ライフサイエンスコーパス: aspartate

1 boxylate chemical shift anisotropy tensor of aspartate.

2 ydrolysis products isoaspartate (isoAsp) and aspartate.

3 physiological extracellular levels of free D-aspartate.

4 he concomitant conversion of oxaloacetate to aspartate.

5 in equal-magnitude gradients of serine than aspartate.

6 sly measured efflux of the charged d-[(14) C]aspartate.

7 glutamate and histidine residues and 4 of 11 aspartates.

8 aspase 6 are responsible for this event, and aspartates 348, 387, and 390 were identified as target s

9 -up of a toxic metabolite: 6-phosphofructose-aspartate (6-P-F-Asp).

10 hment of a methylthio group (-SCH3) to C3 of aspartate 89 of protein S12, one of 21 proteins that com

11 salt-bridges formed between arginine 286 and aspartates 96 and 107 are key to dimer formation.

12 Titration of aspartate, a competitive inhibitor of Ans, revealed an i

13 showed that mutation either in the histidine-aspartate acid (HD) domain (a quadruple mutation) or in

14 % (three studies), which was associated with aspartate amino transferase, hemoglobin and ferritin lev

15 In contrast to aspartate-amino-transferase and M65, M30 levels increase

16 573 patients vs six [1%] of 570), increased aspartate aminotransferase (103 [18%] vs 16 [3%]), hyper

17 e (15%), alanine aminotransferase (12%), and aspartate aminotransferase (11%).

18 %] of 573 vs one [<1%] of 570) and increased aspartate aminotransferase (14 [2%] vs one [<1%]).

19 nd elevations in alanine aminotransferase or aspartate aminotransferase (25 [12%]).

20 group, SG induced significant improvement in aspartate aminotransferase (32.4 +/- 17.4 vs 21.5 +/- 6.

21 288 patients vs four [3%] of 140), elevated aspartate aminotransferase (51 [18%] vs four [3%]), hype

22 mia (86 [34%]), fatigue (83 [33%]), elevated aspartate aminotransferase (65 [26%]), and increased ala

23 In aspartate aminotransferase (AAT), an extended hydrogen b

24 ctivity of PLP in both GabR and a homologous aspartate aminotransferase (Asp-AT) from Escherichia col

25 eiver operating characteristics curve showed aspartate aminotransferase (AST) had highest area under

26 of vomiting, lower platelet count, elevated aspartate aminotransferase (AST) level, positivity in th

27 ension with grade 3 rash and fevers, grade 4 aspartate aminotransferase (AST) or alanine aminotransfe

28 ses in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (

29 e (GGT), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), among a discovery set

30 Transplant albumin, day-1 aspartate aminotransferase (AST), day-1 lactate, day-3 b

31 Aspartate aminotransferase (AST)-to-platelet ratio (APRI

32 We evaluated the diagnostic accuracy of aspartate aminotransferase (AST)-to-platelet ratio index

33 aminotransferase (42 versus 27, P = 0.005), aspartate aminotransferase (AST; 26 versus 21, P = 0.01)

34 aminotransferase (five [6%]), and increased aspartate aminotransferase (four [5%]).

35 creatine phosphokinase (n=2), and increased aspartate aminotransferase (n=2) each occurring in more

36 (affecting >/=2% of patients) were elevated aspartate aminotransferase (six [2%] vs none), dyspnoea

37 seven [7%]), and increased concentration of aspartate aminotransferase (six [3%] vs two [2%]).

38 hydrogenase < 100 U/L, below analyzer range; aspartate aminotransferase 0 hour, 15.6 +/- 9.3 U/L vs 7

39 atelet ratio (APRI) was calculated as = 100*(aspartate aminotransferase [AST]/upper limit of AST)/pla

40 ed NASH as reflected by reductions in plasma aspartate aminotransferase and alanine aminotransferase

41 sis, decreased platelet count, and increased aspartate aminotransferase and alpha-fetoprotein levels

42 Aspartate aminotransferase and lactate dehydrogenase as

43 d predictive clinical variables and revealed aspartate aminotransferase as an important, albeit previ

44 ration (24 [21%] vs one [1%]), and increased aspartate aminotransferase concentration (16 [14%] vs on

