ライフサイエンスコーパス: aspartate

1 ated import and conversion of L-malate and L-aspartate.

2 id (DABA), which is further catabolized to l-aspartate.

3 Glt(Ph) is the coupled binding of sodium and aspartate.

4 ase (gene: Nat8l) from acetyl-coenzyme A and aspartate.

5 nol intermediate) to glucose-6-phosphate and aspartate.

6 as a key residue that forms a salt bridge to aspartate-25 in the patient protein fibril structure.

7 caspase-2 (Casp2)-catalyzed tau cleavage at aspartate 314 mediates synaptic dysfunction and memory i

8 LtgG containing a site directed mutation in aspartate 343, confirmed the essentiality of this amino

9 ing properties, as well as a single residue, aspartate 348, that determines both cation selectivity a

10 glutamate in infected tissue, which inhibits aspartate acquisition by S. aureus Together, these data

11 minotransferase (ALT) (-49%; P = 0.009), and aspartate aminotransferase (-42%; P = 0.019).

12 nine aminotransferase (ALT) (-67% and -60%), aspartate aminotransferase (-57% and -52%), and fibrogen

13 %] among 68 who received placebo), increased aspartate aminotransferase (11 [8%] vs two [3%]), anaemi

14 quent grade 3-4 adverse events were elevated aspartate aminotransferase (14 of 44, 32%), elevated gam

15 in alanine aminotransferase (7 [11.3%] SAD), aspartate aminotransferase (4 [6.5%] SAD), and creatinin

16 levels of alanine aminotransferase (64%) and aspartate aminotransferase (60%), hypoalbuminemia (55%),

17 Mean postoperative day (POD) 7, aspartate aminotransferase (61.13 + 24.77 vs 73.17 + 53.

18 /tissue volume (BV/TV) by micro-CT analysis; aspartate aminotransferase (ASAT) and alanine aminotrans

19 mitted COVID-19 patients had elevated plasma aspartate aminotransferase (AST) and 35% had elevated al

20 Aspartate aminotransferase (AST) and alanine aminotransf

21 They found that an increase in aspartate aminotransferase (AST) and its dynamicity corr

22 d lower serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST) levels and less hepatic

23 g NMP grafts showed significantly lower peak aspartate aminotransferase (AST) levels than those recei

24 cerides, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) using a general linear

25 analysis older patient's age, abnormal serum aspartate aminotransferase (AST) value, Hepatitis C viru

26 Median aspartate aminotransferase (AST) was higher than alanine

27 According to reported data, patients with aspartate aminotransferase (AST)>100 IU/L and 50 IU/L sh

28 Peak values of aspartate aminotransferase (AST), alanine aminotransfera

29 hepatotoxicity with improved blood levels of aspartate aminotransferase (AST), alanine transaminase (

30 ood glucose, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase,

31 nd change in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl tra

32 od levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), glucose, total cholest

33 the upper limit of normal (ULN), platelets, aspartate aminotransferase (AST), hemoglobin, sodium, pa

34 tal protein, alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase

35 lular carcinoma (HCC) and the performance of aspartate aminotransferase (AST)-platelet ratio index (A

36 alkaline phosphatase (R = 0.543, P = 0.003), aspartate aminotransferase (R = 0.420, P = 0.029), and l

37 , hyponatraemia (11 [6%] vs 0) and increased aspartate aminotransferase (six [3%] vs five [5%]).

38 erase (two [<1%] of 260 patients), increased aspartate aminotransferase (two [<1%]), and nausea (two

39 fined by changes in liver aminotransferases (aspartate aminotransferase [AST] and alanine aminotransf

40 Clinical characteristics, liver tests (aspartate aminotransferase [AST], alanine aminotransfera

41 iversity displayed significantly higher mean aspartate aminotransferase and alanine aminotransferase

42 bilirubin and alanine aminotransferase; POD3 aspartate aminotransferase and prothrombin time-internat

43 oncentrations (two [7%] patients), increased aspartate aminotransferase concentration (two [7%] patie

44 ase concentrations (74 [46%]), and increased aspartate aminotransferase concentrations (65 [41%]).

