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1                                              Val to Ala substitution at position 49 (V49A) had partic
2                                              Val(48) and Ile(328) are at the outer end of TM1 and TM2
3                                              Val-136 and adjacent residues may mediate anesthetic bin
4                                              Val-70 follows a newly recognized conserved motif, PXGG
5                                              Val-Pro had the highest ORAC activity (19.45+/-2.15mumol
6                                              Val/Val mice exhibited robust reductions in spatial work
7 1+/-0.1% Arg, 1.07+/-0.05% Asx, 0.96+/-0.05% Val, 0.48+/-0.03% Thr, 0.35+/-0.03% Phe, and 0.28+/-0.03
8 omprising the hydrophobic residues Phe-1012, Val-1025, Tyr-1089, and Leu-1092).
9 hism Leu-108/Thr-189) or b (Prnp(b), Phe-108/Val-189) is associated with short or long incubation tim
10 n of alpha-helix 1 (residues Cys-11, Glu-12, Val-13, Lys-15, and Glu-16) and residue Glu-88.
11 rried on 16 Met (Val/Met and Met/Met) and 16 Val/Val participants selected from a large pool of healt
12 s (N=71; BDNF genotype: Val/Val (N=12, 17%), Val/Met (N=40, 56.3%), and Met/Met (N=19, 26.8%)) receiv
13                  C-terminal residues Ser-178-Val-190 act in concert with the flexible EF3/EF4 loop re
14                           Removal of Ser-178-Val-190 generated a C-terminal truncation mutant that fo
15 unique set of amino acid residues (Gln(218), Val(277), and Ala(286)) at the putative PpORS active sit
16 hobic and aromatic residues (Phe-22, Trp-25, Val-23, and Met-27) predominantly involved.
17        Making strategic mutations at Lys-26, Val-51, and Arg-79, we targeted residues predicted to be
18 ions suggest that C-terminal residues Gly-29-Val-40 form a tightly packed core with intermolecular di
19                                  Position 3 (Val) controls affinity, whereas position 7 (Tyr) acts as
20 ting the hydrophobic core residues, Leu-331, Val-338, and Ile-345, of Hec1 with alanine completely el
21 ydrophobic regions probed at Leu-17, Leu-34, Val-36, and Met-35 side chains were found to be very pro
22  at three amino acid positions (Lys/Asn-392, Val/Met-397, Lys/Arg-409) to alter the strength of inter
23 st that a surface of GRK2, including Leu(4), Val(7), Leu(8), Val(11), and Ser(12), directly interacts
24 sp(10), Tyr(13), Ala(16), Met(17), Gly(475), Val(477), and Ile(485) are more important for kinase dom
25 nase within the amino acid sequence Ser(478)-Val(479)-Leu(480)-Gln(481)-Val(482).
26 sequence Ser(478)-Val(479)-Leu(480)-Gln(481)-Val(482).
27  via the leucine 69 (Leu(69)) and valine 68 (Val(68)) residues.
28 ermediate, thereby establishing the alpha-70(Val-->Ile) intermediate as a reliable guide to mechanism
29  freeze-trapped intermediate of the alpha-70(Val-->Ile) MoFe protein as the Janus intermediate that s
30 residues Phe(63), Leu(64), Glu(77), Thr(78), Val(81), and Arg(82) that underlie IFN-beta-IFNAR1-media
31 e of GRK2, including Leu(4), Val(7), Leu(8), Val(11), and Ser(12), directly interacts with receptors,
32 ping identified the cleavage site as Leu(90)/Val(91) in the 95-amino acid ADRA1D NT domain, suggestin
33  site is only one amino acid N-terminal to a Val/Leu substitution associated with schizophrenia.
34 les conserved nonpolar side chains (Ile(A2), Val(A3), Val(B12), Phe(B24), and Phe(B25)) to engage the
35 rved nonpolar side chains (Ile(A2), Val(A3), Val(B12), Phe(B24), and Phe(B25)) to engage the receptor
36                                  In addition Val-907 was significantly coupled with Asn-1548 in IIIS6
37                   Patients with the A4V (Ala-Val) SOD1 mutation (SOD1(A4V)), the largest mutation pop
38 with azide and alkyne at its termini, N3-Ala-Val-NHCH2-C identical withCH, which is designed to self-
39 ning azide and alkyne at its termini (N3-Ala-Val-NHCH2C identical withCH, 1) was synthesized.
