ライフサイエンスコーパス: Arg

1 Arg starvation induces p300 dissociation, allowing histo

2 Arg starvation induces PHD2 and HDAC2 interaction which

3 Arg, Ornithine and Lys were identified as substrates.

4 in, a novel tetrapeptide scaffold [Ac-Xaa(1)-Arg-(pI)DPhe-Xaa(4)-NH2] is reported.

5 s demonstrate that MazF-mt6 residues Asp-10, Arg-13, and Thr-36 are critical for RNase activity and l

6 ion between IL1B +3954 C/T and FCGR2A 131His/Arg was observed.

7 the variant form of the SNP in FCGR2A 131His/Arg, FCGR2B 232Ile/Thr, TNFA -1031T/C, and TNFA -863C/A

8 Substitution of Arg-72, Tyr-190, Arg-234, or Glu-282 reduced LigY activity over 100-fold.

9 /PEI-4,000 (1:3)] and [Rep/PEI-40,000 (1:2)/(Arg)9] were efficacious in vivo in mice and pigs, where

10 that is largely independent of the Glu(277)-Arg(173)-Glu(282) network and accompanied by irreversibl

11 when using the central cE5 fragment (Asp-31-Arg-62) alone.

12 the protein, encompassing amino acids Asp-31-Arg-62, is the region mainly responsible for alpha-throm

13 The residues of Trp-354, Arg-359, Glu-355, Leu-363, and Glu-367 in DR5 death doma

14 nd the catalytic site with the region Pro-49-Arg-56, which includes the highly conserved DPGR tetrape

15 mutagenesis, indicating that Thr-28, Ser-50, Arg-51, and Arg-55 are important for discriminating betw

16 that MAX Arg36 recognizes 5caC using a 5caC-Arg-Guanine triad, with the next nearest residue to the

17 We mutated Arg-84, Arg-88, and Arg-101 in the ATPase-active B, C, and D sub

18 Charged residues Asp-997, Glu-998, Arg-1000, and Lys-1001 in M10, participating in this bon

19 ting and regulating Abl localization and Abl/Arg activation by Src family kinases.

20 esistance to BRAFi and immunotherapy, as Abl/Arg and Akt inhibitors cooperate to prevent viability, c

21 Importantly, Abl/Arg activation downstream of BRAF(V600E) has functional

22 ot only provide mechanistic insight into Abl/Arg regulation during melanoma development, but also pav

23 Abl kinases (Abl/Arg) are activated in melanomas and drive progression; h

24 ional significance by demonstrating that Abl/Arg cooperate with PI3K/Akt/PTEN, a parallel pathway tha

25 ort that loss of the integrin-regulated Abl2/Arg kinase in vivo yields a subpopulation of "immature"

26 The three most potent MC3R agonists, 18 [Ac-Arg-Arg-(pI)DPhe-Tic-NH2], 1 [Ac-His-Arg-(pI)DPhe-Tic-NH

27 1 [Ac-His-Arg-(pI)DPhe-Tic-NH2], and 41 [Ac-Arg-Arg-(pI)DPhe-DNal(2')-NH2] were more potent (EC50 <

28 One among the synthesized analogue, Ac-Arg-Ala-[d-Cys-Arg-Phe-His-Pen]-COOH (19), displayed sub

29 nt, selective, and plasma stable peptide, Ac-Arg-Ala-[d-Cys-Arg-Phe-Phe-Cys]-COOH (3).

30 Mutagenesis of Nef amino acids Arg-134, Glu-174, and Asp-175, which stabilize Nef for A

31 o positions, namely after Arg(104) and after Arg (1290), resulting in a homogeneous sample lacking 10

32 ch is cleaved at two positions, namely after Arg(104) and after Arg (1290), resulting in a homogeneou

33 (PCA), and the transition state analogue AK:Arg:Mg.ADP:NO3(-) (TSA).

