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1  Ser722 and Ser792 of RAPTOR were mutated to alanine.
2 mpounds, focusing on the smallest amino acid alanine.
3 lf the Pro3 or Pro6 residues are replaced by alanine.
4 y related CLK3 which harbors a smaller DFG-1 alanine.
5 activity is influenced by the abundance of L-alanine.
6  IQGAP1 construct by replacing Tyr-1510 with alanine.
7 ta-hydroxybutyrate, trimethyl uric acid, and alanine.
8 rough condensation of these amines with beta-alanine.
9 elevant two serine residues were replaced by alanine.
10  significant accumulation of extracellular D-alanine.
11 lu residues in the motif were substituted by alanine.
12  types studied, though still more basic than alanine.
13 on substitution of catalytic acid Asp-239 by alanine.
14 l but the arginine residues were replaced by alanine.
15 ed lactate, S-lactoylglutathione, N-acetyl-l-alanine, 2-hydroxyglutarate, and UMP levels.
16 erminal Lys with isotopically labeled acetyl-alanine; (3) thiol Michael addition of an isotopically l
17 pA/PreNAC complex displays a contact between alanine 53 of alpha-synuclein and glutamine 111 in the c
18                                  Mutation of alanine 53 to glutamate, as found in patients with early
19 dequate molecular features, it is, owning an alanine (A) as their penultimate N-terminal residue (e.g
20 recipitation studies reveal that the R205 to alanine (A) mutant of YBX1 (YBX1-R205A) interacted less
21 V FP were substituted with neutrally charged alanines (A).
22 one carrying substitution of IN serine 57 to alanine, a mutation known to impair viral DNA integratio
23 mined whether mutation of these cysteines to alanine affects differentially Tau mediated toxicity and
24                                              Alanine (Ala) accumulated to about 35% of total amino ac
25  at 160 degrees C from d-glucose (Glc) and l-alanine (Ala) as well as from fructosylalanine - the cor
26 1/FLI1-T79A, containing a threonine (Thr) to alanine (Ala) substitution at amino acid 79, failed to i
27 ghly conserved tyrosine residue (Y382), into alanines also delayed the activation rate.
28 tamate (EcE65/AaE64), which, when mutated to alanine, also enhances the production of siRNA-like prod
29 ial protein, the putative N-acetylmuramoyl-l-alanine amidase RC0497.
30  including gamma-glutamyl transferase (GGT), alanine aminopeptidase (AAP), and N-acetyl-beta-d-glucos
31 onths (symptomatic seroconversion illness or alanine aminotransferase > 10 x upper limit of normal) o
32 dermatitis acneiform (20 [9%]) and increased alanine aminotransferase (17 [8%]).
33 mmon adverse events were increased levels of alanine aminotransferase (64%) and aspartate aminotransf
34 lation, including nitrate reductase (NR) and alanine aminotransferase (AlaAT), were induced during se
35 cluded HBV DNA >=2000 IU/mL, with or without alanine aminotransferase (ALT) >=2-fold the upper limit
36 positive women and HBeAg-negative women with alanine aminotransferase (ALT) >=40 IU/L as a predictor
37 amma-glutamyl transferase (-30%; P < 0.001), alanine aminotransferase (ALT) (-49%; P = 0.009), and as
38 pectively), corrected T1 (cT1; -8% and -9%), alanine aminotransferase (ALT) (-67% and -60%), aspartat
39 rtate aminotransferase (AST) was higher than alanine aminotransferase (ALT) at admission (46 vs. 30 U
40  increased BM sproc recruitment, and reduced alanine aminotransferase (ALT) by 92% and 77% at 5 weeks
41 ges in qualitative serum HBsAg, HBV DNA, and alanine aminotransferase (ALT) concentrations in additio
42                   Analysis of peak values of alanine aminotransferase (ALT) during COVID-19 showed mo
43  Interpretations of elevated blood levels of alanine aminotransferase (ALT) for drug-induced liver in
44 otential mediating role of viral load and/or alanine aminotransferase (ALT) in the relation of smokin
45 RS was associated with an increase in plasma alanine aminotransferase (ALT) level of 26% in those wit
46  aminotransferase (AST) and 35% had elevated alanine aminotransferase (ALT) levels on admission.