40   To our knowledge, the peptides Gly-Pro-Ala-Val, Val-Cys, and Phe-Phe have not been previously ident
41 Cys]-OH), PanSB1 (DOTA-PEG2-dTyr-Gln-Trp-Ala-Val-betaAla-His-Phe-Nle-NH2), and DOTA-MG11 (DOTA-dGlu-A
42 thylaniline-diglycolic acid-DPhe-Gln-Trp-Ala-Val-Gly-His-Leu-NHEt), showing excellent tumor localizin
43 -1-carboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Leu-OCH3 (ARBA05, 3) analogues are labeled w
44 -1-carboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Leupsi(CHOH- CH2)-(CH2)2-CH3 (RM7, 2), and t
45 -1-carboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-L eu-NH2 (BAY 86-7548).
46 t GRPr antagonist MJ9, Pip-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH(2) (Pip, 4-amino-1-carboxymethyl-
47 1-carboxymethyl-piperidine-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a synthetic bomb
48 1-carboxymethyl-piperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a synthetic bomb
49 -1-carboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 (RM2, 1; DOTA:1,4,7,10-tetraazac
50  GRPR antagonist JMV594 (H-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2) was conjugated to NODA-MPAA for
51 is DOTA-betaAla-betaAla-[H-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2], and NODA-MPAA is 2-[4-(carboxy
52 DA-MPAA-betaAla-betaAla-[H-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2], JMV4168 is DOTA-betaAla-betaAl
53  in children homozygous for the minor allele Val/Val, aOR: 1.25 (0.98-1.60).
54                   Specifically, Tyr(135) and Val(141) on the DEa loop were shown to be critical resid
55  required conserved loop C ((137)TP(138) and Val(150)) and loop E ((230)HW(231)) amino acids for bind
56 t amino acid stretches Phe(150)-Glu(152) and Val(166)-Glu(170) of FaeGad bind the terminal galactose
57 mprovement to FcgammaRIIIA (both Phe-158 and Val-158 allotypes), increased ADCC activity in vitro, an
58 s-189), and neutrophil elastase (Val-182 and Val-193) sites.
59                                  Met-186 and Val-288 in IFP1.4 are responsible for the formation of a
60 ides were Ile-Gln-Ala (beta-CN f187-189) and Val-Glu-Pro (beta-CN f116-118) having ACE IC50 values of
61 the peptide was cleaved between Ala(195) and Val(196) (i.e., 1 aa upstream of the expected position).
62 ly-78, Asp-79, His-81, Asn-235, Thr-267, and Val-368 are proposed to position appropriately the catal
63 ncludes residues Arg-32, Ile-33, Met-34, and Val-35.
64 n-cleaved skeletal actin (between Gly-42 and Val-43).
65  failed to cleave a peptide in which Ala and Val were reversed.
66 hese residues with equally conserved Glu and Val counterpart residues in NusG destabilized interactio
67 ched-chain amino acids (BCAAs) Leu, Ile, and Val are among nine essential amino acids that must be ob
68 d-chained amino acids (BCAAs) (Leu, Ile, and Val) and their catabolites, propionylcarnitine and butyr
69                                  The Leu and Val isomer investigation and trends revealed by our anal
70 tical functions, S. aureus represses Leu and Val synthesis, instead preferring to acquire them from t
71 t BcaP, is required for transporting Leu and Val to be used for iso-BCFA synthesis.
72  adsorption of structural isomers of Leu and Val, which exhibit a correlation between the position of
73 ts of the methyl groups of the Ile, Leu, and Val residues at two static magnetic fields.
74  for the methyl side chains on Ile, Leu, and Val residues showed changes in conformational exchange d
75 conserved loops; Pro-135 in a short loop and Val-70 in a longer loop.