45 In Study 2, 16 g/d increased mean aspartate aminotransferase from baseline (19 U/L; 95% CI

46 findings, O2 saturation lower than 90%, and aspartate aminotransferase greater than 40 U/L.

47 eased levels of alanine aminotransferase and aspartate aminotransferase in the plasma, indicating les

48 Hair colour changes (67%), fatigue (54%), aspartate aminotransferase increase (39%), nausea (38%),

49 Ewing sarcoma, three [7%] for osteosarcoma), aspartate aminotransferase increase (two [4%] for Ewing

50 e aminotransferase level (in 11%), increased aspartate aminotransferase level (in 9%), hyponatremia (

51 (normal range, 0-29 U/L [0-0.48 ukat/L]), an aspartate aminotransferase level of 98 U/L (1.6 ukat/L)

52 (normal range, 0-29 U/L [0-0.48 ukat/L]), an aspartate aminotransferase level of 98 U/L (1.6 ukat/L)

53 y reduced serum alanine aminotransferase and aspartate aminotransferase levels as well as proinflamma

54 nd creatinine, alanine aminotransferase, and aspartate aminotransferase levels were within normal lim

55 proaches to show that Rv3722c is the primary aspartate aminotransferase of M. tuberculosis, and media

56 culated: NASH clinical scoring system (NCS), aspartate aminotransferase to platelet ratio index (APRI

57 ors and the decline or increase of FIB-4 and aspartate aminotransferase to platelet ratio index (APRI

58 assessed non-invasively via the serum tests Aspartate Aminotransferase to Platelet Ratio Index and H

59 easily available perfusate parameters (PP) (aspartate aminotransferase, alanine aminotransferase, la

60 ean difference for alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and ga

61 pids, cholesterol, alanine aminotransferase, aspartate aminotransferase, and creatinine.

62 concentrations of alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyltransferas

63 eductions in serum alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase,

64 Grade 3 increased aspartate aminotransferase, syncope, pericardial effusio

65 er waist circumference, levels of alanine or aspartate aminotransferase, total and low-density lipopr

66 al cutoffs for three noninvasive biomarkers (aspartate aminotransferase-to-platelet ratio index, Fibr

67 y-4-cholesten-3-one, bile acids, alanine and aspartate aminotransferases, and neoepitope-specific N-t

68 Aspartate analogue 8 with the hydroxy-1,2,3-triazole moi

69 We report a series of glutamate and aspartate analogues designed using the hydroxy-1,2,3-tri

70 Aspartate and alanine transaminase elevations occurring

71 mechanistic role of the distal heme residues aspartate and arginine in the heterolysis of peroxide to

72 We found that MPTP treatment increases D-aspartate and D-serine in the monkey putamen while L-DOP

73 Here, we show that PGC-1alpha1 elevates aspartate and glutamate levels and increases the express

74 Single-site mutations of aspartate and glutamate residues reveal their role in in

75 reaction and the intermediates of the malate-aspartate and glycerol 3-phosphate shuttles.

76 n (ETC), both of which are known to increase aspartate and GOT1 dependencies.

77 et, His, and Tyr, conversion of histidine to aspartate and hydroxyaspartate was identified at four si

78 bolism and brain health metabolites N-acetyl-aspartate and kynurenine.

79 hich is exported by DcuABC in exchange for L-aspartate and L-malate.

80 d enzymes that convert the C4-dicarboxylates aspartate and malate into fumarate (AspA, FumABC), are r

81 osphate and adenylosuccinate, which consumes aspartate and releases fumarate in a manner involving fa

82 (Gln) is converted to excitatory (glutamate, aspartate) and inhibitory (gamma-amino butyric acid) ami

83 of these AAs (tyrosine, alanine, isoleucine, aspartate, and glutamate) were also found to be signific

84 e form of ZnCl(3)(-), together with citrate, aspartate, and N-acetylaspartate on human prostate cance

85 amino acids glutamine, asparagine, arginine, aspartate, and serine activate TORC1 most efficiently fo

86 gel filtration experiments with asparagine, aspartate, and valine as PKM2 ligands, we examined wheth

87 proteins, indicative of the rareness of tri-aspartate architectures, which allows for engineering su

88 hanistically related metabolites citrate and aspartate, are widely reported as reduced in prostate ca

89 tochondria boosts the synthesis of cytosolic aspartate (Asp) and NAA, which is impeded by aralar defi

90 stidine (His), arginine (Arg), lysine (Lys), aspartate (Asp), glutamate (Glu) and cysteine (Cys) phos

91 of amino acids, and effectively transported aspartate, asparagine and glutamate.

