ライフサイエンスコーパス: L-aspartate

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

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

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

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

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

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

7 diated import and conversion of L-malate and L-aspartate.

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

9 acid (DABA), which is further catabolized to l-aspartate.

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

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

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

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

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

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

16 500 s(-1) (at 6 degrees C) with increasing [L-aspartate].

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

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

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

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

21 rs results in acute depletion of N-carbamoyl-L-aspartate, a pyrimidine biosynthesis intermediate, wit

22 L- Aspartate-alpha-decarboxylase catalyzes the decarboxy

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

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

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

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

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

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

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

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

31 250 IU/L alanine aminotransferase and 420 IU/L aspartate aminotransferase 9 hours after gavage.

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

33 e phosphatase (U/L), alanine transaminase (U/L), aspartate aminotransferase (U/L), and bilirubin tota

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

49 l intestine contained high and low levels of l-aspartate and l-malate respectively, whereas fumarate

50 which is exported by DcuABC in exchange for L-aspartate and L-malate.

51 SC_02373 as an LAL with high selectivity for L-aspartate and L-methionine substrates, specifically fo

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

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

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

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

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

57 nd uptake substrates, including L-glutamate, L-aspartate, and D-aspartate, using ion gradients.

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

59 l Na(+): substrate coupling stoichiometry as L-aspartate, and that the affinities (K(d) and K(m)) for

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 articles (poly(ethylene glycol)-poly[(benzyl-l-aspartate)-co-(N-(3-aminopropyl)imidazole-L-aspartamid

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

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

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

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

89 obacter baylyi ADP1 (ADP1), panD (coding for l-aspartate decarboxylase) encodes the only protein know

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

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

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

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

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

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

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

97 ocholine, glycerol-3-phosphate, L-carnitine, L-aspartate, glutathione, prostaglandin G2, alpha-linole

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

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

100 The metabolite is produced by dedicated L-aspartate hydroxylases that use NADPH and molecular ox

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

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

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

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

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

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

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

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

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

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

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

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

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

114 we propose that SAOUHSC_02373 be assigned as L-aspartate-L-methionine ligase (LdmS).

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

116 Data on the use of intravenous L-ornithine L-aspartate (LOLA) in the treatment of overt HE (OHE) is

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

118 The crystal structure of Streptomyces sp. V2 L-aspartate N-hydroxylase outlines a characteristic heli

119 g age was associated with increased N-acetyl-l-aspartate (NAA) in the anterior cingulate and insular

120 ation in the brain concentration of N-acetyl-L-aspartate (NAA) is a characteristic feature of Canavan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 We conclude that l-aspartate plays an important role in providing fumarat

154 relevant polyanions: hyaluronate (HA), poly-L-aspartate (PLD), poly-L-glutamate (PLE), and polyacryl

155 Poly(L-aspartate) (PLD)-coated NPs similarly bind SLC1A5 but

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

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

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

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

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

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

162 carboxylates, such as fumarate, l-malate and l-aspartate represent substrates for anaerobic growth of

163 It is composed of a peptide backbone of L-aspartate residues with L-arginines attached to their

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

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

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

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

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

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

170 d with lasso peptide BGCs first methylate an l-aspartate side chain found within the ring of the lass

171 L-aspartate slides into the catalytic center only when t

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

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

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

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

176 Besides L-glutamate and L-aspartate, they also recognize D-aspartate, which migh

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

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

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

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

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

182 boxyaminoimidazole ribonucleotide (CAIR) and l-aspartate to N-succinylcarboxamide-5-aminoimidazole ri

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

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

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

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

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

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

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

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

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

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

193 ole as a precursor for fumarate respiration, l-aspartate was able to supply all the nitrogen required

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

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

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

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

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

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

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