76 of the reported differences in human Met and Val carriers across working memory, fear processes and s
77  these functions between sibling Met/Met and Val/Val mice.
78 ded an unambiguous identification of Nva and Val since the v ion was generated only when Val was pres
79                   However, when both Nva and Val were present in one peptide, the observation of inte
80 ntrast, the lactotripeptides Ile-Pro-Pro and Val-Pro-Pro, which were widely used as ingredients for h
81 of healthy adolescents stratified by sex and Val(158)Met genotype (n=1133), we examine BOLD responses
82  residue in this core (Met(25) in ssSPTa and Val(25) in ssSPTb) was identified which confers specific
83 acids (Ala, Asp, Glu, His, Lys, Pro, Thr and Val), incorporating a range of side-chain functionality.
84  with binding guanine in VldE (Asn, Thr, and Val) are similar in S. venezuelae OtsA (Asp, Ser, and Ph
85 ing hydrogen bonds between Asn-2-rho-TIA and Val-197, Trp-3-rho-TIA and Ser-318, and the positively c
86 (JA) to at least Ile, Leu, Met, Phe, Trp and Val and both osjar1 alleles had substantial reduction in
87 t high rates and for Gly, Lys, Phe, Tyr, and Val at moderate or low rates, respectively.
88 s with the Methionine (Met)/Valine (Val) and Val/Val genotypes showed higher fractional anisotropy an
89 ntly different between Met/Met, Met/Val, and Val/Val carriers in each group, which indicated that the
90                The PC inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethyl ketone significantly suppressed
91                      Tight packing of ARRDC3 Val-352', part of a 310 helix at the C terminus of PPXY1
92  the most potent peptides were identified as Val-Glu-Leu-Tyr-Pro, Ala-Phe-Val-Gly-Tyr-Val-Leu-Pro and
93 -acrylamido-phenylalanine (AcrF) mutation at Val-216 that leads to an increase in catalytic efficienc
94                                 The valve at Val(27) remains on average quite narrow in all protonati
95 ated changes in estradiol secretion and BDNF Val(66)Met genotype on measures of hippocampal function
96 w PET in 39 healthy women genotyped for BDNF Val(66)Met, and a confirmatory data set was obtained wit
97 ied the effect of the common functional BDNF Val(66)Met (rs6265) polymorphism on rewarding experience
98 effects of scopolamine were assessed in BDNF Val/Met knock-in mice, in which BDNF processing and rele
99 ensor imaging to examine the effects of BDNF Val(66)Met genotype on white matter microstructure in a
100 healthy controls were genotyped for the BDNF Val(66)Met polymorphism and underwent the monetary incen
101 an evidence regarding the effect of the BDNF Val(66)Met polymorphism on DA-mediated responses to stre
102                                     The BDNF Val(66)Met polymorphism, a possible risk variant for men
103 ypothesis that cellular sequelae of the BDNF Val(66)Met SNP interface with aspects of schizophrenic h
104 ration in women that the effects of the BDNF Val/Met polymorphism on hippocampal function are selecti
105                    Individuals with the BDNF Val/Val (valine allele) polymorphism showed better memor
106  and brain-derived neurotrophic factor (BDNF(Val/Val), BDNF(Met)) in the extent to which they moderat
107 ity time in the forced swimming test in BDNF(Val/Val) but not in BDNF(Met/Met) mice.
108                              Wild-type (BDNF(Val/Val)) and homozygous BDNF Val66Met (BDNF(Met/Met)) m
109 3 years, whereas Abeta(+)varepsilon4(+)/BDNF(Val/Val) individuals can expect a similar degree of impa
110  54 months compared with varepsilon4(-)/BDNF(Val/Val) participants (d=0.90-1.02).
111 ced in BDNF(Met/Met) mice compared with BDNF(Val/Val) mice.
112 ent active site inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone.
113 xial contacts do not engage the mutant beta6 Val and its nonmutant receptor region on an adjacent mol
114  results suggest that an interaction between Val(48) and Ile(328) stabilizes the closed channel and t
115 y was, however, found to be stronger between Val-907 in IIS4-S5 and Ile-1013 in IIS6.
