ライフサイエンスコーパス: Val

1 Val amino acid and Val-Val dipeptides imparted low plasm

2 Val-136 and adjacent residues may mediate anesthetic bin

3 Val-Pro had the highest ORAC activity (19.45+/-2.15mumol

4 by inserting its N-terminal dipeptide Ile(1)-Val(2) into the ProT Ile(16) pocket, forming a salt brid

5 uggest that SC variants other than WT Ile(1)-Val(2)-Thr(3) might emerge with similar ProT-activating

6 ith Val(1)-Val(2), Ile(1)-Ala(2), and Leu(1)-Val(2) variants exhibiting ProT(QQQ) affinity and activa

7 ons 1 and 2 were well-tolerated, with Val(1)-Val(2), Ile(1)-Ala(2), and Leu(1)-Val(2) variants exhibi

8 omprising the hydrophobic residues Phe-1012, Val-1025, Tyr-1089, and Leu-1092).

9 active site of class D SBLs (i.e. Trp(105), Val(120), and Leu(158), using OXA-48 numbering) impact o

10 n of alpha-helix 1 (residues Cys-11, Glu-12, Val-13, Lys-15, and Glu-16) and residue Glu-88.

11 nally identify the HG as Val(109), Phe(150), Val(177), and Val(178), which play a critical and exclus

12 rried on 16 Met (Val/Met and Met/Met) and 16 Val/Val participants selected from a large pool of healt

13 s (N=71; BDNF genotype: Val/Val (N=12, 17%), Val/Met (N=40, 56.3%), and Met/Met (N=19, 26.8%)) receiv

14 C-terminal residues Ser-178-Val-190 act in concert with the flexible EF3/EF4 loop re

15 Removal of Ser-178-Val-190 generated a C-terminal truncation mutant that fo

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 Position 3 (Val) controls affinity, whereas position 7 (Tyr) acts as

19 ydrophobic regions probed at Leu-17, Leu-34, Val-36, and Met-35 side chains were found to be very pro

20 st that a surface of GRK2, including Leu(4), Val(7), Leu(8), Val(11), and Ser(12), directly interacts

21 sp(10), Tyr(13), Ala(16), Met(17), Gly(475), Val(477), and Ile(485) are more important for kinase dom

22 nase within the amino acid sequence Ser(478)-Val(479)-Leu(480)-Gln(481)-Val(482).

23 sequence Ser(478)-Val(479)-Leu(480)-Gln(481)-Val(482).

24 via the leucine 69 (Leu(69)) and valine 68 (Val(68)) residues.

25 ermediate, thereby establishing the alpha-70(Val-->Ile) intermediate as a reliable guide to mechanism

26 freeze-trapped intermediate of the alpha-70(Val-->Ile) MoFe protein as the Janus intermediate that s

27 o suggested that autolysis occurs at Glu-729-Val-730 and Glu-732-Ala-733 in the ADAMTS7 Spacer domain

28 residues Phe(63), Leu(64), Glu(77), Thr(78), Val(81), and Arg(82) that underlie IFN-beta-IFNAR1-media

29 e of GRK2, including Leu(4), Val(7), Leu(8), Val(11), and Ser(12), directly interacts with receptors,

30 ping identified the cleavage site as Leu(90)/Val(91) in the 95-amino acid ADRA1D NT domain, suggestin

31 yme with valine at residue 172 accumulates a Val(*); mutation of Val172 to isoleucine or cysteine res

32 G-to-T change at nucleotide 1965 producing a Val-to-Leu substitution at position 330 of the viral env

33 site is only one amino acid N-terminal to a Val/Leu substitution associated with schizophrenia.