47  Correlates of FLD and its relationship with alanine aminotransferase (ALT) overtime were examined in
48 ted positive and had higher initial and peak alanine aminotransferase (ALT) than those who tested neg
49  The primary endpoint was the time for serum alanine aminotransferase (ALT) to fall below 100 U/L.
50  were metabolically abnormal or had elevated alanine aminotransferase (ALT) were higher than among th
51 L), high-density lipoprotein, triglycerides, alanine aminotransferase (ALT), and aspartate aminotrans
52 levated gamma-glutamyl transferase (GGT) and alanine aminotransferase (ALT), and higher number of hea
53 ic acids and flavones reduced blood glucose, alanine aminotransferase (ALT), aspartate aminotransfera
54 of salivary concentrations of total protein, alanine aminotransferase (ALT), aspartate aminotransfera
55 ere constructed using baseline and change in alanine aminotransferase (ALT), aspartate aminotransfera
56 three groups: patients with steatosis/normal alanine aminotransferase (ALT), steatosis/elevated ALT,
57 P( KO) mice fed an HFD exhibited lower serum alanine aminotransferase (ALT)/aspartate aminotransferas
58 ctinib-related adverse events were increased alanine aminotransferase (eight [3%] of 260 patients), a
59 ed by increased leukocyte count (P < .0001), alanine aminotransferase (P = .024), and aspartate trans
60 enia (six [5%] vs three [4%]), and increased alanine aminotransferase (six [5%] vs two [3%]).
61 elated serious adverse events were increased alanine aminotransferase (two [<1%] of 260 patients), in
62  routinely assayed in clinical laboratories (alanine aminotransferase 1, C-reactive protein, and myog
63       In a mouse model of ALD, liver injury (alanine aminotransferase [ALT]) and steatosis were preve
64 ver tests (aspartate aminotransferase [AST], alanine aminotransferase [ALT], alkaline phosphatase [AL
65  histological staining, measurement of serum alanine aminotransferase activity, and expression analys
66 ation was accompanied by decreased levels of alanine aminotransferase and aspartate aminotransferase
67 verse events were rash (89 [56%]), increased alanine aminotransferase concentrations (74 [46%]), and
68 ropenia (15 [50%] of 30 patients), increased alanine aminotransferase concentrations (two [7%] patien
69 0%] of 425 patients in the sunitinib group), alanine aminotransferase increase (54 [13%] vs 11 [3%]),
70  (39.1% vs 28.1%), pyrexia (38.7% vs 26.0%), alanine aminotransferase increased (33.9% vs 22.8%), and
71 rtension (in 21% of the patients), increased alanine aminotransferase level (in 11%), increased aspar
72   Liver enzyme levels were elevated, with an alanine aminotransferase level of 48 U/L (0.80 ukat/L) (
73   Liver enzyme levels were elevated, with an alanine aminotransferase level of 48 U/L (0.80 ukat/L) (
74                                          The alanine aminotransferase levels decreased from 79.9 +/-
75 de association study combining cirrhosis and alanine aminotransferase levels performed in 5 discovery
76 72,705 controls and 362,539 individuals with alanine aminotransferase levels).
77 xcept lactate correlated with EAD, 90-minute alanine aminotransferase showing the highest area under
78 an isolated grade 4 increase in the level of alanine aminotransferase that led to treatment discontin
79                   For all subjects combined, alanine aminotransferase was reduced by 15.8 +/- 8.4% (P
80 on, and hyperkalaemia, and grade 4 increased alanine aminotransferase were reported in one patient ea
81 HBV DNA target not detected, normal level of alanine aminotransferase) after removal of all therapy.
82 ts indicated a causal role of increased ALT (alanine aminotransferase) in the development of type 2 d
83 e, HBV DNA below 2000 IU/mL, normal level of alanine aminotransferase) or functional cure (HBsAg belo
84 ymes than control group (mean difference for alanine aminotransferase, aspartate aminotransferase, al
85                We assessed concentrations of alanine aminotransferase, aspartate aminotransferase, an
86  (P < 0.01) serum total lipids, cholesterol, alanine aminotransferase, aspartate aminotransferase, an
87 ction in ALP had greater reductions in serum alanine aminotransferase, aspartate aminotransferase, ga
88 ver follow-up time, with increasing level of alanine aminotransferase, hemoglobin A1C (P<.05), gamma-
89  values of aspartate aminotransferase (AST), alanine aminotransferase, lactate dehydrogenase, and cre
90 parameters (PP) (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, glucose
91 de levels and improved liver markers such as alanine aminotransferase, NAFLD activity score, and fibr
92 22% had advanced fibrosis and 54% had normal alanine aminotransferase.