45 [19%] vs one [1%]) and increased alanine or aspartate aminotransferase concentration (39 [10%] vs no

46 Elevated alanine and aspartate aminotransferase concentrations and profound e

47 The aspartate aminotransferase gene AAT1 was found to be a c

48 e in two patients at 20 mg/kg, and increased aspartate aminotransferase in one patient at 1 mg/kg, an

49 increase (five [14%]), pyrexia (four [11%]), aspartate aminotransferase increase (three [8%]), and ej

50 hrombocytopenia (70 [14%] of 490), increased aspartate aminotransferase levels (22 [5%]), and anaemia

51 demonstrated by decreased serum alanine and aspartate aminotransferase levels and numbers of TUNEL-p

52 inotransferase levels, four (33%) had raised aspartate aminotransferase levels, and two (17%) had inc

53 elevated serum alanine aminotransferase and aspartate aminotransferase levels.

54 Aspartate aminotransferase was significantly higher in D

55 lar injury markers lactate dehydrogenase and aspartate aminotransferase were persistently low (lactat

56 e 3 increase of alanine aminotransferase and aspartate aminotransferase) and two (13%) patients given

57 increases (40% alanine aminotransferase, 17% aspartate aminotransferase), maculopapular rash (17%), a

58 ties (grade 3 diarrhoea and grade 3 elevated aspartate aminotransferase).

59 ed plasma glucose, alanine aminotransferase, aspartate aminotransferase, AGEs and insulin levels.

60 aspartate aminotransferase, alanine aminotransferase (AL

61 of serum liver tests (alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase) an

62 (international normalized ratio, bilirubin, aspartate aminotransferase, alanine aminotransferase) an

63 s the elevation in alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and ga

64 increases in alanine aminotransferase and in aspartate aminotransferase, and hyponatraemia, each occu

65 ed concentrations of asymptomatic alanine or aspartate aminotransferase, or gamma-glutamyltransferase

66 cture of a homodimeric PLP-dependent enzyme, aspartate aminotransferase, which was reacted in situ wi

67 Liver fibrosis was predicted using the aspartate aminotransferase-to-platelet ratio index (APRI

68 OMA-IR) and liver fibrosis defined using the aspartate aminotransferase-to-platelet ratio index (APRI

69 us co factor for diverse enzymes, among them aspartate aminotransferase.

70 serum levels of alanine aminotransferase and aspartate aminotransferase.

71 na that control the electronic modulation in aspartate aminotransferase.Pyridoxal 5'-phosphate (PLP)

72 aline phosphatase; alanine aminotransferase; aspartate aminotransferase; gamma-glutamyltransferase; a

73 essed the release of radiolabelled d-[(14) C]aspartate and [(3) H]taurine.

74 r water-mediated hydrogen bonding between an aspartate and a cysteine (D156-O...S-C128) that would de

75 Elevations of aspartate and alanine aminotransferase concentrations of

76 hile erasers for the MARylation of glutamate/aspartate and arginine have been identified, the respect

77 ach enabled the relative quantification of d-aspartate and d-glutamate in individual neurons mechanic

78 Two natural and nonbiocidal CAs (aspartate and glucose) were used to attract bacteria to

79 bstrate specificity as mono(ADP-ribosyl)ated aspartate and glutamate but not lysine residues.

80 In order to measure the d- and l-forms of aspartate and glutamate, we developed and applied a stac

81 Asparagine synthetase (ASNS) converts aspartate and glutamine to asparagine and glutamate in a

82 th ammonia-lowering therapy by l-ornithine l-aspartate and rifaximin orally for 4 weeks.

83 the amino acid neurotransmitters glutamate, aspartate and taurine.

84 shows a hydrogen bond between the iron bound aspartate and the bridging solvent molecule, the DFT cal

85 ured by the levels of lactate dehydrogenase, aspartate, and alanine aminotransferase.

86 ced changes in self-processing and decreased aspartate (Asp) content.

87 ution of serum markers of liver damage, high aspartate (AST, >49.9 IU/L) and alanine aminotransferase

88 Here, we show that an aspartate at position 1261 is the most critical residue

89 Substitution of serine with aspartate at position 3 (S3D) is widely used to mimic co

90 Although the aspartate at position Asp-50 was indispensable for dival

91 Aspartate beta-hydroxylase (ASPH) is an enzyme overexpre

92 acidification through its essential role in aspartate biosynthesis.