92 The human 2-oxoglutarate dependent oxygenase aspartate/asparagine-beta-hydroxylase (AspH) catalyses t

93 Human aspartate/asparagine-beta-hydroxylase (AspH) is a 2-oxog

94 tions, respectively; and is stabilized by an aspartate at +6 position, which creates a network of int

95 ing its autophosphorylation at the conserved aspartate at position 54.

96 hat rice (Oryza sativa L.) roots can acquire aspartate at soil concentration, and that japonica subsp

97 g the phosphate binding loop and a conserved aspartate at the tip of beta2.

98 Genetically introducing aspartates at these N-glycosylation sites bypasses the r

99 Disruption of caa1 (+) resulted in aspartate auxotrophy, a finding that prompted us to asse

100 ates cancer cell proliferation by increasing aspartate availability for pyrimidine synthesis by the e

101 based on the bacterial periplasmic glutamate/aspartate binding protein with either an endogenously fl

102 functions as the extracellular gate for the aspartate binding site, in the coupled binding of sodium

103 ich predict high-affinity Na(+)-low-affinity aspartate binding, and the experimental results in which

104 Our results identify aspartate biosynthesis and nitrogen distribution as pote

105 Kat inhibition with carbidopa impairs aspartate biosynthesis, mitochondrial respiration, and r

106 Comparison of the L- and D-aspartate bound Glt(Tk) structures revealed that D-aspar

107 Aspartate content was significantly reduced in cerebral

108 lasticity of use of a non-limiting resource, aspartate, controls both resource production and the eme

109 lular loop 2 (K210) and a negatively charged aspartate (D112) in extracellular loop 1 that helps dete

110 ubstitution, replacing asparagine (N40) with aspartate (D40), and has been linked with an increased r

111 in Mycobacterium tuberculosis by binding to aspartate decarboxylase PanD.

112 way by triggering degradation of its target, aspartate decarboxylase.

113 alanine- (DNA-PKcs(PQR)) or phospho-mimetic aspartate (DNA-PKcs(SD)) substitutions at the S2053 clus

114 This metabolic plasticity of aspartate enables carbon-nitrogen budgeting, thereby dri

115 Aspartate formation was influenced by storage time after

116 methyl-4-isoxazole propionic acid/N-methyl-D-aspartate glutamate currents.

117 Aralar/AGC1/Slc25a12, the mitochondrial aspartate-glutamate carrier expressed in neurons, is the

118 s in neurotransmitter signaling, urea cycle, aspartate-glutamate metabolism, and glutathione synthesi

119 ntermediate metabolism in the urea cycle and aspartate-glutamate pathways disrupting mitochondrial bi

120 characterized by the presence of a conserved aspartate-glutamate-leucine-leucine-alanine motif) compe

121 subtype I-D systems, however, the histidine-aspartate (HD) nuclease domain is encoded as part of a C

122 cose ester (ABA-GE) and low indole-3-acetate aspartate (IAA-Asp) and isopentenyladenine (iP) contents

123 Bacterial synthesis of aspartate in particular is absolutely essential for stap

124 in V and a histidine in place of a catalytic aspartate in plasmepsin III.

125 We propose to use the formation of aspartate in stored salmon flesh as a marker of salmon f

126 the invariant lysine in subdomain II or the aspartate in the DYG-loop of GC-A and GC-B failed to dec

127 s promoted by phosphorylation on a conserved aspartate in the receiver domain of the type-A ARRs.

128 Exhaustion of aspartate in these cells resulted in immediate depletion

129 nding that prompted us to assess the role of aspartate in TORC1 activation.