93                POD3 of 7 total bilirubin and alanine aminotransferase; POD3 aspartate aminotransferas
94 o resulted in hypersusceptibility to DCS, an alanine analogue antibiotic that inhibits alanine racema
95 Mutational analysis of the LLI sequence with alanine and arginine substitutions showed that its overa
96 alpha-hydroxy-4-cholesten-3-one, bile acids, alanine and aspartate aminotransferases, and neoepitope-
97  residues (seven in both TMHs 6 and 12) with alanine and generated a mutant termed 14A.
98 so show that Dat mediates the synthesis of D-alanine and its activity is influenced by the abundance
99 ate the general applicability of our method, alanine and other amino acids were analyzed from soy sau
100 rammes a metabolic network involving serine, alanine and pyruvate that drives the endogenous synthesi
101 e stalled polypeptides with carboxy-terminal alanine and threonine residues (CAT tails).
102 APC [APC with lysine 191-193 replaced with 3 alanines and arginine 229/230 replaced with 2 alanines])
103 a-(piperidin-1-yl)alanine, beta-(azepan-1-yl)alanine, and fluorescent and ciprofloxacin-containing am
104 is instantaneously hydrolyzed to [1-(13)C]-l-alanine, and subsequently metabolized to [1-(13)C]lactat
105 sparagine (Asx), glutamic acid/glutamine and alanine are positively correlated with seawater pCO(2) a
106 noncanonical 1-deoxysphingolipids when using alanine as a substrate(4,5).
107         Glutamate, glutathione, lactate, and alanine, as well as interleukin (IL)-1beta and IL-8, inc
108              Substitution to helix-enhancing alanine at either of these positions dramatically enhanc
109 in sensitivity, and that simply changing the alanine at position 578 in the S4-S5 helix of the chicke
110 to PKa was prepared by replacing Arg371 with alanine at the activation cleavage site (PK-R371A, or si
111 d gene, dat, can support slow growth of an L-alanine auxotroph.
112 th tetrapeptide alanine-valine-phenylalanine-alanine (AVFA), a fragment of RuBisCO.
113 lysophosphatidic acid, trypsin, SLIGRL, beta-alanine, BAM8-22), and scratching was assessed using a m
114  method to show that skeletal muscle-derived alanine becomes rate controlling for hepatic mitochondri
115 lysophosphatidylcholines, triglycerides, and alanine before GADA-first.
116 eta-benzylaminoalanine, beta-(piperidin-1-yl)alanine, beta-(azepan-1-yl)alanine, and fluorescent and
117 ed the major enzymes involved in B. subtilis alanine biosynthesis and identified an alanine permease,
118 ugh some of the purified enzymes involved in alanine biosynthesis have been shown to catalyze reversi
119                         beta-N-methylamino-l-alanine (BMAA) is a nonproteinogenic amino acid that has
120  environmental neurotoxin beta-methylamino-L-alanine (BMAA).
121 iscrete, we generated six charged cluster-to-alanine (CCTA) mutants within the UL148 ectodomain and c
122 orus (i.e. the junction with the stomach) of alanine, choline compounds, creatine, leucine and valine
123 s: Valine (coded by GUX [X = U, C, A or G]), alanine (coded by GCX), aspartic acid (coded by GAY [Y =
124  class of Ser codons, UCX, were derived from alanine codons, GCX, distinctly different from the other
125                               Methionine and alanine, compounds produced in BCAA metabolism and fatty
126 e skeletal total amino acid, Asx, serine and alanine concentrations combined with the calcification m
127 ders glucose binding because its mutation to alanine converts the AncMsPFK enzyme into a specific ADP
128                      One ATP-grasp enzyme, d-alanine-d-alanine ligase (Ddl), catalyzes ATP-dependent
129 rs, two novel variants of genes encoding a D-alanine-D-alanine ligase (ddl6 and ddl7) located within
130                        Their substitution to alanine decreased high-molar-mass alternan yield by a th
131                    Finally, we discover that alanine dehydrogenase is involved in ammonium assimilati
132            SigG1 regulates the expression of alanine dehydrogenase, ald and the WhiB-like regulator,
133  conclude that the lack of AnxA6 compromises alanine-dependent GNG and liver regeneration in mice.