34 ate free), the Michaelis complex analogue AK:Arg:Mg.AMPPNP (MCA), a product complex analogue AK:pAIE:

35 of different polarity and length (i.e. Ala, Arg, Cys, His, Glu, and Leu) on transporter stability an

36 Oxidation of Tyr-Ala-Ala-Ala-Arg (YAAAR) produces Tyr-O radicals by combined electron

37 HBO) cells with five arginyl dipeptides: Ala-Arg (AR), Arg-Ala (RA), Arg-Pro (RP), Arg-Glu (RE), and

38 Seven synthetases, Ala-, Arg-, Asp-, Asn-, Leu-, Lys- and TyrRS, appear to associ

39 Although Arg-Gly-Asp (RGD) integrin ligand and matrix softening c

40 the substrate-kinase interaction enabled an Arg/Lys two to three amino acids C-terminal to the phosp

41 third position of Vbeta11 CDR3 can encode an Arg or Ser residue as a result of somatic rearrangement.

42 C3 harbors an Arg-Gly-Asp (RGD) motif, which is the major integrin-bin

43 Third, an Arg-Asp dipeptide immediately preceding the ZF helix, co

44 ions independently of IGF binding through an Arg-Gly-Asp (RGD) integrin-binding motif.

45 ly local stresses on the cell surface via an Arg-Gly-Asp-coated magnetic bead.

46 cated that Asp-168 is important in anchoring Arg-155 for ligand binding but is not critical for Lys-1

47 te conserved residues Tyr(40), Asp(181), and Arg(100)and a reacting duplex 5'-phosphate.

48 ed two GAPDH arginine residues, Arg(197) and Arg(200), and that these two residues were essential for

49 S1 silencing is controlled by HIF-1alpha and Arg starvation-reactivated ASS1 is associated with HIF-1

50 esents the sites of cleavage at Arg(271) and Arg(320) to factor Xa in different orientations by pivot

51 ted regulation of SOD2 and that Glu(446) and Arg(447) cooperate with other amino acid residues in the

52 rough cleavage of the receptor at Arg-46 and Arg-41 protease recognition sites, respectively.

53 indicating that Thr-28, Ser-50, Arg-51, and Arg-55 are important for discriminating between NADP(+)

54 63), Leu(64), Glu(77), Thr(78), Val(81), and Arg(82) that underlie IFN-beta-IFNAR1-mediated signaling

55 ubstituted Cys for two residues (Glu-816 and Arg-1229) forming a salt bridge between the NADPH/FAD an

56 E active site residues Phe(79), His(85), and Arg(245) to interrogate their roles in substrate binding

57 We mutated Arg-84, Arg-88, and Arg-101 in the ATPase-active B, C, and D subunits of Sac

58 ative mutations Arg-126-Gln, Asp-49-Asn, and Arg-126-Lys, we inferred that a crystallographic water a

59 easing the levels of IL-10, LIGHT, CCL1, and Arg-1.

60 onal explanation, demonstrating that Glu and Arg form salt bridges more commonly, utilize a wider ran

61 hin the low dielectric binding interface and Arg(506) functions to orient Glu(550) and to stabilize t

62 assess the relative stoichiometry of Lys and Arg modifications (QuARKMod) in complex biological setti

63 scover unexpected and possibly novel Lys and Arg modifications.

64 residues, in contrast to the larger Lys and Arg residues in yeast and plant orthologs.

65 membrane domain (out of 16 potential Lys and Arg sites).

66 on properties of lipid-exposed His, Lys, and Arg side chains in lipid bilayer membranes.

67 high activity against the abundant Lys- and Arg-rich protein, myosin.

68 pectroscopy, shows the importance of Phe and Arg interactions in driving the phase separation of Ddx4

69 tween an N-terminal Asp of the pheromone and Arg-153 within the proposed pheromone-binding pocket of

70 utagenesis of SR34 RNA-binding sequences and Arg/Ser-rich (RS) domain, we further show that functiona

71 alpha24 low- and high-intensity subsets, and Arg-encoding TCR Vbeta11 chains were more frequently iso

72 scarce reciprocal inhibition between TEA and Arg was found, while the biguanide metformin was able to

73 translational modifications (PTM) of Trp and Arg amino acid residues.