93 ed under high CO2, the canB mutant grew on L-aspartate but not on the key C3 compounds L-serine, pyru

94 the absence and presence of sodium ions and aspartate, but stall in sodium alone, providing a direct

95 include HIV-1 proteinase, function with two aspartate carboxy groups at the active site.

96 rbon C5 atom hydrogen bond directly with the aspartate carboxylate of the E446D variant.

97 measured by the ratio of choline to N-acetyl-aspartate (Cho/NAA) may provide additional information o

98 , tramadol, lidocaine, and/or the N-methyl-d-aspartate class of glutamate receptor antagonists have b

99 II)-mediated intramolecular cross-linking of aspartate-containing polyolefins in water.

100 Strikingly, mutation of Glu181 to aspartate converts TbPRMT7 into a type I PRMT, producing

101 oxazole propionic acid (AMPA) and N-methyl-D-aspartate currents and the ability to exhibit long-term

102 hese synapses as measured by AMPA/N-methyl-D-aspartate currents.

103 AMHD1 (sterile alpha motif and histidine (H) aspartate (D) domain-containing protein 1) is known for

104 Exposing brain slices to Glut and D-aspartate (D-Asp) before recording resulted in an increa

105 by exogenous preexposure to the amino acid D-aspartate (D-Asp).

106 in vitro and in vivo after NMDA (N-methyl-d-aspartate) damage in young mice.

107 We further identify N-methyl-d-aspartate-dependent long-term depression (NMDA-LTD) at p

108 sion or exogenous 2OG treatment, resulted in aspartate depletion that was specifically manifested as

109 Reduced levels of aspartate deregulated the malate-aspartate shuttle, whic

110 ral polymorphism at residue 35, glutamate to aspartate (E35D), alone and in conjunction with residue

111 ules to a pocket near the p38alpha glutamate-aspartate (ED) substrate-docking site rather than the ca

112 N-methyl-d-aspartate-encephalitis or inborn errors of metabolism ma

113 nolysis, an anaplerotic pathway, replenished aspartate for anabolic biosynthesis, which was critical

114 P46A1 is activated by l-glutamate (l-Glu), l-aspartate, gamma-aminobutyric acid, and acetylcholine, w

115 nvestigated the catalytic contribution of an aspartate general base in ketosteroid isomerase (KSI) by

116 is further posited to result from N-methyl-D-aspartate glutamate receptor (NMDAR) hypofunction.

117 aptic strengthening by increasing N-methyl D-aspartate glutamate receptor (NMDAR) internalization thr

118 epressant effects of ketamine, an N-methyl-D-aspartate glutamate receptor antagonist, have not been f

119 ans, particularly those involving N-methyl-D-aspartate glutamate receptor antagonists, to illustrate

120 e, iso-leucine; aminoacyl-tRNA; and alanine, aspartate, glutamate.

121 of alpha-ketoglutarate dehydrogenase and the aspartate-glutamate carrier 1.

122 ARALAR/AGC1/Slc25a12, the aspartate-glutamate carrier from brain mitochondria, is

123 boxylate ion, and sidechain carbon-oxygen of aspartate/glutamate and serine/threonine in zinc-peptide

124 enzymes, the peptide transporter CstA, PEB1 aspartate/glutamate transporter, LutABC lactate dehydrog

125 event peptide backbone cleavage, but whether aspartate glycosylation occurred was not examined.

126 -specific nuclease activity in the histidine-aspartate (HD) domain of the Cmr2 subunit of the complex

127 Replacing glutamate with aspartate in an HCF-1 proteolytic repeat was shown to pr

128 Mutating Ca(2+)-coordinating aspartates in the C2A-domain localizes Doc2B permanently

129 a3-alpha3 loop while keeping the active-site aspartate intact resulted in suppression of CKI1 functio

130 s negatively regulated by c-di-AMP, and high aspartate levels can be restored by expression of a c-di

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

132 ids from leaves of transgenic plants such as aspartate, lysine, glycine, leucine and threonine with n

133 tion of the five modified Runx1 tyrosines to aspartate markedly reduced co-immunoprecipitation with H

134 ects are very likely caused by an N-methyl-d-aspartate-mediated non-opioid mechanism as Dyn A peptide

135 and motility were recorded after N-methyl-d-aspartate microinjection in the SNpc and/or optogenetic

136 ctivity of XXT5 require the aspartate-serine-aspartate motif.