116 otocol and Amyloid beta (39-42) peptide (Boc-Val-Val-IIe-Ala-OMe), following solution-phase strategy
117 loop A ((63)EKP(65) and Asp(69)) and loop C (Val(141), His(151), and Leu(154)).
118  implications for future satellite lidar Cal/Val efforts, because planned satellite lidars measuring
119                               Meaningful Cal/Val requires intercomparison data sets with small enough
120 ble along-track averaging for meaningful Cal/Val.
121          Several Calibration/Validation (Cal/Val) studies for CALIOP conducted with ground-based lida
122 tive PREP inhibitor, N-(pyridine-3-carbonyl)-Val-boroPro (ARI-3531, 22).
123 n between prenatal maternal smoking and COMT Val(158)Met in conduct problems and crime in the 1993 Pe
124 t mouse lines, which carry either human COMT Val or Met alleles via gene targeting.
125  recall of remote memories as silencing COMT Val overexpression starting from 30 days after the initi
126 overexpressing the human COMT-Val gene (COMT-Val-tg) present exaggerated remote memories (>50 days) w
127 ransgenic mice overexpressing the human COMT-Val gene (COMT-Val-tg) present exaggerated remote memori
128 cue the altered remote memory recall in COMT-Val-tg mice and increased PFC dopamine levels.
129 hereas the weakest-binding analogs contained Val, Ile, and Leu substitutions.
130 up B (CsA, 30 mg/kg per day), group C (CsA + Val, 30 + 30 mg/kg per day), and group D (Val, 30 mg/kg
131 that replacement of Lys-377 with either Cys, Val, Arg, or Asp disables both Na(+) and melibiose bindi
132 H-Glu-Thr-Pro-Asp-c[Cys-Phe-Trp-Lys-Tyr-Cys]-Val-OH) fragment 4-11 were synthesized to explore the in
133  + Val, 30 + 30 mg/kg per day), and group D (Val, 30 mg/kg per day).
134 near tripeptide l-delta-aminoadipoyl-l-Cys-d-Val (ACV) on the pathways to a number of important antib
135 nt of C-terminal di-Gly of ubiquitin with di-Val or di-Arg enhances CXCR4 mediated effects on cAMP le
136 , w ions, which can be used to differentiate Val and Nva.
137  in the corresponding HbA Evans (alpha62(E11)Val --> Met).
138 of adult Hb (HbA) Bristol-Alesha (beta67(E11)Val --> Met) that were associated with hemolytic anemia.
139 ts of human fetal Hb Toms River (gamma67(E11)Val --> Met) and beta subunits of adult Hb (HbA) Bristol
140  plasmin (Lys-189), and neutrophil elastase (Val-182 and Val-193) sites.
141         Thus, these two residues, especially Val-89 at the lobby region, are crucial for the entrance
142 n of any of the 20 canonical amino acids for Val-216, indicating that an expanded genetic code may of
143 ation of the adjacent GUA triplet coding for Val at the aminoacyl (A) site.
144 d SERCA-PLB binding, intermolecular FRET for Val(49)-stop (V49X) truncation mutant was paradoxically
145  as base, beta-ketosulfonamides derived from Val, Leu or Ile gave the expected beta-keto-alpha,alpha-
146 o characterize Nva and differentiate it from Val (Valine), a systematic study was conducted using hot
147 etermined mainly by steric restrictions from Val-136 on the beta2-subunit and favorable interactions
148 anchors in a hydrophobic pocket on Galphai1 (Val-34, Leu-194, Phe-196, Phe-336, Thr-340, Ile-343, and
149               Patients (N=71; BDNF genotype: Val/Val (N=12, 17%), Val/Met (N=40, 56.3%), and Met/Met
150 ly possessing lower activity BDNF genotypes (Val/Met, Met/Met).
151  stretches of rare codons, Leu(UUA)-Gly(GGU)-Val(GUA).
152 is-Asn-Pro, Cys-Ile-Gln-Pro-Val, Cys-Arg-Gln-Val-Phe) vs. 14 volatile compounds belonging to relevant
153 tics and a caspase-3 enzyme specific Asp-Glu-Val-Asp (DEVD) peptide.