130 ith conservative substitutions (glutamate to aspartate) in either of two positions in the proton-tran

131 In gluconeogenic cells, aspartate is a carbon source for trehalose production, w

132 ate bound Glt(Tk) structures revealed that D-aspartate is accommodated with only minor rearrangements

133 rved selectivity filter (SF) domain II (DII) aspartate is essential for CDI.

134 provide evidence that a Ln(3+)-coordinating aspartate is essential for the enzymatic functions of Xo

135 glycolytic cells using trehalose for carbon, aspartate is predominantly a nitrogen source for nucleot

136 To investigate the consequences of aspartate isomerization, we investigated two alphaA crys

137 o produce threonine leads to deregulation of aspartate kinase, causing flux imbalance and lysine and

138 Here we show that a turgor-sensing histidine-aspartate kinase, Sln1, enables the appressorium to sens

139 degree of similarity and harbor a conserved aspartate kinase-chorismate mutase-tyrA (prephenate dehy

140 tion demonstrating a causal role of elevated aspartate level in cardiomyocyte hypertrophy.

141 d simple method to detect zinc, citrate, and aspartate levels as a biomarker signature for prostate c

142 glucose consumption and higher intracellular aspartate levels, resulting in increased synthesis of nu

143 changing the electronegativity of the unique aspartate ligand.

144 (5) glutamate-aspartate metabolism (N-acetyl aspartate: lower in AD, p = 0.002); and (6) neurotransmi

145 petitive colonization assays to describe how aspartate/malate can trigger initial Salmonella Typhimur

146 ing, along with increased levels of N-acetyl-aspartate measured by (1)H-MRS; and hypomyelination in P

147 Here, we demonstrate that the DIME-aspartate mediates a Ca(2+)-modulated electrostatic inte

148 mate: lower in AD, p < 0.001); (5) glutamate-aspartate metabolism (N-acetyl aspartate: lower in AD, p

149 d crystallographic characterization of a tri-aspartate metal-binding site previously identified on th

150 ino-5-phosphonopentanoic acid, or N-methyl-d-aspartate modulation of native or recombinant glycine re

151 Over the past decade, various N-methyl-D-aspartate modulators have failed in clinical trials, und

152 discovery, to identify inhibitors targeting aspartate N-acetyltransferase (ANAT), a promising target

153 N-acetylaspartate (NAA) is synthesized by aspartate N-acetyltransferase (gene: Nat8l) from acetyl-

154 ion in the brain concentration of N-acetyl-L-aspartate (NAA) is a characteristic feature of Canavan d

155 utamate, along with the compounds N-methyl-d-aspartate (NMDA) and d-(-)-2-amino-5-phosphonopentanoic

156 med to be mediated by blockade of N-methyl-D-aspartate (NMDA) glutamate receptors, our experiments de

157 The N-methyl-D-aspartate (NMDA) receptor antagonist ketamine is associa

158 Ketamine, an N-methyl-d-aspartate (NMDA) receptor antagonist, can rapidly allevi

159 nt response to ketamine and other N-methyl-D-aspartate (NMDA) receptor antagonists.

160 es, which could be reversed by an N-methyl-D-aspartate (NMDA) receptor blocker.

161 N-methyl-D-aspartate (NMDA) receptor-dependent LTP requires trans-s

162 lease of H(2) O(2) resulting from N-methyl-D-aspartate (NMDA) receptor-mediated activation of nicotin

163 N-Methyl-d-aspartate (NMDA) receptors are Ca(2+)-permeable channels

164 ory neurotransmission mediated by n-methyl-d-aspartate (NMDA) receptors following stimulation of non-

165 N-methyl-D-aspartate (NMDA) receptors mediate synaptic excitatory s

166 urotransmitter receptors, such as N-methyl-d-aspartate (NMDA) receptors, affect whole cell currents o

167 structures, and elevated synaptic N-methyl-d-aspartate (NMDA) receptors, thereby increasing synaptic

168 hat targets the GluN2B subunit of N-methyl-d-aspartate (NMDA) receptors.

169 tion of the glutamatergic agonist N-methyl-d-aspartate (NMDA).