137 We report here that OGT glycosylates aspartate much faster than it glycosylates glutamate in

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

139 d in oligodendroglia that cleaves N-acetyl-l-aspartate (NAA) to acetate and l-aspartic acid, elevates

140 ocampus levels of the neuron marker N-acetyl aspartate (NAA), along with higher levels of glutamate (

141 solute metabolite concentration for N-acetyl-aspartate (NAA), choline (Cho) and creatine (Cr).

142 ondria, is the regulatory step in the malate-aspartate NADH shuttle, MAS.

143 gets, including GluN2A and GluN2B N-methyl-D-aspartate (NMDA) and GluA2 alpha-amino-3-hydroxy-5-methy

144 In healthy subjects (HS), N-methyl-D-aspartate (NMDA) antagonists like memantine and ketamine

145 In vivo imaging of N-methyl-d-aspartate (NMDA) glutamate receptor and gamma-aminobutyr

146 matergic compound that acts as an N-methyl-D-aspartate (NMDA) modulator with glycine-like partial ago

147 soxazole propionic acid (AMPA) to N-methyl-D-aspartate (NMDA) ratios, and matrix metalloproteinase ac

148 nction and plasticity, especially N-methyl-d-aspartate (NMDA) receptor (NMDAR)-dependent long-term po

149 the time interval between spikes, N-methyl-D-aspartate (NMDA) receptor activation, and Calcium/calmod

150 een used successfully to quantify N-methyl-d-aspartate (NMDA) receptor binding in humans.

151 l research with modulators at the N-methyl-d-aspartate (NMDA) receptor GluN2B N-terminal domain (NTD)

152 ieve the first time, we show that N-methyl-d-aspartate (NMDA) receptor-dependent Ca(2+) transients ar

153 Evoked, N-methyl-D-aspartate (NMDA) receptor-mediated currents were recorde

154 , calcium ion (Ca2+) flux through N-methyl-D-aspartate (NMDA) receptors activates Ca2+/calmodulin sig

155 euron expression of glutamatergic N-methyl-D-aspartate (NMDA) receptors and decreased expression of a

156 N-methyl-d-aspartate (NMDA) receptors are glutamate- and glycine-ga

157 N-Methyl-D-aspartate (NMDA) receptors are glutamate-gated excitator

158 N-methyl-d-aspartate (NMDA) receptors are ligand-gated, cation-sele

159 her with the strong expression of N-methyl-D-aspartate (NMDA) receptors by its cells, are consistent

160 Activation of extrasynaptic N-methyl-d-aspartate (NMDA) receptors causes neurodegeneration and

161 A distinctive characteristic of N-methyl-D-aspartate (NMDA) receptors containing a GluN2A subunit i

162 roaches, we find that ablation of N-methyl-D-aspartate (NMDA) receptors during postnatal development

163 Competitive antagonists against N-methyl-D-aspartate (NMDA) receptors have played critical roles th

164 The physiology of N-methyl-d-aspartate (NMDA) receptors is fundamental to brain devel

165 y, mediated by overstimulation of N-methyl-D-aspartate (NMDA) receptors, is a mechanism that causes s

166 lease activating Ca(2+)-permeable N-methyl-D-aspartate (NMDA) receptors.

167 ed in influencing learning is the N-methyl-D-aspartate (NMDA) subtype 2B glutamate receptor (NR2B).

168 ted by glutamate receptors of the N-methyl-d-aspartate (NMDA) subtype and resulted in removal of gluc

169 uR) agonists, kainic acid (KA) or N-methyl-D-aspartate (NMDA), contributed to significant, progressiv

170 unimNPs with the glutamate analog N-methyl-d-aspartate (NMDA), which is excito-toxic and induces RGC

171 N-methyl-d-aspartate (NMDA)-type ionotropic glutamate receptors med

172 e endogenous NMDA receptor (NMDAR) agonist D-aspartate occurs transiently in the mammalian brain beca

173 onses, which only appeared in the leaves for aspartate or in the roots for asparagine, serine and gly

174 ic acid functionality of FPMPs with a diamyl aspartate phenoxyamidate group led to a novel generation

175 Ratios of N-acetyl-aspartate plus N-acetyl-aspartyl-glutamate (NAA) to crea

176 The aspartate pool in L. lactis is negatively regulated by c

177 In vitro, GLS1 inhibition blocked aspartate production and reprogrammed cellular prolifera

178 utilized glucose oxidation for glutamate and aspartate production.