154 Leu-Ala-Pro, Leu-Leu-Ala-Pro and Met-Ala-Gly-Val-Asp-His-Ile, with IC50 values in the range 43-159 mu
155        % MS SI restoration for the Z-Gly-Gly-Val and bradykinin peptides were 75-83% while % MS SI re
156 sense mutations Lys27Met (K27M) and Gly34Arg/Val (G34R/V) in genes encoding histone H3.3 (H3F3A) and
157 Ile > His >3,4-dihydroxyphenylalanine, Arg > Val > Lys, Tyr, Pro > hydroxyproline > alpha-aminobutyri
158 gnificant effect of BDNF (Met(66) carriers > Val/Val) on brain responses during the anticipation of m
159 lls lines carrying homozygous YARS2 p.191Gly>Val and m.11778G>A mutations.
160 ents both carrying homozygous YARS2 p.191Gly>Val and m.11778G>A mutations.
161                                   The 191Gly>Val mutation reduced the YARS2 protein level in the muta
162                           The YARS2 p.191Gly>Val mutation worsened the respiratory phenotypes associa
163 or both m.11778G>A and heterozygous p.191Gly>Val mutations and symptomatic subjects harboring m.11778
164 harboring m.11778G>A and homozygous p.191Gly>Val mutations) and controls lacking these mutations.
165 ON susceptibility allele (c.572G>T, p.191Gly>Val) in YARS2 gene encoding mitochondrial tyrosyl-tRNA s
166                    The hierarchy Leu>Met>Ile>Val at the C-terminal position was determined for all me
167 and acyl carrier protein (65-74) fragment (H-Val-Gln-Ala-Ala-Ile-Asp-Tyr-Ile-Asn-Gly-OH), following t
168 s have Met in position 129 and the other has Val.
169  The branched-chain amino acids (BCAAs) Ile, Val, and Leu are essential nutrients that humans and oth
170       The last 3 residues of NaV1.5 (Ser-Ile-Val) constitute a PDZ domain-binding motif that interact
171 idespread increases in radial diffusivity in Val/Val homozygotes compared with Met-allele carriers, p
172 hydrogenase, AtHDH1 (At4g20930), involved in Val degradation.
173 recollection increased significantly more in Val/Val individuals than in Met carriers in parietal and
174 s points to a role of the enzyme not only in Val but possibly also in Ile metabolism.
175 YXXPhi (where X is any amino acid and Phi is Val, Leu, or Ile) endocytic motif that, when transferred
176 eduction in content of JA-Ile, JA-Leu and JA-Val in florets.
177 at the N terminus: the tertiary amino acid L-Val induces a left-handed type II beta-turn in both the
178 f two different dipeptide nanotubes: l-Ala-l-Val and its retro-analog l-Val-l-Ala.
179        A designed beta-sheet-forming l-Ala-l-Val dipeptide containing azide and alkyne at its termini
180 anotubes: l-Ala-l-Val and its retro-analog l-Val-l-Ala.
181 ormula of the native L3P as D-Phe-N-Methyl-L-Val-L-Ala-OMe attached in N-ter to a 20-carbon fatty aci
182  the results for D + L mixtures of Ala, Leu, Val, and Pro.
