ライフサイエンスコーパス: L-aspartate

1 f adenylosuccinate from 6-phosphoryl-IMP and l-aspartate.

2 he purine ring into the alpha-amino group of l-aspartate.

3 omponent of peptidoglycan, and L-lysine from L-aspartate.

4 ransport of acidic amino acids, particularly l-aspartate.

5 ate/transition state analog N-phosphonacetyl-L-aspartate.

6 ition of the phosphonate of N-phosphonacetyl-l-aspartate.

7 ral intermediate analogue, N-phosphonomethyl-L-aspartate.

8 f the amide bond of the substrate, N-acetyl- l-aspartate.

9 was synthesized in 7 steps from beta-benzyl L-aspartate.

10 th products, phosphate (P(i)) and N-carbamyl-L-aspartate.

11 best inhibitor, competitive with respect to L-aspartate.

12 -glutamate first excreted and then destroyed l-aspartate.

13 st antagonism between CAIR and either ATP or L-aspartate.

14 500 s(-1) (at 6 degrees C) with increasing [L-aspartate].

15 tissue and K(m) parameters for GTP, IMP, and l-aspartate (12, 45, and 140 microm, respectively) simil

16 The channels were activated by L-aspartate (250-500 nM) in the presence of saturating g

17 -malic enzyme from Ascaris suum will utilize L-aspartate, (2S,3R)-tartrate, and meso-tartrate as subs

18 e significant response of WT cells to 3.2 nM L-aspartate, a concentration three orders of magnitude l

19 L- Aspartate-alpha-decarboxylase catalyzes the decarboxy

20 Homozygous lines expressing E. coli L- aspartate-alpha-decarboxylase had significantly great

21 The Escherichia coli pan D gene encoding L- aspartate-alpha-decarboxylase was expressed under a c

22 rowth of homozygous lines expressing E. coli L- aspartate-alpha-decarboxylase was less affected than

23 tothenate biosynthesis enzymes from E. coli, l-aspartate-alpha-decarboxylase (ADC) and ketopantoate r

24 l-Aspartate-alpha-decarboxylase (PanD) catalyzes the dec

25 for the events leading to maturation of the L-aspartate-alpha-decarboxylase (PanD) enzyme that conve

26 Our results indicated that E. coli L-aspartate-alpha-decarboxylase was correctly processed

27 topantoate hydroxymethyltransferase (KPHMT), L: -aspartate-alpha-decarboxylase (ADC), pantothenate sy

28 250 IU/L alanine aminotransferase and 420 IU/L aspartate aminotransferase 9 hours after gavage.

29 mg/dL), alanine aminotransferase (2288.82 U/L), aspartate aminotransferase (1251.76 U/L), gamma-glut

30 ver enzymes (alanine aminotransferase, 657 U/L, aspartate aminotransferase, 1401 U/L), blood urea (53

31 For instance, l-aspartate aminotransferase (l-AspAT) is inactivated by

32 As in L-aspartate aminotransferase (L-AspAT), the cofactor in

33 The high-resolution structure of l-aspartate ammonia-lyase from Escherichia coli has rece

34 The X-ray crystal structure of l-aspartate ammonia-lyase has been determined to 2.8 A r

35 Iontophoresis of l-aspartate, an NMDAR agonist, onto basket cell axon col

36 ts to hydrolyze N-acetylaspartate (NAA) into l-aspartate and acetate, but the connection between ASPA

37 etylation of N-acetyl-L-aspartate to produce L-aspartate and acetate.

38 l-Glutamate, l-aspartate and d-serine are simultaneously quantified i

39 in the de novo biosynthesis of AMP, coupling L-aspartate and IMP to form adenylosuccinate.

40 ate (CP) and l-aspartate to form N-carbamoyl-l-aspartate and inorganic phosphate.

41 ylaspartic acid (NAA) to produce acetate and L-aspartate and is the only brain enzyme that has been s

42 erfamily, is shown to mediate uptake of both L-aspartate and L-glutamate as well as having sensitivit

43 oscopy that purified recombinant PEB1a binds L-aspartate and L-glutamate with sub microM K(d) values.

44 ATP-dependent formation of L-asparagine from L-aspartate and L-glutamine, via a beta-aspartyl-AMP int

45 with ammonia-lowering therapy by l-ornithine l-aspartate and rifaximin orally for 4 weeks.

46 These compounds liberated L-aspartate and the fluorophore 8-hydroxypyrene 1,3,6-tr

47 Nonetheless, the Km value for L-aspartate and the Ki value for hadacidin (a competitiv

48 richia coli mediates attractant responses to L-aspartate and to maltose.