179 Caspases are cysteine aspartate proteases that are major players in key cellul

180 bstrate; moreover, once formed, the glycosyl aspartate reacts further to form a succinimide intermedi

181 antibody-positive patients, anti-N-methyl-d-aspartate receptor (5 patients), had normal MRI results

182 d demonstrated that it acts as an N-methyl D-aspartate receptor (NMDA-R) agonist, leading to calcium

183 in 1 [LGI1] Ab), and 4 (3.6%) had N-methyl-D-aspartate receptor (NMDAR) Ab.

184 ty subsequent to the reduction in N-methyl-D-aspartate receptor (NMDAR) activity.

185 We recorded N-methyl-D-aspartate receptor (NMDAR) and alpha-amino-3-hydroxy-5-m

186 s to search for antibodies to the N-methyl-D-aspartate receptor (NMDAR) and contactin-associated prot

187 laments to examine the roles that N-methyl-D-aspartate receptor (NMDAR) and hyperpolarization-activat

188 ing EtOH abstinence utilizing the N-methyl D-aspartate receptor (NMDAR) antagonist and antidepressant

189 on-competitive, voltage-dependent N-Methyl-D-aspartate receptor (NMDAR) antagonist, has been shown to

190 rough the fortuitous discovery of N-methyl-D-aspartate receptor (NMDAR) antagonists as effective anti

191 to mice treated chronically with N-methyl-d-aspartate receptor (NMDAR) antagonists, we demonstrate t

192 NALE: Encephalitis caused by anti-N-methyl-d-aspartate receptor (NMDAR) antibodies is the leading cau

193 ed in schizophrenia research, and N-methyl-d-aspartate receptor (NMDAR) dysfunction can provide insig

194 he majority of patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis.

195 Mutations in the N-methyl-D-aspartate receptor (NMDAR) gene GRIN2A cause epilepsy-ap

196 oantibodies against glutamatergic N-methyl-D-aspartate receptor (NMDAR) have been reported in a propo

197 N-methyl-D-aspartate receptor (NMDAR) hypofunction in parvalbumin-e

198 excess in schizophrenia and that N-methyl-d-aspartate receptor (NMDAR) hypofunction on gamma-aminobu

199 The activation of the N-methyl D-aspartate receptor (NMDAR) is controlled by a glutamate-

200 RIN2A and GRIN2B) subunits of the N-methyl-D-aspartate receptor (NMDAR), a ligand-gated ion channel w

201 KYNA depletion then leads, in an N-methyl D-aspartate receptor (NMDAR)-dependent manner, to activati

202 nked to underlying dysfunction of N-methyl-D-aspartate receptor (NMDAR)-mediated neurotransmission.

203 especially antibodies against the N-methyl-D-aspartate receptor (NMDAR)-more commonly than do healthy

204 pyramidal neurons that relied on N-methyl-d-aspartate receptor activation and calcium/calmodulin-dep

205 N-methyl-D-aspartate receptor activation requires the binding of a

206 findings implicate dysfunction of N-methyl-D-aspartate receptor and glutamatergic neurotransmission i

207 single sub-anesthetic dose of the N-methyl-D-aspartate receptor antagonist ketamine may work to corre

208 t can be partially blocked by the N-methyl-d-aspartate receptor antagonist MK-801.

209 Ketamine is a potent N-methyl-D-aspartate receptor antagonist with a potentially novel m

210 tory genes, and that ketamine (an N-methyl-D-aspartate receptor antagonist) would reduce or block thi

211 Ketamine is an N-methyl-D-aspartate receptor antagonist, which on administration p

212 Additionally, the NR2B-selective N-methyl-D-aspartate receptor antagonists ifenprodil and CP-101,606

213 confirmed identification of anti-N-methyl-D-aspartate receptor antibodies in the cerebrospinal fluid

214 thought to reflect glutamatergic N-methyl-d-aspartate receptor function and excitatory-inhibitory ne

215 lutamateric neurotransmission and N-methyl-D-aspartate receptor hypofunction in the pathophysiology o

216 The N-methyl-D-aspartate receptor hypofunction model of schizophrenia p

217 e receptor (GLY-R) in 5 patients, N-methyl-d-aspartate receptor in 4 patients and gamma-aminobutyric

218 nobutyric acid type A receptor or N-methyl-D-aspartate receptor inhibition.