183 Phe-Leu, Trp-Val, His-Leu, Glu-Lys, Ala-Leu, Val-Ala, Ser-Leu and Gly-Leu) inhibited DPP-IV.
184  analysis of a polar mixture composed of Leu-Val, Leu-Tyr, Gly-Tyr, and Ala-Tyr dissolved in DMSO-d6/
185  by the thrombin specific cleavage site (Leu-Val-Pro-Arg-Gly-Ser) has been used to fabricate an ultra
186  were observed in other behaviors, with male Val/Val mice exhibited lower prepulse inhibition compare
187  a single-pulse TMS study carried on 16 Met (Val/Met and Met/Met) and 16 Val/Val participants selecte
188 significantly different between Met/Met, Met/Val, and Val/Val carriers in each group, which indicated
189 es would produce the tripeptide Phe-N-Methyl-Val-Ala with a lipid moiety, termed lipotripeptide (L3P)
190  that a substitution in the penultimate MftA Val-29 position causes the accumulation of an MftA** min
191 measurements further suggest that Lys[Z-NO2]-Val interacts with discrete residues in TMH 2 that are i
192          After demonstrating that Lys[Z-NO2]-Val, the strongest inhibitor of hPEPT1, also acts as a h
193                            Administration of Val might lead to amelioration of CsA nephrotoxicity by
194 R) also revealed that oral administration of Val-Glu-Leu-Tyr-Pro can decrease systolic blood pressure
195 ucial for the unambiguous differentiation of Val and Nva.
196 es access to the backbone carbonyl groups of Val 494 and Pro 495.
197  of FGF14 where an alanine (Ala) mutation of Val-160 impaired binding to Nav1.6 but had no effect on
198 COX-2 interactions revealed that mutation of Val-434 to Ile significantly reduces inhibition by melox
199                    In contrast, mutations of Val(168) or Asn(171) in the upper site, which are unique
200 the mutants if cultivated in the presence of Val or Ile but not in the presence of leucine.
201 aintained when Cys63 is replaced with Ala or Val.
202 ps based on the administration of CsA and/or Val: group A (control, 1 mL/kg per day of olive oil as v
203 dary structure are hydrophobic (e.g., Ile or Val) or only moderately polar (e.g., Thr).
204 idue 129 is polymorphic, being either Met or Val.
205 aa-Ala-Y (where Glp=pyroglutamyl; Xaa=Phe or Val; and Y=pNA [p-nitroanilide], AMC [4-amino-7-methylco
206 st increases in antibodies containing Trp or Val motifs.
207 han-containing dipeptides such as Ile-Trp or Val-Trp, which were recently found in food protein hydro
208 amily members: a hydrophobic residue (Tyr or Val) in the +2 position specifies interaction with SEC24
209 and Trp-483 could form a pocket that orients Val-250 to interact with the dNTP.
210 R. hookeri wine contained more (p<0.05) Phe, Val, Ala, Gly, Pro, Asp, Asn, His and Lys than E. guinee
211 scribe new HsTX1 analogues with an Ala, Phe, Val or Abu substitution at position 14.
212 e identified as Val-Glu-Leu-Tyr-Pro, Ala-Phe-Val-Gly-Tyr-Val-Leu-Pro and Glu-Lys-Ser-Tyr-Glu-Leu-Pro.
213 ICHOS membrane insertion is promoted by poly-Val peptides present in the membrane.
214 con-mediated folding of the WT pro-SP-C poly-Val and a designed poly-Leu transmembrane (TM) segment i
215      The human gene contains a polymorphism (Val(158)Met) that alters enzyme activity and influences
216 Ala-Cys-Cys-Glu-His-dPhe-Arg-Trp-Cys-Arg-Pro-Val-NH 2}, RTD-beta-Ala-(Arg(11))CCMSH (2), RVD-beta-Ala
217 ides Cys-Ile-His-Asn-Pro and Cys-Ile-Gln-Pro-Val while low response was achieved for the dipeptide.
218 thione, Cys-Ile-His-Asn-Pro, Cys-Ile-Gln-Pro-Val, Cys-Arg-Gln-Val-Phe) vs. 14 volatile compounds belo
219 the decapeptide Gramicidin S cyclo(d-Phe-Pro-Val-Orn-Leu-)2 (GS).