49 The conversion of ATP, L-aspartate, and 5-aminoimidazole-4-carboxyribonucleotid

50 Lactulose, probiotics, L-ornithine-L-aspartate, and potassium-iron-phosphate-citrate have b

51 din (a competitive inhibitor with respect to L-aspartate) are 29-57-fold lower in the presence of IMP

52 g pocket of the homologous GltPh coordinates L-aspartate as well as the sodium ion Na1.

53 The amino acid L-aspartate (ASP) is one of the most abundant excitatory

54 tructure and function of another PLP enzyme, l-aspartate beta-decarboxylase.

55 ion of dihydrodipicolinate from pyruvate and L-aspartate beta-semialdehyde (ASA).

56 ized slices of rat hippocampus to 400 microM L-aspartate-beta-hydroxamate for 8 min results in the co

57 partate = MPDC > beta-glutamate > L-CCG-IV = L-aspartate-beta-hydroxamate.

58 g(2+) interaction element) and loop 298-304 (L-aspartate binding element).

59 ely inhibits this enzyme by interfering with L-aspartate binding.

60 Data suggest that the monoanion of L-aspartate binds to enzyme and that the same general ba

61 ted by the structure with N-(phosphonacetyl)-L-aspartate bound).

62 ulfinic acid bound with higher affinity than L-aspartate but involved lower saturating rates, whereas

63 NADP-dependent dehydrogenase activity toward l-aspartate but no aspartate oxidase activity.

64 Remarkably, GltPh-M362T exhibited l-aspartate but not l-glutamate transport.

65 ated under high CO2, the canB mutant grew on L-aspartate but not on the key C3 compounds L-serine, py

66 of Thr(301) abolishes catalysis supported by l-aspartate, but has no effect on catalysis supported by

67 acellular messenger: enzymatic scavenging of l-aspartate, but not glutamate, blocked stimulation of C

68 f Thr(300) to alanine increases the K(m) for l-aspartate by 30-fold.

69 ersion of l-aspartate (l-Asp) to N-carbamoyl-l-aspartate by PyrB may reduce the amount of l-Asp avail

70 ylosuccinate forms from 6-phosphoryl-IMP and l-aspartate by the movement of the purine ring into the

71 ease the K(i) for dicarboxylate analogues of l-aspartate by up to 40-fold.

72 pyrimidine biosynthetic pathway, N-carbamyl-L-aspartate (CA-asp) is converted to L-dihydroorotate (D

73 r studies of other ligands (N-phosphonacetyl-L-aspartate, carbamyl phosphate plus malonate, phosphono

74 a high-affinity Na+-dependent L-glutamate/D,L-aspartate cell-membrane transport protein.

75 estimate of about 0.18 s(-1) for V/E(t) with L-aspartate compared to a value of 39 s(-1) obtained wit

76 hich catalyzes the deacetylation of N-acetyl-l-aspartate, correlate with Canavan Disease, a neurodege

77 ne from l-aspartate is a pyruvoyl-containing l-aspartate decarboxylase (PanD), the enzyme in M. janna

78 hii is a pyridoxal phosphate (PLP)-dependent l-aspartate decarboxylase encoded by MJ0050, the same en

79 ral arteries via binding to L-arginyl-glycyl-L-aspartate-dependent integrin receptors and prevented v

80 h the enzymatic inhibitor N-(phosphonacetyl)-L-aspartate did not induce CHOP.

81 The binding kinetics of L-aspartate differed from the binding kinetics of two al

82 natural substrates, carbamoyl phosphate and L-aspartate, do not induce in the Q137A enzyme the same

83 Val(273) and Thr(300) in the recognition of l-aspartate, even though these residues do not or cannot

84 reonine, or asparagine increase the K(m) for l-aspartate from 15- to 40-fold, and concomitantly decre

85 CYP46A1 is activated by l-glutamate (l-Glu), l-aspartate, gamma-aminobutyric acid, and acetylcholine,

86 igated to products (phosphate and N-carbamyl-l-aspartate) has been determined at 2.37 A resolution (R

87 L-glutamate as well as having sensitivity to L-aspartate hydroxamate.

88 Values of D- and L-aspartate in different tissues agreed well with those

89 eins capable of converting l-isoaspartate to l-aspartate in small peptide substrates.