34 hepsin G), plasma elastase footprint (Aalpha-Val(360)), and markers of elastin degradation (desmosine

35 resulted in the discovery of compound 42 (Ac-Val-Gln-(pI)DPhe-DTic-NH(2)), a full MC3R agonist that i

36 The adjacent Val-557 is in direct contact with the template base, and

37 Patients with the A4V (Ala-Val) SOD1 mutation (SOD1(A4V)), the largest mutation pop

38 ubstituted Val285 with Ala (V285A) in an Ala-Val dipeptide, to mimic the conserved Ala-Ala in many me

39 with azide and alkyne at its termini, N3-Ala-Val-NHCH2-C identical withCH, which is designed to self-

40 ning azide and alkyne at its termini (N3-Ala-Val-NHCH2C identical withCH, 1) was synthesized.

41 To our knowledge, the peptides Gly-Pro-Ala-Val, Val-Cys, and Phe-Phe have not been previously ident

42 Cys]-OH), PanSB1 (DOTA-PEG2-dTyr-Gln-Trp-Ala-Val-betaAla-His-Phe-Nle-NH2), and DOTA-MG11 (DOTA-dGlu-A

43 thylaniline-diglycolic acid-DPhe-Gln-Trp-Ala-Val-Gly-His-Leu-NHEt), showing excellent tumor localizin

44 -1-carboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Leu-OCH3 (ARBA05, 3) analogues are labeled w

45 -1-carboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Leupsi(CHOH- CH2)-(CH2)2-CH3 (RM7, 2), and t

46 1-carboxymethyl-piperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a synthetic bomb

47 1-carboxymethyl-piperidine-D-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 ((68)Ga-RM2) is a synthetic bomb

48 -1-carboxymethylpiperidine-d-Phe-Gln-Trp-Ala-Val-Gly-His-Sta-Leu-NH2 (RM2, 1; DOTA:1,4,7,10-tetraazac

49 VH4-34-encoded antibodies with unmutated Ala-Val-Tyr and Asn-His-Ser motifs, which recognize both ery

50 ical significance in the distribution of Ala/Val genotype between suicide attempters and non-attempte

51 Specifically, Tyr(135) and Val(141) on the DEa loop were shown to be critical resid

52 required conserved loop C ((137)TP(138) and Val(150)) and loop E ((230)HW(231)) amino acids for bind

53 t amino acid stretches Phe(150)-Glu(152) and Val(166)-Glu(170) of FaeGad bind the terminal galactose

54 the HG as Val(109), Phe(150), Val(177), and Val(178), which play a critical and exclusive role in pr

55 Met-186 and Val-288 in IFP1.4 are responsible for the formation of a

56 ncludes residues Arg-32, Ile-33, Met-34, and Val-35.

57 under DI, RNA-seq was performed in C-76 and Val-C.

58 Val amino acid and Val-Val dipeptides imparted low plasma exposure of the p

59 Concurrent delivery of Dox and Val showed the greatest difference at 16 days post injec

60 ings demonstrate that co-delivery of Dox and Val via ISFI can avoid systemic toxicity issues seen wit

61 hese residues with equally conserved Glu and Val counterpart residues in NusG destabilized interactio

62 ched-chain amino acids (BCAAs) Leu, Ile, and Val are among nine essential amino acids that must be ob

63 d-chained amino acids (BCAAs) (Leu, Ile, and Val) and their catabolites, propionylcarnitine and butyr

64 tical functions, S. aureus represses Leu and Val synthesis, instead preferring to acquire them from t

65 t BcaP, is required for transporting Leu and Val to be used for iso-BCFA synthesis.

66 3)C-methyl relaxation study of Ile, Leu, and Val (ILV) residues of PTP1B, which, because of its subst

67 e, in general, more rigid than Ile, Leu, and Val methyl probes in protein side chains.

68 ts of the methyl groups of the Ile, Leu, and Val residues at two static magnetic fields.

69 of the reported differences in human Met and Val carriers across working memory, fear processes and s

70 these functions between sibling Met/Met and Val/Val mice.

71 etic site in pre-transfer editing of Nva and Val also appears to be similar.

