative diseases such as pantothenate kinase-associated neurodegeneration (PKAN)
162 den-Spatz syndrome, the disorder was renamed pantothenate kinase-associated neurodegeneration after d
163 e shown great potential for the treatment of pantothenate kinase-associated neurodegeneration and pro
165 PanK2(G521R), the most frequent mutation in pantothenate kinase-associated neurodegeneration, was de
177 ry properties exhibited by the family of the pantothenate kinases allowed the rate of CoA biosynthesi
178 , both active sites of the dimeric mammalian pantothenate kinases coordinately switch between the on
179 coside phosphotransferase [APH(3')-IIIa] and pantothenate kinases from Escherichia coli (EcPanK) and
182 quence that is more similar to the mammalian pantothenate kinases than the prototypical bacterial Coa
183 in human brain, distinguishing it from other pantothenate kinases that do not possess mitochondrial-t
185 CoaX regulates PanB abundance in response to pantothenate levels by modulating its vulnerability to p
186 ontrast plants expressing KPHMT had elevated pantothenate levels in leaves, flowers siliques and seed
188 delian randomization analysis that elevating pantothenate levels significantly contributes to the pro
189 lants are capable of de novo biosynthesis of pantothenate, making this pathway a potential target for
190 both purine and thiamine; however, exogenous pantothenate may be substituted for the thiamine require
192 the effects of supplementary choline and/or pantothenate on the carnitine and lipid status of free-l
194 hip between the cDNA-specific uptake rate of pantothenate or biotin and Na+ concentration is sigmoida
195 Low-RFI steers had greater abundances of pantothenate (P = 0.02) based on fold change (high/low R
196 lysis of DEGs in DeltaMAP3773c revealed that pantothenate (Pan) biosynthesis, polysaccharide biosynth
197 r proteins responsible for the conversion of pantothenate (Pan) to CoASH in Escherichia coli are cons
199 own that pantothenate analogs interfere with pantothenate phosphorylation and block asexual blood sta
200 n normal cells providing clear evidence that pantothenate phosphorylation was a rate-controlling step
201 teracting with the hydrophobic dome over the pantothenate pocket, which is also accessed by the beta-
202 beta expression eliminated the intracellular pantothenate pool and triggered a 13-fold increase in in
203 Fusobacteriia and/or greater proportions of pantothenate-producing bacteria, such as Flavobacteriia,
204 ns, was necessary and sufficient to increase pantothenate production and allow PurF-independent thiam
206 rences in the binding modes for both ATP and pantothenate substrates, and suggests that these differe
208 dent multivitamin transporter for biotin and pantothenate), SVCT (for vitamin C), and CaT1 (for Ca up
213 T), L: -aspartate-alpha-decarboxylase (ADC), pantothenate synthetase (PS) and ketopantoate reductase
216 antoate hydroxymethyltransferase (KPHMT) and pantothenate synthetase (PtS) catalyse the first and las
218 e reactions have therefore demonstrated that pantothenate synthetase catalyzes the formation of a pan
219 9, Q72, and K160 residues in M. tuberculosis pantothenate synthetase caused a greater than 1000-fold
220 hree-dimensional structural determination of pantothenate synthetase from Mycobacterium tuberculosis
223 [betagamma-(18)O(6)]-ATP was incubated with pantothenate synthetase in the presence of d-pantoate, a
226 tion studies showed the kinetic mechanism of pantothenate synthetase to be Bi Uni Uni Bi Ping Pong, w
231 In contrast to the uptake mechanisms for pantothenate, the cellular uptake mechanisms for PanSH a
232 ) coupled with hydrogen bonding of the C1 of pantothenate to Asp-127 suggests different interpretatio
236 vidence for an essential role of a candidate pantothenate transport in malaria transmission to Anophe
239 onal characterization of the first protozoan pantothenate transporter, PfPAT, from P. falciparum.
240 nts the growth defect of the yeast fen2Delta pantothenate transporter-deficient mutant and mediates t
243 armacological analyses, we show that altered pantothenate utilization dramatically alters the suscept
245 nce for the importance of the early steps of pantothenate utilization in the regulation of CoA biosyn
248 s in cell culture to include [(13)C(3)(15)N]-pantothenate (vitamin B(5)), a CoA precursor, instead of
255 fold), nicotinamide/vitamin B(3) (1.5-fold), pantothenate/vitamin B(5) (1.3-fold), and pyridoxine/vit
257 tions for the formation of pyrophosphate and pantothenate were determined using rapid quench techniqu
258 mational changes upon binding of folate than pantothenate, which could explain the kinetic difference
259 thiamine auxotrophs are predicted to produce pantothenate, which we show is required for growth of Va
260 thenate was prepared by hydrolysis of methyl pantothenate with Na(18)OH, followed by enzymatic phosph
261 ts that they bind in the same orientation as pantothenate with their alkyl chains interacting with th