220 ntly of AHAS and IPMS AHAS and IPMS regulate Val and Leu homeostasis, where AHAS affects total Val+Le
221                   We mutagenized the residue Val-136, which lines the anesthetic-binding cavity, its
222 nts identified three transmembrane residues (Val-86, Lys-93, and Asn-258) that form a putative barrie
223 ar docking studies suggested three residues, Val(567), Glu(568), and Glu(571), located at the interfa
224 0.53-0.79, P=1.81 x 10(-5)) and COMT rs4680 (Val (G) allele: OR=1.27, 95% CI: 1.14-1.42, P=2.49 x 10(
225  mammals, the Cebidae Pro(8)OXT and Saguinus Val(3)Pro(8)OXT taxon-specific variants act as equi-effi
226 e residues contribute to cation selectivity (Val-86 and Asn-258), the transition between the two open
227   ELPs are protein polymers of the sequence (Val-Pro-Gly-Xaa-Gly)n, where the identity of Xaa and n d
228 hr-18 residue in the small subunit with Ser, Val, Gln, Gly, or Asp, and we analyzed the effects of th
229 airs d/l-Ala, -Asp, -Glu, -His, -Leu, -Ser, -Val and the three achiral amino acids Gly, beta-Ala, and
230                                          Ser-Val and Ile-Phe were shown to exhibit ACE inhibitory act
231 substitutions at the Val-65-equivalent site (Val-64) in Kir6.2 indicated no major effects on channel
232                           The site-specific (Val(344)-Thr(345)) and rapid (seconds to minutes) NE-bas
233  the transition between the two open states (Val-86), open channel stability, and the hydrogen-bondin
234                                  By swapping Val (V63) with Phe, AtPOT1bOB1 gained the capacity to bi
235 xploitative, behavior in Met/Met rather than Val/Val subjects.
236                          We demonstrate that Val-boroPro mediates tumor eradication by accelerating t
237                        Finally, we show that Val-boroPro has potent adjuvant properties resulting in
238                    We therefore suggest that Val(3)Pro(8)OXT and Pro(8)OXT are functional variants, w
239 urthermore, mutagenesis studies suggest that Val-499 is the primary site responsible for these change
240           Lineweaver-Burk plots suggest that Val-Glu-Leu-Tyr-Pro acts as a non-competitive inhibitor
241 ly lower frontal DA based on genotype at the Val(158)Met polymorphism in the COMT gene.
242  of leucine and alanine substitutions at the Val-65-equivalent site (Val-64) in Kir6.2 indicated no m
243 ed analogues have a cis-configuration at the Val-Dil amide bond in their functionally relevant tubuli
244   The present study is aim at evaluating the Val effect in alleviation of CsA nephrotoxicity by proba
245 mparison individuals with genotyping for the Val(66)Met SNP and [(15)O]H(2)O positron emission tomogr
246 the simulations for the Met-129, but not the Val-129, protein.
247 (2h)J(NN), attributed to optimization of the Val N-H...Ndelta1 His H-bond.
248 ngs are convergent with human studies of the Val(158)Met polymorphism, and suggest that COMT's effect
249 plasma and reduced global flexibility of the Val-213 variant most likely improve its local availabili
250 capone treatment significantly reversing the Val/Val alternation deficits.
251 antly lower functional connectivity than the Val/Val genotype.
252               These structures show that the Val-216-AcrF mutation leads to conformational changes in
253               These results suggest that the Val-Glu-Leu-Tyr-Pro would be a beneficial ingredient for
254 MTS did not open P2X2 receptors in which the Val(48) side chain was removed (P2X2(V48G/I328C)).
255 s among the three protein variants, with the Val-36 site displaying the most variability.
256 BDNF Val66Met genotype (30 patients with the Val/Val BDNF allele, 25 patients with the Met-66 allele)
257 n of Asp-96 to Val in mitoNEET or Asp-123 to Val in Miner1 facilitates nitric oxide binding in the [2
258                One mutant, GVSK (Gly(159) to Val, Ser(208) to Lys), contains mutations in regions of
259 nitric oxide, a single mutation of Asp-96 to Val in mitoNEET or Asp-123 to Val in Miner1 facilitates
260 ary core around Lys(11) but makes changes to Val(8) on the exterior side of the beta-strand, possibly
261 visuomotor associative learning, compared to Val homozygotes.