72 f isoleucyl-tRNA synthetase (IleRS), Nva and Val are activated and transferred to tRNA at similar rat

73 ost-transfer editing misincorporated Nva and Val in the proteome to a similar extent and at the same

74 ded an unambiguous identification of Nva and Val since the v ion was generated only when Val was pres

75 However, when both Nva and Val were present in one peptide, the observation of inte

76 ntrast, the lactotripeptides Ile-Pro-Pro and Val-Pro-Pro, which were widely used as ingredients for h

77 acids (Ala, Asp, Glu, His, Lys, Pro, Thr and Val), incorporating a range of side-chain functionality.

78 with binding guanine in VldE (Asn, Thr, and Val) are similar in S. venezuelae OtsA (Asp, Ser, and Ph

79 t high rates and for Gly, Lys, Phe, Tyr, and Val at moderate or low rates, respectively.

80 s with the Methionine (Met)/Valine (Val) and Val/Val genotypes showed higher fractional anisotropy an

81 ntly different between Met/Met, Met/Val, and Val/Val carriers in each group, which indicated that the

82 suggest that the lipid substrate approaches Val-906 during the translocation.

83 The PC inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethyl ketone significantly suppressed

84 or the pharmacologic inhibitor Decanoyl-Arg-Val-Lys-Arg-chloromethylketone repressed PD-1 and exhaus

85 We functionally identify the HG as Val(109), Phe(150), Val(177), and Val(178), which play a

86 the most potent peptides were identified as Val-Glu-Leu-Tyr-Pro, Ala-Phe-Val-Gly-Tyr-Val-Leu-Pro and

87 -acrylamido-phenylalanine (AcrF) mutation at Val-216 that leads to an increase in catalytic efficienc

88 ated changes in estradiol secretion and BDNF Val(66)Met genotype on measures of hippocampal function

89 w PET in 39 healthy women genotyped for BDNF Val(66)Met, and a confirmatory data set was obtained wit

90 ied the effect of the common functional BDNF Val(66)Met (rs6265) polymorphism on rewarding experience

91 effects of scopolamine were assessed in BDNF Val/Met knock-in mice, in which BDNF processing and rele

92 an evidence regarding the effect of the BDNF Val(66)Met polymorphism on DA-mediated responses to stre

93 ration in women that the effects of the BDNF Val/Met polymorphism on hippocampal function are selecti

94 Individuals with the BDNF Val/Val (valine allele) polymorphism showed better memor

95 and brain-derived neurotrophic factor (BDNF(Val/Val), BDNF(Met)) in the extent to which they moderat

96 ity time in the forced swimming test in BDNF(Val/Val) but not in BDNF(Met/Met) mice.

97 the BDNF(Val66Met) carriers compared to BDNF(Val) homozogytes.

98 Wild-type (BDNF(Val/Val)) and homozygous BDNF Val66Met (BDNF(Met/Met)) m

99 3 years, whereas Abeta(+)varepsilon4(+)/BDNF(Val/Val) individuals can expect a similar degree of impa

100 54 months compared with varepsilon4(-)/BDNF(Val/Val) participants (d=0.90-1.02).

101 ced in BDNF(Met/Met) mice compared with BDNF(Val/Val) mice.

102 Because Val-17, Gly-22, Leu-25, Asn-26, and Pro-29 are predicted

103 otocol and Amyloid beta (39-42) peptide (Boc-Val-Val-IIe-Ala-OMe), following solution-phase strategy

104 loop A ((63)EKP(65) and Asp(69)) and loop C (Val(141), His(151), and Leu(154)).

105 types revealed C76-16 (C-76) and Valencia-C (Val-C) as the best and poor performers under deficit irr

106 implications for future satellite lidar Cal/Val efforts, because planned satellite lidars measuring

107 Meaningful Cal/Val requires intercomparison data sets with small enough

108 ble along-track averaging for meaningful Cal/Val.

109 Several Calibration/Validation (Cal/Val) studies for CALIOP conducted with ground-based lida

110 ells, and increases the rate of near-cognate Val-tRNA(Val) reacting on a PsiUU codon.