90 ), which catalyzes deacetylation of N-acetyl-L-aspartate in the central nervous system (CNS), result

91 Upon binding l-aspartate in the presence of a saturating concentratio

92 The beta-RAH-P then condenses with l-aspartate in the presence of ATP to form 4-(beta-d-rib

93 apillary electrophoresis to determine D- and L-aspartate in tissue samples obtained from rats.

94 rifluoromethyl)benzoyl]amino]phenyl]methoxy]-l-aspartate increased neuronal loss after OGD or NMDA, a

95 eas the bisubstrate analog N-phosphonoacetyl-L-aspartate induced a significant change in the scatteri

96 where the enzyme producing beta-alanine from l-aspartate is a pyruvoyl-containing l-aspartate decarbo

97 coli taxis toward the amino acid attractant L-aspartate is mediated by the Tar receptor.

98 Strikingly, in subunit II, carbamoyl L-aspartate is observed binding near the binuclear metal

99 Our results indicate that conversion of l-aspartate (l-Asp) to N-carbamoyl-l-aspartate by PyrB m

100 random motility and chemotactic responses to L-aspartate, L-serine, L-leucine, and Ni(2+) of WT and c

101 -quality data on the efficacy of L-ornithine L-aspartate (LOLA) in patients with cirrhosis and bouts

102 e presence of IMP, hadacidin (an analogue of L-aspartate), Mg2+, and GTP.

103 rs after the induction of ischemia, N-acetyl-L-aspartate (NAA) levels in the lateral caudo-putamen an

104 Genetic suppression of N-acetyl-l-aspartate (NAA) synthesis, previously shown to block b

105 hed in oligodendroglia that cleaves N-acetyl-l-aspartate (NAA) to acetate and l-aspartic acid, elevat

106 mutations that prevent cleavage of N-acetyl-L-aspartate (NAA), resulting in marked elevations in cen

107 The glutamate analog N-methyl-D,L-aspartate (NMA) affects the regulation of GnRH and LH

108 In contrast, N-methyl-L-aspartate (NMLA) reverse microdialysed in to the LH (6

109 acellular calcium following iontophoresis of l-aspartate or two-photon uncaging of glutamate.

110 proteolysis in the presence of a substrate, L-aspartate, or an inhibitor, DL-TBOA in the presence of

111 each substrate and enhanced selectivity for L-aspartate over D-aspartate and L-glutamate, and lost t

112 rofile to that of GltPh, with preference for l-aspartate over l-glutamate.

113 minoaspartate is generated via the action of l-aspartate oxidase (NadB), which catalyzes the first st

114 d S after treatment with N-(phosphonoacetyl)-L-aspartate (PALA) at concentrations that normally lead

115 on in response to the drug N-phosphonoacetyl-L-aspartate (PALA) compared to TGF-beta 1-expressing con

116 f p53, cells treated with N-(phosphonacetyl)-L-aspartate (PALA) continue to synthesize DNA slowly and

117 oacetamide and malonate, or N-phosphonacetyl-l-aspartate (PALA) have previously been made in the spac

118 midine synthesis inhibitor N-phosphonoacetyl-l-aspartate (PALA) produced a pyrimidine deficit with mi

119 of the bisubstrate analogue N-phosphonacetyl-L-aspartate (PALA) required to activate the mutant enzym

120 not develop resistance to N-(phosphonacetyl)-L-aspartate (PALA), an inhibitor of the synthesis of pyr

121 t by the antimetabolite, N-(phosphonoacetyl)-L-aspartate (PALA), is defective, whereas p53 induction

122 the bisubstrate analogue N-(phosphonoacetyl)-l-aspartate (PALA), or the aspartate analogue succinate,

123 he phosphonate moiety of N-(phosphonoacetyl)-l-aspartate (PALA), the carboxylates of Asp interact wit

124 transcarbamylase inhibitor N-phosphonacetyl-l-aspartate (PALA), which blocks the synthesis of pyrimi

125 The potent inhibitor N-phosphonacetyl-l-aspartate (PALA), which combines the binding features

126 When treated with N-(phosphonacetyl)-L-aspartate (PALA), which inhibits pyrimidine nucleotide

127 rily in G1 in response to N-(phosphonacetyl)-L-aspartate (PALA), which starves them for pyrimidine nu

128 the UMP synthesis inhibitor N-phosphonacetyl-L-aspartate (PALA), which, in addition to selecting for

129 frequency of formation of N-(phosphoacetyl)-L-aspartate (PALA)-resistant (PALA(R)) colonies, mediate

130 with the bisubstrate analog N-phosphonacetyl-L-aspartate (PALA).