262                                   One Glu to Val mutation in the active site of the homologous alpha-
263        Here we show that a de novo Glu183 to Val (E183V) mutation in the CaMKIIalpha catalytic domain
264 ele for 3-week vernalization, was mutated to Val(180) in vrn-A1b, encoded by the recessive allele for
265                                The Ala212-to-Val (A212V) mutant profoundly limits the product to 5hmC
266                            Finally, a Thr-to-Val replacement, which eliminates the Thr Ogamma-H...Nde
267 nd Leu homeostasis, where AHAS affects total Val+Leu and IPMS controls partitioning between these ami
268 ant enzyme revealed that BCAT6 transaminates Val, Leu and Ile as well as the corresponding 2-oxo acid
269 rolled in the Valsartan Heart Failure Trial (Val-HeFT), 3519 had a baseline left ventricular EF of <3
270 valine-m-tyrosine-piperazic acid tripeptide (Val-m-Tyr-Pip) in the sanglifehrin core, stereocenters a
271 A(Gly) and tRNA(Leu), the mitochondrial tRNA(Val) and tRNA(Pro)) were strongly associated with the ob
272 uman mitoribosome when levels of the mt-tRNA(Val) are depleted.
273 ikingly, when steady-state levels of mt-tRNA(Val) are reduced, human mitoribosome biogenesis displays
274 bosomes have been shown to integrate mt-tRNA(Val) compared with the porcine use of mt-tRNA(Phe) We ha
275       Our data demonstrate that only mt-tRNA(Val) or mt-tRNA(Phe) are found in the mitoribosomes of f
276 t of mitochondrial valine transfer RNA (tRNA(Val)) to play an integral structural role, and changes i
277                                          Trp-Val was predicted to be intestinally neutral (between 25
278  and Trp) and eight dipeptides (Phe-Leu, Trp-Val, His-Leu, Glu-Lys, Ala-Leu, Val-Ala, Ser-Leu and Gly
279 petitive inhibition observed, docking of Trp-Val to the secondary binding sites of XO and DPP-IV is r
280  and Trp-containing dipeptides (Arg-Trp, Trp-Val, Val-Trp, Lys-Trp and Ile-Trp) inhibited XO.
281 nsitized ubiquitin variant that contains two Val to Ala mutations.
282        The BRAF kinase is mutated, typically Val 600-->Glu (V600E), to induce an active oncogenic sta
283  as Val-Glu-Leu-Tyr-Pro, Ala-Phe-Val-Gly-Tyr-Val-Leu-Pro and Glu-Lys-Ser-Tyr-Glu-Leu-Pro.
284 (gamma-melanocyte-stimulating hormone, H-Tyr-Val-Met-Gly-His-Phe-Arg-Trp-Asp-Arg-Phe-Gly-OH), with it
285 our knowledge, the peptides Gly-Pro-Ala-Val, Val-Cys, and Phe-Phe have not been previously identified
286 Trp-containing dipeptides (Arg-Trp, Trp-Val, Val-Trp, Lys-Trp and Ile-Trp) inhibited XO.
287 CAAs) leucine, isoleucine (Ile), and valine (Val) in the mitochondria efficiently allows the formatio
288   Subjects with the Methionine (Met)/Valine (Val) and Val/Val genotypes showed higher fractional anis
289     It has been demonstrated that Valsartan (Val) as an angiotensin receptor blocker has renoprotecti
290 clear phenotypic differences between various Val-containing haplotypes on COMT-3' untranslated region
291  Val since the v ion was generated only when Val was present, not Nva within the electron energy rang
292       We investigated the mechanism by which Val-boroPro, a boronic dipeptide that inhibits post-prol
293 ports showed that overexpressed ILK in which Val(386) and Thr(387) were substituted with glycine resi
294 y efficacious on Gq and beta-arrestin, while Val(3)Pro(8)OXT showed reduced relative efficacy toward
295 ly, dendritic cell vaccination combined with Val-boroPro treatment results in complete regression of
296 eduction in enzymatic activity compared with Val/Val mice.
297    (1) For steric reasons, epoxyketones with Val or Ile at the P1 position are weak inhibitors of all
298  cortex during failed-inhibition trials with Val homozygotes displaying elevated activation compared
299 e investigated three mutant forms (I14X; X = Val, Ala, Gly) of the enzyme that have increased active
300 pentenyl)alanine at positions 92 and 96; Z = Val, Gly, or Asn at position 95)).

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