219 r understanding D-serine-mediated N-methyl-D-aspartate receptor plasticity in the amygdala and how th

220 isions of ACC with different AMPA/N-methyl-D-aspartate receptor profiles.

221 compound 1 (Cmpd-1), a novel A2AR/N-methyl d-aspartate receptor subtype 2B (NR2B) dual antagonist and

222 key synaptic proteins, including N-methyl-d-aspartate receptor subunit 2B (NR2B) and PSD-95.

223 d spine pruning and switch in the N-methyl-D-aspartate receptor subunit, which are relevant to autism

224 litation, and interactions of the N-methyl D-aspartate receptor with opioids at the level of the spin

225 ated spine that depends on NMDAR (N-methyl-d-aspartate receptor) and CaMKII signalling and on postsyn

226 (Sp1)-binding site resulted in an N-methyl-d-aspartate receptor-dependent enhancement of COX-2 promot

227 N-methyl-D-aspartate receptor-dependent plasticity in the amygdala

228 ptic activity and was shown to be N-methyl-d-aspartate receptor-dependent.

229 and was predicted best when both N-methyl-D-aspartate receptor-IgG and aquaporin-4-IgG coexisted (71

230 non-competitive antagonist at the N-methyl-d-aspartate receptor.

231 of synaptic connections by NMDA (N-methyl-d-aspartate) receptor-dependent long-term potentiation (LT

232 in the pharmacological profile of N-methyl-d-aspartate receptors (NMDAR) in the NAc core, TLR4.KO ani

233 on between synaptic activation of N-methyl-D-aspartate receptors (NMDARs) and intrinsic oscillatory m

234 accumulation of GluN2B-containing N-methyl-D-aspartate receptors (NMDARs) and pathological pain are c

235 d-Serine modulates N-methyl d-aspartate receptors (NMDARs) and regulates synaptic plas

236 N-methyl-D-aspartate receptors (NMDARs) are glycoproteins in the br

237 N-methyl-d-aspartate receptors (NMDARs) are heterotetrameric ion ch

238 N-methyl-D-aspartate receptors (NMDARs) are necessary for the induc

239 The significant role played by N-methyl-d-aspartate receptors (NMDARs) in both the pathophysiology

240 Postsynaptic N-methyl-d-aspartate receptors (NMDARs) phasically activated by pre

241 N-Methyl-D-aspartate receptors (NMDARs) play pivotal roles in synap

242 Synaptic activation of N-methyl-d-aspartate receptors (NMDARs) plays a key role in synapti

243 Alcohol may act on N-methyl-d-aspartate receptors (NMDARs) within cortical circuits to

244 have shown altered expression of N-methyl-D-aspartate receptors (NMDARs).

245 g of 'Delay cells' is mediated by N-methyl-d-aspartate receptors and weakened by cAMP-PKA-potassium c

246 Blocking N-methyl-D-aspartate receptors or activation of extracellular signa

247 n alpha-syn and GluN2D-expressing N-methyl-D-aspartate receptors, represents a precocious biological

248 inases as well as NR2B-containing N-methyl-D-aspartate receptors.

249 een domain layers, reminiscent of N-methyl-D-aspartate receptors.

250 yl-4-isoxazole propionic acid and N-methyl-D-aspartate receptors.

251 lpha7 nicotinic acetylcholine and N-methyl-D-aspartate receptors.

252 N-methyl-D-aspartate-receptors (NMDARs) are ionotropic glutamate re

253 (MSCRAMM) family, exemplified by the serine-aspartate repeat protein D (SdrD), which serve key roles

254 t of homophilic binding forces by the serine-aspartate repeat protein SdrC and their inhibition by a

255 Recently, a conserved aspartate residue (D303, or D46) of hedgehog was identif

256 Moreover, a conserved aspartate residue trigger was found to affect mitochondr

257 onversion are modulated by protonation of an aspartate residue, establishing the power of MD & MSMs i

258 enriched in alternating lysine and glutamate/aspartate residues (KEKE motifs).