134 -/-) mice was the consequence of an impaired alanine-dependent GNG in AnxA6(-/-) hepatocytes.
135           Here, we developed a (13)C-labeled alanine derivative, [1-(13)C]-l-alanine ethyl ester, as
136 es ATP-dependent formation of the d-alanyl-d-alanine dipeptide essential for bacterial cell wall bios
137 nd that mutation of threonine (T) T923 to an alanine disrupted synaptic trafficking.
138 ank3 residues (949)Arg-Arg-Lys(951) to three alanines disrupts CaMKII binding in vitro and CaMKII ass
139  the S/T residues have been substituted with alanines does not.
140 a knockin mouse in which S600 was mutated to alanine (Drp1S600A).
141 ral studies of antibody-antigen complexes by Alanine et al., Urusova et al., and Rawlinson et al. def
142        Following cell transport, [1-(13)C]-l-alanine ethyl ester is instantaneously hydrolyzed to [1-
143                                              Alanine ethyl ester readily crosses cell membrane while
144 13)C-labeled alanine derivative, [1-(13)C]-l-alanine ethyl ester, as a viable DNP probe whose chemica
145                                Expression of alanine-expanded PABPN1 is linked to the formation of nu
146 odel where altered protein interactions with alanine-expanded PABPN1 that lead to loss or gain of fun
147             Soil microbes appeared to remove alanine from soil solution within 1 min and release enou
148 ow has a major role in the assimilation of D-alanine from the environment.
149 type, a charge-scrambled, a phenylalanine-to-alanine (FtoA), and an arginine-to-lysine (RtoK) mutant
150 share a glycine-phenylalanine-hydroxyproline/alanine (GFO/A) motif that is recognised by the enzyme i
151  Strecker aldehydes was also demonstrated in alanine/glucose and in a bread model systems using [(13)
152 ponent analysis, we observed that glutamine, alanine, glutathione, and lactate were positively associ
153  of hexose monophosphate, pyruvate, lactate, alanine, glycerol-3 phosphate, and isocitrate were signi
154 glutamine catabolism, such as glutamic acid, alanine, glycine, pyrimidine, and creatine.
155        Herein, we present a versatile acetyl-alanine-glycine (Ac-AG) tag that conceals quantitative i
156 tant mice in which Ser21 is substituted with alanine (GRK1-S21A), preventing dark-dependent phosphory
157 he DDR, tyrosine 142 (Y142), is converted to alanine (H2ax-Y142A).
158 l arylsulfones as dipolarophiles and glycine/alanine iminoesters as azomethine ylide precursors has b
159 framework, whereby serine is substituted for alanine in the fifth position, provided the most potent
160                      We mutated K4 or K36 to alanine in the histone variant H3.3 and showed that the
161 econd threonine of the TTVGYG sequence by an alanine in the hKv2.1 and hKv3.1 channels, which are kno
162 tes on serines 63, 68, and 69 are mutated to alanines), in which phospholemman is rendered unphosphor
163 ates of alanine turnover, assessed by [3-13C]alanine, in a subgroup of participants under similar fas
164 racemase and d-alanine ligase required for d-alanine incorporation into cell wall peptidoglycan.
165 n channel downstream of MrgprD, and the beta-alanine-induced calcium signal was attributed mostly to
166             Mutation of H3K36 to arginine or alanine inhibits H3K27 methylation by PRC2 on nucleosome
167 ing a single and double deletion or a single alanine insertion in the large (L) polymerase protein th
168 ying a single or double deletion or a single alanine insertion were genetically stable, highly attenu
169 te alanine, the primary synthetic enzyme for alanine is encoded by alaT, although a second gene, dat,
170 te of the polymerase domain were replaced by alanine is highly toxic to E. coli cells.