111 n between prenatal maternal smoking and COMT Val(158)Met in conduct problems and crime in the 1993 Pe

112 recall of remote memories as silencing COMT Val overexpression starting from 30 days after the initi

113 overexpressing the human COMT-Val gene (COMT-Val-tg) present exaggerated remote memories (>50 days) w

114 ransgenic mice overexpressing the human COMT-Val gene (COMT-Val-tg) present exaggerated remote memori

115 cue the altered remote memory recall in COMT-Val-tg mice and increased PFC dopamine levels.

116 hereas the weakest-binding analogs contained Val, Ile, and Leu substitutions.

117 41-RBD were evaluated along with two control Val-to-Ala substitutions.

118 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

119 that replacement of Lys-377 with either Cys, Val, Arg, or Asp disables both Na(+) and melibiose bindi

120 H-Glu-Thr-Pro-Asp-c[Cys-Phe-Trp-Lys-Tyr-Cys]-Val-OH) fragment 4-11 were synthesized to explore the in

121 + Val, 30 + 30 mg/kg per day), and group D (Val, 30 mg/kg per day).

122 near tripeptide l-delta-aminoadipoyl-l-Cys-d-Val (ACV) on the pathways to a number of important antib

123 ntains l-Val, d-Lys, and l-Ile (instead of d-Val, l-Lys, and l-allo-Ile) and is a hydroxylated brunsv

124 , w ions, which can be used to differentiate Val and Nva.

125 dissociation (HECD) is able to differentiate Val from Nva by producing diagnostic w ions on custom de

126 Dox + Val ISFIs showed a 2-fold reduction in tumor growth and

127 Dox + Val showed a 4-fold reduction in the 50% lethal dose (LD

128 al intratumoral Dox intensity with the Dox + Val ISFIs compared to Dox alone ISFIs (0.54 +/- 0.11 vs

129 in the corresponding HbA Evans (alpha62(E11)Val --> Met).

130 lation initiation from a GTG codon (encoding Val) within eNISTmAb.

131 Thus, these two residues, especially Val-89 at the lobby region, are crucial for the entrance

132 side of the effector cell, the FcgammaRIIIa-Val/Phe158 polymorphism influenced ADCC potency, with NK

133 n of any of the 20 canonical amino acids for Val-216, indicating that an expanded genetic code may of

134 ation of the adjacent GUA triplet coding for Val at the aminoacyl (A) site.

135 as base, beta-ketosulfonamides derived from Val, Leu or Ile gave the expected beta-keto-alpha,alpha-

136 o characterize Nva and differentiate it from Val (Valine), a systematic study was conducted using hot

137 etermined mainly by steric restrictions from Val-136 on the beta2-subunit and favorable interactions

138 Patients (N=71; BDNF genotype: Val/Val (N=12, 17%), Val/Met (N=40, 56.3%), and Met/Met

139 ly possessing lower activity BDNF genotypes (Val/Met, Met/Met).

140 stretches of rare codons, Leu(UUA)-Gly(GGU)-Val(GUA).

141 is-Asn-Pro, Cys-Ile-Gln-Pro-Val, Cys-Arg-Gln-Val-Phe) vs. 14 volatile compounds belonging to relevant

142 -binding proteins 3 and 4 (LTBP3/4) at a Glu-Val and Glu-Ala site, respectively.

143 Leu-Ala-Pro, Leu-Leu-Ala-Pro and Met-Ala-Gly-Val-Asp-His-Ile, with IC50 values in the range 43-159 mu

144 % MS SI restoration for the Z-Gly-Gly-Val and bradykinin peptides were 75-83% while % MS SI re

145 Ile > His >3,4-dihydroxyphenylalanine, Arg > Val > Lys, Tyr, Pro > hydroxyproline > alpha-aminobutyri

146 sed by a single point mutation (beta6 Glu -> Val) on the beta-chain of adult hemoglobin (HbA) that re

147 (2)I side-chain interactions, and the Gly -> Val change broke the essential Mg(2+) coordination.