170 Binding free energies for Na(+) and aspartate obtained using this intermediate state are in

171 Our results indicate that the invariant aspartate of the J-domain perturbs a conserved intramole

172 Golgi compartments depends on the N-terminal aspartate of the mature peptides.

173 as guanidine, which interacts strongly with aspartate of the protease catalytic triad, as well as mi

174 isplays a good biosafety profile, eliminates aspartate only in OXPHOS-incompetent tumors, and prevent

175 tal heme site of DyPs can be tuned to select aspartate or arginine for the rate enhancement of peroxi

176 ino acid specificity of PARP1 and PARP2 from aspartate or glutamate to serine residues(5-10).

177 ino acid specificity of PARP1 and PARP2 from aspartate or glutamate to serine(9,10).

178 ccelerated by substituting this glycine with aspartate or glutamate.

179 Together these findings demonstrate that the aspartate pathway in Mtb relies on a combination of meta

180 ulations of related enzymes suggest that the aspartate plays an important role in enhancing the catal

181 is predominantly mediated by the N-methyl-d-aspartate receptor (NMDA) receptor, although NMDA-indepe

182 ling events were dependent on the N-methyl-d-aspartate receptor (NMDA-R) and low-density lipoprotein

183 Increased synaptic N-methyl-d-aspartate receptor (NMDAR) activity in the hypothalamic

184 entiation occurred independent of N-methyl-D-aspartate receptor (NMDAR) activity, was accompanied by

185 inhibition hypothesis posits that N-methyl-d-aspartate receptor (NMDAR) antagonists such as ketamine

186 ntibodies from patients with anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis alter the levels

187 Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is an immune-med

188 Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most comm

189 Of these, the N-methyl-d-aspartate receptor (NMDAR) family has many critical role

190 orokynurenic acid (7-Cl-KYNA), an N-methyl-D-aspartate receptor (NMDAR) glycine site antagonist, and

191 this is unclear but may be due to N-methyl-D-aspartate receptor (NMDAR) hypofunction and parvalbumin

192 N-methyl-D-aspartate receptor (NMDAR) hypofunction has been implica

193 The N-methyl-d-aspartate receptor (NMDAR) is an ion channel that mediat

194 Downward FRH did not require N-methyl-D-aspartate receptor (NMDAR) signaling and was associated

195 Alterations of the N-methyl-d-aspartate receptor (NMDAR) subunit GluN2A, encoded by GR

196 emonstrate that the developmental N-methyl-D-aspartate receptor (NMDAR) subunit switch from GluN2B to

197 nine cycle, is a known agonist of N-methyl-d-aspartate receptor (NMDAR), a glutamate receptor subtype

198 All three compounds reduced N-methyl-D-aspartate receptor (NMDAR)-mediated currents 1 week afte

199 We previously showed that N Methyl D Aspartate Receptor (NMDARs), expressed on cerebral endot

200 ne neuroinflammation (due to anti-N-methyl-D-aspartate receptor [NMDA] encephalitis and multiple scle

201 es of ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist(2,3), provide rapid and lo

202 id antidepressant efficacy of the N-methyl-D-aspartate receptor antagonist, ketamine, for treating ma

203 ts of ketamine, a non-competitive N-methyl-D-aspartate receptor antagonist, which produces rapid and

204 patients and measurements of anti-N-methyl-D-aspartate receptor antibodies were taken in 49 (14%) pat

205 ebo-controlled clinical trials of N-methyl-D-aspartate receptor augmentation of psychotropic drug tre

206 ng in reduced availability of the N-methyl-D-aspartate receptor coagonists glycine and D-serine and N

207 ed encephalomyelitis, and 6% anti-N-methyl-d-aspartate receptor encephalitis; and 17% (95% CI, 13%-21

208 also present in a mouse model of N-methyl-D-aspartate receptor hypofunction (Ppp1r2cre/Grin1 knockou

209 agonists glycine and D-serine and N-methyl-D-aspartate receptor hypofunction.

210 ostsynaptic current frequency and N-methyl-D-aspartate receptor hypofunction.

211 uch deficits in humans, including N-methyl-D-aspartate receptor modulators (ketamine, D-cycloserine),

212 substantially upon addition of an N-methyl-D-aspartate receptor peptide analog but not ATP.