171                      Under metabolic stress, alanine is the main hepatic gluconeogenic substrate, and
172            One ATP-grasp enzyme, d-alanine-d-alanine ligase (Ddl), catalyzes ATP-dependent formation
173 vel variants of genes encoding a D-alanine-D-alanine ligase (ddl6 and ddl7) located within gene casse
174 ibiotic that inhibits alanine racemase and d-alanine ligase required for d-alanine incorporation into
175 utamic acids (mdxS3E) or nonphosphorylatable alanines (mdxS3A).
176 pulses with either N-acetylmuramic acid or D-alanine metabolic probes showed that cell wall growth is
177 g auxotrophic markers, the genes involved in alanine metabolism have not been characterized fully.
178    This work provides valuable insights into alanine metabolism that suggests that the relative abund
179 SPT therefore links serine and mitochondrial alanine metabolism to membrane lipid diversity, which fu
180                            Ten (lactic acid, alanine, methionine, fumaric acid, inosine, inosine mono
181 ests that the relative abundance of D- and L-alanine might be linked with cytosolic pool of D and L-g
182 ion in murine Nkx3.1 to code for a serine to alanine missense at amino acid 186, the target for Dyrk1
183 onserved aspartate-glutamate-leucine-leucine-alanine motif) competitively inhibit the GID1-NGR5 inter
184                                           An alanine mutagenesis analysis reveals that two receptor s
185                                              Alanine mutagenesis has identified residues that disrupt
186 Furthermore, kinetic analysis of active site alanine mutants indicates that carbapenem hydrolysis is
187                                    Serine-to-alanine mutation at position 53 of the Kv7.5 amino termi
188                                         Each alanine mutation elicited a distinctive off-pathway dist
189                 Yeast cells with arginine-to-alanine mutations in the H4 basic patch (H4(2RA)) exhibi
190                                              Alanine mutations in the sequence between amino acids 37
191                                              Alanine mutations of all 11 phosphorylation sites on the
192 n the fifth glycine of cross-bridges and the alanine of the adjacent stem peptide.
193 e, and higher waist circumference, levels of alanine or aspartate aminotransferase, total and low-den
194     Replacement of Arg-177 in PKG1alpha with alanine or methionine also increased basal activity.
195                      Mutations of Cys69 with alanine or serine show 5hmC-specificity that mirrors the
196 APC [APC with lysine 191-193 replaced with 3 alanines] or 5A-APC [APC with lysine 191-193 replaced wi
197  the mitochondrial pyruvate carrier promotes alanine oxidation to mitigate deoxysphingolipid synthesi
198                                              Alanine (p <= 0.011), tyrosine (p <= 0.014) and formate
199 t changes an aspartic acid at position 50 to alanine (p.D50A), resulting in intellectual disability i
200           Introducing the cleavable arginine-alanine peptide into the NAc attenuated expression of co
201 tilis alanine biosynthesis and identified an alanine permease, AlaP (YtnA), which we show has a major
202 derwent simultaneous fluorodihydroxyphenyl-l-alanine PET (18F-DOPA-PET) and resting state functional
203                          Rather, amino acids alanine, phenylalanine, glutamic acid, valine, and leuci
204                       Both isomeric forms of alanine play a crucial role in bacterial growth and viab
205 mutant human superoxide dismutase glycine to alanine point mutation at amino acid 93 (hSOD1(G93A)) mo
206  active site of pol beta, 35, 68, and 72, to alanine (pol beta KDelta3A) increased the binding affini
207 cted a prospective [(18)F]-dihydroxyphenyl-L-alanine positron emission tomography study in antipsycho
208 m metabolites, 1-(13) C-lactate and 1-(13) C-alanine, predicted histological viability.
209 on of a single residue in beta1, Cys-162, to alanine prevented palmitoylation, reduced the level of b
210                           Mutating Ser162 to Alanine produces constitutive activity, whereas the phos
211 ffect on S-acylation, but extended and rigid alanine-proline repeats perturbed it.