148 lls lines carrying homozygous YARS2 p.191Gly>Val and m.11778G>A mutations.

149 ents both carrying homozygous YARS2 p.191Gly>Val and m.11778G>A mutations.

150 The 191Gly>Val mutation reduced the YARS2 protein level in the muta

151 The YARS2 p.191Gly>Val mutation worsened the respiratory phenotypes associa

152 or both m.11778G>A and heterozygous p.191Gly>Val mutations and symptomatic subjects harboring m.11778

153 harboring m.11778G>A and homozygous p.191Gly>Val mutations) and controls lacking these mutations.

154 ON susceptibility allele (c.572G>T, p.191Gly>Val) in YARS2 gene encoding mitochondrial tyrosyl-tRNA s

155 The hierarchy Leu>Met>Ile>Val at the C-terminal position was determined for all me

156 and acyl carrier protein (65-74) fragment (H-Val-Gln-Ala-Ala-Ile-Asp-Tyr-Ile-Asn-Gly-OH), following t

157 kers (e.g., Dat, Comt, and Th) between hBDNF(Val/Val) and hBDNF(Met/Met) mice, implicating involvemen

158 amily, composed of tandemly repeated Pro-Hyp-Val-X-Lys pentapeptide motifs, is found primarily in the

159 The branched-chain amino acids (BCAAs) Ile, Val, and Leu are essential nutrients that humans and oth

160 The last 3 residues of NaV1.5 (Ser-Ile-Val) constitute a PDZ domain-binding motif that interact

161 hydrogenase, AtHDH1 (At4g20930), involved in Val degradation.

162 s points to a role of the enzyme not only in Val but possibly also in Ile metabolism.

163 Additionally, we perform a case study in Val d'Agri (VA), an area of Basilicata Region, Southern

164 neri and the small molecule DPP8/9 inhibitor Val-boroPro, focusing on recent mechanistic insights and

165 Conversely, introducing Val in place of Cys(93) stabilized the hydrophobic core

166 f two different dipeptide nanotubes: l-Ala-l-Val and its retro-analog l-Val-l-Ala.

167 A designed beta-sheet-forming l-Ala-l-Val dipeptide containing azide and alkyne at its termini

168 anotubes: l-Ala-l-Val and its retro-analog l-Val-l-Ala.

169 Mozamide A contains l-Val, d-Lys, and l-Ile (instead of d-Val, l-Lys, and l-al

170 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

171 012, oxaline, questiomycin A, cyclo (l-Pro-l-Val), cyclo (l-Pro-l-Tyr), bikaverin, kojic acid and 3-n

172 analysis of a polar mixture composed of Leu-Val, Leu-Tyr, Gly-Tyr, and Ala-Tyr dissolved in DMSO-d6/

173 a single-pulse TMS study carried on 16 Met (Val/Met and Met/Met) and 16 Val/Val participants selecte

174 significantly different between Met/Met, Met/Val, and Val/Val carriers in each group, which indicated

175 es would produce the tripeptide Phe-N-Methyl-Val-Ala with a lipid moiety, termed lipotripeptide (L3P)

176 that a substitution in the penultimate MftA Val-29 position causes the accumulation of an MftA** min

177 sing the degradation-refractory K78V mutant, Val-SDE2Ct, fail to induce RPA phosphorylation and singl

178 mals with PH, treatment with Sac/Val but not Val resulted in significant reduction in RV pressure (mm

179 both Asn and Asp can restore the activity of Val-inhibited PKM2.

180 Administration of Val might lead to amelioration of CsA nephrotoxicity by

181 R) also revealed that oral administration of Val-Glu-Leu-Tyr-Pro can decrease systolic blood pressure

182 The majority of amino acids were composed of Val, Pro, Tyr, Met, Leu, Trp, Phe, Lys and Glu.

183 ucial for the unambiguous differentiation of Val and Nva.