213 ifically successive impairment of N-methyl-d-aspartate receptor subunit 2B (NR2B), postsynaptic densi

214 related to an upregulation of the N-methyl-D-aspartate receptor subunits NR1 and NR2A.

215 aging the NR2B subunit within the N-methyl-d-aspartate receptor with PET.

216 iated nociception modulation, and N-methyl-D-aspartate receptor, NMDAR, antagonism.

217 maging the GluN2B subunits of the N-methyl-d-aspartate receptor.

218 CSF from patients with either N-methyl-D-aspartate-receptor-antibody (pCSF(NMDAR), n = 7) or Leuc

219 ghtly controlled by activation of N-methyl-D-aspartate receptors (NMDAR) containing the GluN2A subuni

220 N-methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion cha

221 N-methyl-D-aspartate receptors (NMDARs) are required to shape activ

222 Antibodies against neuronal N-methyl-D-aspartate receptors (NMDARs) in patients with anti-NMDAR

223 by glutamate receptors including N-methyl-D-aspartate receptors (NMDARs) is pivotal to brain develop

224 N-Methyl-D-aspartate receptors (NMDARs) play critical roles in the

225 d characteristics for imaging the N-methyl-d-aspartate receptors (NMDARs) subtype 2B (GluN1/2B), we i

226 bodies against natively expressed N-methyl-D-aspartate receptors (NMDARs), or the surface of live hip

227 N-methyl d-aspartate receptors are ligand-gated ionotropic receptor

228 effect requires open presynaptic N-methyl-d-aspartate receptors but not plasmin generation.

229 alcium signaling, and presynaptic N-methyl-D-aspartate receptors coupled with calcineurin signaling,

230 hibitors of the GluN2B subunit of N-methyl-d-aspartate receptors in the ionotropic glutamate receptor

231 rs, and GluN2B-subunit containing N-methyl-D-aspartate receptors, but not GluA1 subunit containing al

232 n-receptor tyrosine kinase Src or N-methyl-D-aspartate receptors.

233 bGCs directly excite mGCs through N-methyl-d-aspartate receptors.

234 Surprisingly, aspartate replacements mimicking the negative charge of

235 r-filled pocket surrounding an nNOS-specific aspartate residue (absent in eNOS).

236 on to the vital hydrogen bonding between the aspartate residue (Asp53) of beta2M and methionine (Met9

237 ediates the conversion of a highly conserved aspartate residue in a cyclic substrate into a succinimi

238 acid asparagine 285, which is replaced by an aspartate residue in type P(O) SadP, was required for bi

239 evealed the presence of a water-coordinating aspartate residue that limits esterase activity.

240 ysis of ALG6 variants identified a catalytic aspartate residue that probably acts as a general base.

241 rtance of a proposed lanthanide-coordinating aspartate residue.

242 preQ(1)-recognition site by pushing back an aspartate residue.

243 active site variants identified two central aspartate residues Asp-99 and Asp-219 as essential for c

244 ins and a cluster of conserved histidine and aspartate residues capable of binding two metal atoms in

245 within the lens wherein the isomerization of aspartate residues in crystallin peptides differentially

246 Expression of a gp5 variant in which aspartate residues in the metal-binding site of the poly

247 ective cleavage at only 6 solvent accessible aspartate residues was observed.

248 Two conserved aspartate residues, Asp-163 and Asp-164, are essential f

249 marily directs PAR modification to glutamate/aspartate residues.

250 eins, and reveal tripeptide Arginine-Glycine-Aspartate (RGD) domains that bind and signal through int

251 fically, ICOSL contains the arginine-glycine-aspartate (RGD) motif, which allowed for a high-affinity

252 hanism, while tight binding of Gd(3+) to the aspartate ring blocks the channel and prevents Na(+) fro

253 ases the expression of glycolysis and malate-aspartate shuttle (MAS) genes.

254 Here, we studied the role of malate-aspartate shuttle (MAS)-dependent substrate supply in OX

255 echanisms with consequent compromised malate-aspartate shuttle and changes in allosteric effectors of

256 mitochondrial citrate export and the malate-aspartate shuttle promote histone acetylation, and speci

257 findings support a model in which the malate-aspartate shuttle, mitochondrial citrate export and comp

258 drial transporter that is part of the malate-aspartate shuttle, which regulates the NAD+/NADH ratio b

259 the regulatory component of the NADH malate-aspartate shuttle.