212 an alanine analogue antibiotic that inhibits alanine racemase and d-alanine ligase required for d-ala
213           FigC belongs to a new subfamily of alanine racemase-fold PLP-dependent decarboxylases that
214 exposed residues that, when substituted with alanine, reduce antagonism of GDF8 in full-length WFIKKN
215                         Here, we report that alanine repeat expansions in the HOXD13 TF, which cause
216                   Moreover, we found that an alanine residue adjacent to the GXXG loop is critical fo
217 e alcove through introduction of the smaller alanine residue in the F229A variant diminishes conversi
218 e-derived fatty acid and a rare dehydro-beta-alanine residue.
219         Replacement of Asp506 and Asp571 for alanine residues abolishes enzyme activity, thus identif
220 cterized by a stretch of amino acids rich in alanine residues that are organized into a hydrophobic,
221 hich the 2 cysteine residues are replaced by alanine residues, impairs the generation of induced plur
222 ides, containing either normal or deuterated alanine residues, were used to confirm the presence and
223                           The pH-insensitive alanine resonance was used as a reference.
224           Replacement of these residues with alanine results in decreased methylation activity and ch
225 nism of substrate-buffering by myristoylated alanine-rich C kinase substrate (MARCKS) and two newly c
226 phospholipid binding domain of Myristoylated alanine-rich C-kinase substrate (MARCKS) could serve as
227                                Myristoylated alanine-rich C-kinase substrate (MARCKS) is an intracell
228 odels with an original marker, myristoylated alanine-rich C-kinase substrate phosphorylated at serine
229 ed increased activation of the Ste20 proline alanine-rich kinase-Na+-Cl- cotransporter (SPAK-NCC) pho
230 g a SUMO acceptor site, a central disordered alanine-rich motif, a proline-rich domain, and a transac
231 e report that mice harboring a serine 365-to-alanine (S365A) mutation in STING are unexpectedly resis
232              Utilizing Mut-Seq to analyze an alanine scan library of Lit alleles, we identified two s
233  an important paramyxoviral model to perform alanine scan mutagenesis and a series of multidisciplina
234                         Here we conducted an alanine scan of active site constituents that engage the
235                                           An alanine scan of apelin-17 reveals that the integrity and
236 hin the target peptide through computational alanine scanning anticipates not only the key residues f
237                       Furthermore, in silico alanine scanning calculations of the last 21 residues of
238                          In combination with alanine scanning mutagenesis and activity measurements w
239                    Here, we use a systematic alanine scanning mutagenesis approach to understand the
240                                              Alanine scanning revealed decreased inhibition by the ap
241  per-residue decomposition calculations, and alanine scanning studies are done to provide further ins
242       By sequence analysis and computational alanine scanning we identify key residues and motifs inv
243 gar binding and catalysis were identified by alanine scanning, D36 being a critical residue for F6P b
244 raction, demonstrating that structure-guided alanine-scanning and computational modeling can serve as
245 t of programmes for performing computational alanine-scanning mutagenesis (CASM) to guide experiments
246 ne the Rab5-p110beta interface, we performed alanine-scanning mutagenesis and analyzed Rab5 binding w
247         In experimental protein engineering, alanine-scanning mutagenesis involves the replacement of
248 ght interact and bind alpha2-AP, and used an alanine-scanning mutagenesis method to select residues h
249                                              Alanine-scanning mutagenesis of Qtip shows that its loca
250             Herein, we used structure-guided alanine-scanning mutagenesis to map the functional epito
251                                              Alanine-scanning of the peptide identified three key res
252                                        Using alanine-substituted BigDyn analogs, we find that the Big
253                                Expression of alanine-substituted, phosphodeficient GFP-gle1A(6A) prom
254 d repressor activities, using a ParA with an alanine substitution at Arg(351), a residue previously p
255 t that knock-in mice harboring a cysteine-to-alanine substitution at Krt14's codon 373 (C373A) exhibi
256  Sprouty1 knockin mice bearing a tyrosine-to-alanine substitution in position 53, corresponding to th
257 ling process because a YAP1 mutant harboring alanine substitutions (Mt-YAP5SA) in LATS1 kinase recogn
258 ino acids 363 and 394 having four additional alanine substitutions (STANT + 7A) reduced desensitizati
259  of Klebsiella oxytoca NasR to site-directed alanine substitutions and measured RNA-binding activity.