131 y the bisubstrate analog, N-(phosphonacetyl)-L-aspartate (PALA).

132 eotides by treatment with N-(phosphonacetyl)-l-aspartate (PALA).

133 y enzyme in the presence of N-phosphonacetyl-L-aspartate (PALA).

134 solid state or in solution, poly(beta-benzyl-L-aspartate) (PBLA) differs from the other helical polya

135 may destabilize binding of the ligand to the L-aspartate pocket by disrupting hydrogen bonds that mai

136 osphoryl-IMP and GDP (hadacidin absent), the L-aspartate pocket can retain its fully ligated conforma

137 deoxy-6-phosphoryl-IMP and GDP, however, the L-aspartate pocket is poorly ordered.

138 major factor in destabilizing ligands at the L-aspartate pocket.

139 pathway in which the nucleophilic attack of l-aspartate precedes the phosphoryl transfer reaction.

140 Binding isotope effects for l-aspartate reacting with the inactive K258A mutant of P

141 At low millimolar [Na(+)], the addition of L-aspartate resulted in complex time courses of W130 flu

142 ps lead to the biosynthesis of L-lysine from L-aspartate semialdehyde and pyruvate in bacteria.

143 that 6-deoxy-5-ketofructose 1-phosphate and l-aspartate semialdehyde are precursors to DHQ.

144 on, undergoes an aldol condensation with the l-aspartate semialdehyde to form 2-amino-3,7-dideoxy-D-t

145 tween 6-deoxy-5-ketofructose 1-phosphate and l-aspartate semialdehyde to yield ADH.

146 tions activated with bath-applied N-methyl-D,L-aspartate, serotonin, and dopamine, the coordination b

147 As shown here, l-aspartate substituted for l-glutamate in this context

148 Control retinas given vehicle, N-methyl-L-aspartate (the L-isomer of NMDA), or NMDA plus MK-801,

149 se to lactulose, probiotics, and L-ornithine-L-aspartate therapy in minimal hepatic encephalopathy (M

150 nse to lactulose, probiotics and L-ornithine-L-aspartate therapy in minimal hepatic encephalopathy ha

151 steine sulphinate = L-CCG-III = L-cysteate = L-aspartate = threo-beta-hydroxyaspartate > trans-PDC >

152 carboxylase catalyzes the decarboxylation of L -aspartate to generate Beta-alanine and carbon dioxide

153 artoacylase catalyzes hydrolysis of N-acetyl-l-aspartate to aspartate and acetate in the vertebrate b

154 lian aspartate racemase (DR), which converts L-aspartate to D-aspartate and colocalizes with D-aspart

155 eaction between carbamoyl phosphate (CP) and l-aspartate to form N-carbamoyl-l-aspartate and inorgani

156 DH and thus decrease the rate of the coupled L-aspartate to oxaloacetate to malate sequence only if t

157 e that catalyzes the beta-decarboxylation of l-aspartate to produce l-alanine and CO(2).

158 that catalyzes the deacetylation of N-acetyl-L-aspartate to produce L-aspartate and acetate.

159 rikingly, after addition of N-phosphonacetyl-l-aspartate to the enzyme, the transition rate was more

160 The induction of sodium-depending L-aspartate transport was inhibited by single amino acid

161 of glutamine synthetase (GS) and L-Glutamate/L-Aspartate Transporter (GLAST) functions.

162 lial L-glutamate transporter and L-glutamate/L-aspartate transporter) along the abscess margins.

163 amma-benzyl-L-glutamate and poly-beta-benzyl-L-aspartate under conditions in which their molecular or

164 or the bisubstrate analogue N-phosphonacetyl-L-aspartate unexpectedly leads to the reformation of hex

165 contrast to the wild type transporter, only l-aspartate was able to activate the uncoupled anion con

166 However, the K(m) of this mutant for l-aspartate was increased approximately 30-fold.

167 ) at 70 degrees C for the decarboxylation of l-aspartate was measured for the recombinant enzyme.

168 ating, step-like additions of the attractant L-aspartate were measured.

169 mutant enzymes ligated with N-phosphonacetyl-L-aspartate, were similar to that observed for the unlig

170 more than a 4-fold increase in the K(m) for l-aspartate, while increasing k(cat) by 3-fold.

171 A Km of approximately 0.80 mM for l-aspartate with a specific activity of 0.09 mumol min(-

172 iate by His41 may require the association of L-aspartate with the active site.