259 to phytaspases hydrolyzed prosystemin at two aspartate residues flanking the systemin sequence.

260 Three aspartate residues in Cx30 (Asp-50, Asp-172, and Asp-179

261 n include PARPs, enzymes known to ribosylate aspartate residues in the process of poly(ADP-ribosyl)at

262 rs, it has been assumed that two ion-binding aspartate residues transport the two protons that are la

263 to enable alignment with oppositely charged aspartate residues within CD3zeta and activation of CD3z

264 phosphorylation sites with either alanine or aspartate residues.

265 proliferation pathways, while application of aspartate restored proliferation.

266 structured winged helix domain and glutamate/aspartate-rich domain, which is sufficient to induce (H3

267 The absence of a Mg(2+) binding, aspartate-rich, DDXXD motif places these enzymes in a no

268 ity of both the translated phenylalanine and aspartate Runx1 variants.

269 ation of E. coli speed races in gradients of aspartate, serine and combinations thereof.

270 vitro catalytic activity of XXT5 require the aspartate-serine-aspartate motif.

271 found reliance on glucose metabolism, malate-aspartate shuttle deregulation leads to a specific proli

272 d levels of aspartate deregulated the malate-aspartate shuttle, which is important for cytoplasmic NA

273 stead, we identified a band of glutamate and aspartate side chains at the lower end of the pore that

274 ) selectivity of TRPV6 arises from a ring of aspartate side chains in the selectivity filter that bin

275 d activation of programmed cell death is the aspartate-specific cysteine protease (caspase)-8.

276 rmone systemin, is performed by phytaspases, aspartate-specific proteases of the subtilase family.

277 rchaebacterium Pyrococcus horikoshii, sodium/aspartate symporter GltPh, suggested the molecular basis

278 Glutamine can also generate aspartate, the carbon source for pyrimidine biosynthesis

279 hich converts glutamine-derived nitrogen and aspartate to asparagine) impaired EC sprouting even in t

280 n addition to OGT, enzymes that may catalyze aspartate to isoaspartate isomerization include PARPs, e

281 own that VHL-/- RCC cells rely on RC-derived aspartate to maintain de novo pyrimidine biosynthesis.

282 abled other amino acids, such as proline and aspartate, to directly acquire this nitrogen.

283 The reciprocal substitution of aspartate-to-histidine-193 in Pto abolished AvrPto recog

284 Aspartate-to-isoaspartate isomerization in proteins occu

285 (32%), alanine transaminase increase (20%), aspartate transaminase increase (15%), anemia and thromb

286 Time to significant fibrosis (defined as an aspartate transaminase level to platelet count ratio ind

287 with other renal injury markers (creatinine, aspartate transaminase, and heart-type fatty acid bindin

288 nor age, steatosis, cold ischemic time, peak aspartate transaminase, day 5 bilirubin or international

289 ount, urea, bilirubin, alanine transaminase, aspartate transaminase, international normalized ratio,

290 upon formation of a dodecameric complex with aspartate transcarbamoylase (ATC).

291 glutamate dysfunction by targeting glutamate-aspartate transporter (GLAST), a crucial glial transport

292 endent downregulation of the glial glutamate-aspartate transporter (GLAST), which causes an enhanceme

293 Glutamate aspartate transporter levels were higher and glial gluta

294 glutamate transporter expression (glutamate/aspartate transporter) were also examined in WT and Cln3

295 ical manipulation targeted at the N-methyl-D-aspartate type glutamate receptor (NMDAR).

296 loned a pollen-expressed P. rhoeas threonine-aspartate-tyrosine (TDY) MAPK, PrMPK9-1 Rather few data

297 and analyzed the conversion of asparagine to aspartate using NMR.

298 In contrast, the release of d-[(14) C]aspartate was preferentially sensitive to deletion of LR

299 Conversely, release of charged osmolytes (d-aspartate) was strongly reduced by deletion of LRRC8A or

300 metabolite generated from Q utilization was aspartate, which is generated from a transaminase reacti