184 es access to the backbone carbonyl groups of Val 494 and Pro 495.

185 ty of HECD for unambiguous identification of Val and Nva especially in structure characterization of

186 of FGF14 where an alanine (Ala) mutation of Val-160 impaired binding to Nav1.6 but had no effect on

187 In contrast, mutations of Val(168) or Asn(171) in the upper site, which are unique

188 the mutants if cultivated in the presence of Val or Ile but not in the presence of leucine.

189 ries of C-terminally truncated analogues of [Val(4)]dDAVP, 2, modified in positions 2, 3, and 7 and/o

190 lacing Pro-29 together with either Leu-25 or Val-17 of TM4SF20 with the corresponding residues of TM4

191 aintained when Cys63 is replaced with Ala or Val.

192 ps based on the administration of CsA and/or Val: group A (control, 1 mL/kg per day of olive oil as v

193 usly reported Gly -> Xaa (Xaa = Ala, Arg, or Val) vEDS substitutions within a high-affinity integrin

194 aa-Ala-Y (where Glp=pyroglutamyl; Xaa=Phe or Val; and Y=pNA [p-nitroanilide], AMC [4-amino-7-methylco

195 st increases in antibodies containing Trp or Val motifs.

196 han-containing dipeptides such as Ile-Trp or Val-Trp, which were recently found in food protein hydro

197 y 6-week treatment with placebo, Sac/Val, or Val alone.

198 ts+placebo (n=34); PH+Sac/Val (N=24); and PH+Val (n=16).

199 scribe new HsTX1 analogues with an Ala, Phe, Val or Abu substitution at position 14.

200 e identified as Val-Glu-Leu-Tyr-Pro, Ala-Phe-Val-Gly-Tyr-Val-Leu-Pro and Glu-Lys-Ser-Tyr-Glu-Leu-Pro.

201 ICHOS membrane insertion is promoted by poly-Val peptides present in the membrane.

202 con-mediated folding of the WT pro-SP-C poly-Val and a designed poly-Leu transmembrane (TM) segment i

203 The human gene contains a polymorphism (Val(158)Met) that alters enzyme activity and influences

204 ariants including four amino acid positions, Val-750, Ile-552, Ile-839, and Trp-500, located within a

205 thione, Cys-Ile-His-Asn-Pro, Cys-Ile-Gln-Pro-Val, Cys-Arg-Gln-Val-Phe) vs. 14 volatile compounds belo

206 the decapeptide Gramicidin S cyclo(d-Phe-Pro-Val-Orn-Leu-)2 (GS).

207 ntly of AHAS and IPMS AHAS and IPMS regulate Val and Leu homeostasis, where AHAS affects total Val+Le

208 cts of substitutions to the adjacent residue Val-906 (i.e. V906A/E/F/L/Q/S) suggest that the lipid su

209 The binding pocket flanking residue Val-339, unlike the equivalent Arg-343 in the homologous

210 We mutagenized the residue Val-136, which lines the anesthetic-binding cavity, its

211 nts identified three transmembrane residues (Val-86, Lys-93, and Asn-258) that form a putative barrie

212 ar docking studies suggested three residues, Val(567), Glu(568), and Glu(571), located at the interfa

213 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(

214 Sac/Val reduces pulmonary pressures, vascular remodeling, as

215 (n=18); PH-Su/Hx rats+placebo (n=34); PH+Sac/Val (N=24); and PH+Val (n=16).

216 Also, PH+Sac/Val animals had altered expression of PKC isozymes in RV

217 ypertrophy (RV/LV+S: PH: 0.74+/-0.06, PH+Sac/Val: 0.46+/-0.06), collagen content (ug/50 ug protein: P

218 ovement in RVs (mm/s: PH: 31.2+/-1.8, PH+Sac/Val: 43.1+/-3.6) compared with placebo.