260            Except for P478A and K505A R508A, alanine substitutions at conserved residues abolished GP
261 nt ASIC1a bearing truncation or glutamate-to-alanine substitutions at distal NT causes constitutive c
262 Using the DNA-PKcs (5A) mouse model carrying alanine substitutions at the T2609 cluster, here we show
263                              The 3D(pol) NLS alanine substitutions of T19 and L21 results in aberrant
264 ted by the orthosteric agonists GABA or beta-alanine, the allosteric agonist propofol, or combination
265 ave a biochemical activity that can generate alanine, the primary synthetic enzyme for alanine is enc
266 composition-arginine, lysine, aspartic acid, alanine, threonine and low levels of isoleucine and meth
267 ate; that transition was abolished with high-alanine TnT.
268 es the replacement of selected residues with alanine to determine the energetic contribution of each
269 ng tRNA, as exemplified by AlaRS mischarging alanine to G4:U69-containing tRNAThr.
270  viruses containing amino acid substitutions alanine to threonine at residues 125 (A125T) and 151 (A1
271                      Addition of glycine and alanine together doubled high impact pyrazines and addit
272 actate dehydrogenase ([1-(13)C]lactate), and alanine transaminase ([1-(13)C]alanine) was assessed.
273 ndex (BMI) (aOR, 1.58 per 1 kg/m2; P < .01), alanine transaminase (ALT) (aOR, 1.76 per 10 U/L; P < .0
274 ociation of rs72613567 with plasma levels of alanine transaminase (ALT) and clinical liver disease an
275 (87%) were asymptomatic, detected by routine alanine transaminase (ALT) or HCV monitoring.
276  levels of aspartate aminotransferase (AST), alanine transaminase (ALT), and mitochondrial aspartate
277 MA-IR), uric acid, C-reactive protein (CRP), alanine transaminase (ALT), aspartate transaminase (AST)
278 transaminase 15.0% (95% CI, 13.6%-16.5%) and alanine transaminase 15.0% (95% CI, 13.6%-16.4%).
279          Asymptomatic transient increases in alanine transaminase and aspartate transaminase were obs
280      These markers were predictors of severe alanine transaminase flares, after treatment withdrawal,
281 re not significantly affected; elevations in alanine transaminase occurred in combination with atazan
282                              Except for ALT (alanine transaminase), all GRSs were significantly assoc
283 -) mice had elevated liver weights and serum alanine transferase values.
284                        These findings reveal alanine transport as a new therapeutic target to enhance
285                                              Alanine transport was impaired in the cycA mutant, and t
286 eening assay coupled to MS, which identified alanine tRNA synthetase 1 (AARS1) as a direct substrate
287 ctions were associated with reduced rates of alanine turnover, assessed by [3-13C]alanine, in a subgr
288 -) hepatocytes 48 hours after PHx, impairing alanine uptake and, consequently, glucose production.
289 ) 2 and 4 are believed to facilitate hepatic alanine uptake.
290             The NLS residues were mutated to alanine using a type A full-genome cDNA clone, and the v
291 ulosis, in addition to its essential role in alanine utilisation as a nitrogen source.
292 he concentrate-rich diet showed increases in alanine, valerate, propionate, glucose, tyrosine, prolin
293 utoclaved seawater amended with tetrapeptide alanine-valine-phenylalanine-alanine (AVFA), a fragment
294              Separately, kinetic analysis of alanine variants has demonstrated that many of these sam
295  together with substitution of Trp(273) with alanine (W273A), generated an active site mimicking that
296 lactate), and alanine transaminase ([1-(13)C]alanine) was assessed.
297 ruvate-derived molecules such as acetoin and alanine were also increased.
298                         Baseline lactate and alanine were associated with baseline and 1-y changes of
299 ation upon substitution of histidine-43 with alanine; whereas x-ray absorption spectroscopy/extended
300 lanines and arginine 229/230 replaced with 2 alanines]) with normal cytoprotective properties, but gr

 
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