260 re directly coordinated by a ring of anionic aspartate side chains.

261 The aspartate-specific cysteine protease caspase-8 suppresse

262 Furthermore, aspartate supplementation was sufficient to reverse the

263 We consider the trimeric Na(+)-aspartate symporter Glt(Ph), a homolog of an important c

264 within a model archaeal homolog, sodium, and aspartate symporter Glt(Ph).

265 This dependence on endogenous aspartate synthesis derives from the presence of excess

266 d glucose consumption is required to support aspartate synthesis that drives the increase of biomass

267 by targeting their dependence upon GOT1 for aspartate synthesis.

268 he TCA cycle while accumulating pyruvate and aspartate that rescue their redox defects.

269 Besides L-glutamate and L-aspartate, they also recognize D-aspartate, which might

270 e mutation of the FXIII-A Isoleucine-Leucine-Aspartate-Threonine (ILDT) motif prevented Lys679Met FXI

271 trations, thereby sequestering nitrogen from aspartate through glutamic-oxaloacetic transaminase 1 (G

272 pus, tCho in hippocampus, and total N-acetyl aspartate (tNAA) in hippocampus.

273 g site, in the coupled binding of sodium and aspartate to Glt(Ph) In this study, we develop a fluores

274 events in the coupled binding of sodium and aspartate to Glt(Ph).

275 xyaminoimidazole ribonucleotide (CAIR) and l-aspartate to N-succinylcarboxamide-5-aminoimidazole ribo

276 e protein (CRP), alanine transaminase (ALT), aspartate transaminase (AST), and liver fat content.

277 lanine transaminase (ALT), and mitochondrial aspartate transaminase (m-AST).

278 1), alanine aminotransferase (P = .024), and aspartate transaminase (P = .0040); elevated lactate deh

279 levated liver abnormalities were as follows: aspartate transaminase 15.0% (95% CI, 13.6%-16.5%) and a

280 / degrees C increase (p = 0.005)], increased aspartate transaminase [OR, 2.47 (p = 0.019)], and decre

281 nsient increases in alanine transaminase and aspartate transaminase were observed at Day 7, resolving

282 DCD-NEVLP-groups showed significantly lower aspartate transaminase-levels compared with the SCS-grou

283 The glutamate aspartate transporter (GLAST) shields the auditory synap

284 e 1 Family Member L1 (ALDH1L1) and Glutamate Aspartate Transporter (GLAST); the reactive markers: Gli

285 GltPh, a homotrimeric aspartate transporter from Pyrococcus horikoshii, is an

286 survival in bone, despite the presence of an aspartate transporter, which we identified as GltT and c

287 We show that protonation of a conserved aspartate triggers conformational transition from outwar

288 (68)Ga-labeled arginine-glycine-aspartate tripeptide sequence (RGD) PET/CT imaging may p

289 Localization of the N-methyl-D-aspartate type glutamate receptor (NMDAR) to dendritic s

290 N-Methyl-d-aspartate type glutamate receptors (NMDARs) are key medi

291 Contributions of N-methyl-D-aspartate-type glutamate receptors (NMDARs) to cDCS-medi

292 HT1) as a candidate gene associated with the aspartate uptake trait.

293 Furthermore, it was detected that aspartate was formed in the flesh of only thawed fish af

294 h measurements, the rise in Lactate/N-acetyl aspartate was reduced in white (p = 0.030) and grey matt

295 Zinc, citrate, and aspartate were correlated with each other (range r = 0.4

296 lpha-His-20, alpha-His-50, and beta-His-2 to aspartate were significantly decreased.

297 amate and L-aspartate, they also recognize D-aspartate, which might participate in mammalian neurotra

298 ine contributed to increased biosynthesis of aspartate, which supplied nitrogen for nucleotide synthe

299 Most notably, substituting aspartate with glutamate (RGE) was shown to eliminate in

300 , where two Na(+) ions coexist and couple to aspartate with similar strengths, boosting its affinity.