219 on in RV pressure (mm Hg: PH: 62+/-4, PH+Sac/Val: 46+/-5), hypertrophy (RV/LV+S: PH: 0.74+/-0.06, PH+

220 ent (ug/50 ug protein: PH: 8.2+/-0.3, PH+Sac/Val: 6.4+/-0.4), pressures and improvement in RVs (mm/s:

221 llowed by 6-week treatment with placebo, Sac/Val, or Val alone.

222 rilysin inhibitor, sacubitril/valsartan (Sac/Val, LCZ696), will attenuate PH and improve RV function

223 In animals with PH, treatment with Sac/Val but not Val resulted in significant reduction in RV

224 mammals, the Cebidae Pro(8)OXT and Saguinus Val(3)Pro(8)OXT taxon-specific variants act as equi-effi

225 e residues contribute to cation selectivity (Val-86 and Asn-258), the transition between the two open

226 hr-18 residue in the small subunit with Ser, Val, Gln, Gly, or Asp, and we analyzed the effects of th

227 airs d/l-Ala, -Asp, -Glu, -His, -Leu, -Ser, -Val and the three achiral amino acids Gly, beta-Ala, and

228 Ser-Val and Ile-Phe were shown to exhibit ACE inhibitory act

229 An RCL-derived peptide with the sequence Ser-Val-Ala-Phe-Ser (SVAFS) displayed robust blocking activi

230 substitutions at the Val-65-equivalent site (Val-64) in Kir6.2 indicated no major effects on channel

231 The site-specific (Val(344)-Thr(345)) and rapid (seconds to minutes) NE-bas

232 the transition between the two open states (Val-86), open channel stability, and the hydrogen-bondin

233 By swapping Val (V63) with Phe, AtPOT1bOB1 gained the capacity to bi

234 noacylates Nva-tRNA(Ile) at slower rate than Val-tRNA(Ile).

235 xploitative, behavior in Met/Met rather than Val/Val subjects.

236 istranslation inflicted higher toxicity than Val, in agreement with IleRS editing being optimized for

237 ar) and Asp (charged) activate PKM2 and that Val (hydrophobic) inhibits it.

238 We therefore suggest that Val(3)Pro(8)OXT and Pro(8)OXT are functional variants, w

239 Lineweaver-Burk plots suggest that Val-Glu-Leu-Tyr-Pro acts as a non-competitive inhibitor

240 The Val to Met substitution in the S4-S5 loop induced a larg

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 For catechol-O-methyltransferase (COMT), the Val(158)Met polymorphism (rs4680) markedly affected enzy

244 The present study is aim at evaluating the Val effect in alleviation of CsA nephrotoxicity by proba

245 peloprasum var. holmense) collected from the Val di Chiana area (Tuscany, Italy).

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 antly lower functional connectivity than the Val/Val genotype.

251 These structures show that the Val-216-AcrF mutation leads to conformational changes in

252 These results suggest that the Val-Glu-Leu-Tyr-Pro would be a beneficial ingredient for

253 s among the three protein variants, with the Val-36 site displaying the most variability.

254 Two compounds 19 (c(Bua-Cpa-Thi-Val-Asn-Cys)-Pro-Agm) and 38 (c(Bua-Cpa-Thi-Val-Asn-Cys)

255 -Val-Asn-Cys)-Pro-Agm) and 38 (c(Bua-Cpa-Thi-Val-Asn-Cys)-Pro-d-Arg-NEt(2)) have been selected for cl

256 cts between the carbonyl groups from the Thr-Val-Gly-Tyr-Gly signature filter sequence and the permea

257 n of Asp-96 to Val in mitoNEET or Asp-123 to Val in Miner1 facilitates nitric oxide binding in the [2

258 nitric oxide, a single mutation of Asp-96 to Val in mitoNEET or Asp-123 to Val in Miner1 facilitates

259 ary core around Lys(11) but makes changes to Val(8) on the exterior side of the beta-strand, possibly

260 visuomotor associative learning, compared to Val homozygotes.

261 Here we show that a de novo Glu183 to Val (E183V) mutation in the CaMKIIalpha catalytic domain

262 esis by changing every amino acid residue to Val, Ala, or Gly, and then screening the drug resistance

263 ts with subtype B HIV-1 identified an Ala-to-Val mutation at SP1 residue 1 and a Pro-to-Ala mutation

264 The Ala212-to-Val (A212V) mutant profoundly limits the product to 5hmC

265 Finally, a Thr-to-Val replacement, which eliminates the Thr Ogamma-H...Nde

266 nd Leu homeostasis, where AHAS affects total Val+Leu and IPMS controls partitioning between these ami

267 ant enzyme revealed that BCAT6 transaminates Val, Leu and Ile as well as the corresponding 2-oxo acid

268 rolled in the Valsartan Heart Failure Trial (Val-HeFT), 3519 had a baseline left ventricular EF of <3

269 valine-m-tyrosine-piperazic acid tripeptide (Val-m-Tyr-Pip) in the sanglifehrin core, stereocenters a

270 luding tRNA(Glu), tRNA(Gly), tRNA(Lys), tRNA(Val), tRNA(His), tRNA(Asp), and tRNA(SeC) to produce tRN

271 ntified a mutation in the mitochondrial tRNA(Val) (mt-tRNA(Val) ) gene, m.1661A>G, present at nearly

272 A(Gly) and tRNA(Leu), the mitochondrial tRNA(Val) and tRNA(Pro)) were strongly associated with the ob

273 tion in the mitochondrial tRNA(Val) (mt-tRNA(Val) ) gene, m.1661A>G, present at nearly 100% heteropla

274 wed severe reduction in abundance of mt-tRNA(Val) , and mildly increased mt-tRNA(Phe) , in subjects c

275 oth (CMT) disease, a mutation in the mt-tRNA(Val) , in a Venezuelan family.

276 uman mitoribosome when levels of the mt-tRNA(Val) are depleted.

277 ikingly, when steady-state levels of mt-tRNA(Val) are reduced, human mitoribosome biogenesis displays

278 bosomes have been shown to integrate mt-tRNA(Val) compared with the porcine use of mt-tRNA(Phe) We ha

279 Our data demonstrate that only mt-tRNA(Val) or mt-tRNA(Phe) are found in the mitoribosomes of f

280 increases the rate of near-cognate Val-tRNA(Val) reacting on a PsiUU codon.

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 our knowledge, the peptides Gly-Pro-Ala-Val, Val-Cys, and Phe-Phe have not been previously identified

285 CAAs) leucine, isoleucine (Ile), and valine (Val) in the mitochondria efficiently allows the formatio

286 Isomeric amino acid residues such as valine (Val) and norvaline (Nva) are common in recombinant prote

287 esis, to the proteinogenic, branched valine (Val) in their propensity to mistranslate isoleucine (Ile

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 inhibitor, either Pluronic P85 or Valspodar (Val).

291 o the aggregation of the hexapeptide VEALYL (Val-Glu-Ala-Leu-Tyr-Leu), the B-chain residue 12-17 segm

292 BDNF levels among the smokers who were Val allele carriers were correlated with the degree of c

293 Val since the v ion was generated only when Val was present, not Nva within the electron energy rang

294 y efficacious on Gq and beta-arrestin, while Val(3)Pro(8)OXT showed reduced relative efficacy toward

295 (1) For steric reasons, epoxyketones with Val or Ile at the P1 position are weak inhibitors of all

296 positions 1 and 2 were well-tolerated, with Val(1)-Val(2), Ile(1)-Ala(2), and Leu(1)-Val(2) variants

297 e investigated three mutant forms (I14X; X = Val, Ala, Gly) of the enzyme that have increased active

298 is derived was identified as a Pro-Ser-X-X-X-Val motif.

299 ino-terminal residues of the chemokine XCL1 (Val(1), Gly(2), Ser(3), and Glu(4)) contribute a large f

300 pentenyl)alanine at positions 92 and 96; Z = Val, Gly, or Asn at position 95)).