74 and activity of enzymes involved in Trp and Arg catabolism (IDO1, IDO2, Trp 2,3-dioxygenase [TDO], a

75 and activity of enzymes involved in Trp and Arg catabolism, as well as to investigate amino acid cat

76 with five arginyl dipeptides: Ala-Arg (AR), Arg-Ala (RA), Arg-Pro (RP), Arg-Glu (RE), and Glu-Arg (E

77 3HC1 (rs11556924), resulting in an arginine (Arg) to histidine (His) substitution in its encoded prot

78 he quantitative determination of L-arginine (Arg) has been developed.

79 Here, we show that L-arginine (Arg) uptake through the host cell's SLC7A2-encoded trans

80 ncies lack de novo biosynthesis of arginine (Arg) as the key enzyme argininosuccinate synthetase 1 (A

81 zyme that controls biosynthesis of arginine (Arg).

82 itution from glutamine (Gln, Q) to arginine (Arg, R) at codon 460 of the purinergic P2X7 receptor (P2

83 s of the hD4R are substituted with arginine (Arg) residues, cellular hD4R protein levels increase.

84 y, while positively charged residues such as Arg suppressed N-glycosylation.

85 arged residues (either Glu(-)/Arg(+), Asp(-)/Arg(+), or Glu(-)/Lys(+)).

86 ls, our study demonstrates an age-associated Arg-II upregulation, which promotes TNF-alpha release th

87 istone H4 Arg-17 regulates PRMT5 activity at Arg-3 in the same protein.

88 ombin-2 (Pre2), which is further attacked at Arg-320-Ile-321 to yield mature alphaT.

89 where Lnk2 presents the sites of cleavage at Arg(271) and Arg(320) to factor Xa in different orientat

90 Most interestingly, monomethylation at Arg-17 in histone H4 not only raised the general activit

91 Processing at Arg(162) was not required for cleavage at Lys(158) or re

92 on the platelet surface, FXa cleaves ProT at Arg-271, generating the inactive precursor prethrombin-2

93 (PCs) proteolytically process human Pxdn at Arg-1336, a location relatively close to its C terminus.

94 al cells through cleavage of the receptor at Arg-46 and Arg-41 protease recognition sites, respective

95 vels of symmetric dimethylarginine (SDMA) at Arg-3 on histone H4, leading to the repression of genes

96 However, Gln and Trp substitution at Arg-1150 significantly decreased glibenclamide potency.

97 g-range columbic interactions between basic (Arg/Lys) residues located N-terminally to the phosphoryl

98 Because Arg(104) is a key catalytic residue responsible for stab

99 for activity, whereas an interaction between Arg-126 and Asp-49 is essential for catalysis.

100 g for survival, and depleting this source by Arg-depleting recombinant enzyme ADI-PEG20 results in ce

101 ials for targeting Arg auxotrophic tumors by Arg starvation therapy.

102 heir actions are subunit-specific with RFC-C Arg-88 serving as an accelerator that enables rapid ATP

103 ge isomer (optical antipode) of cyclodal, c[-Arg-d-Phe-d-Lys-d-Dmt-] (2), also turned out to be a sel

104 showed that mutation of a positively charged Arg residue at the beta-dimer interface and high NaCl co

105 est contribution from the positively charged Arg-1119 in the extracellular pore region in repeat III

106 corresponding to residues 14-24, containing Arg-14 and Lys-17.

107 ngrafted aorta, selected peptides containing Arg or Arg-Asn, not Arg-Met, with a 0 or +1 charge, sign

108 the synthesized analogue, Ac-Arg-Ala-[d-Cys-Arg-Phe-His-Pen]-COOH (19), displayed subnanomolar affin

109 and plasma stable peptide, Ac-Arg-Ala-[d-Cys-Arg-Phe-Phe-Cys]-COOH (3).

110 Oxygen sensing via the Cys-Arg/N-end rule in higher eukaryotes is linked through a

111 se multiple abiotic stresses through the Cys-Arg/N-end rule pathway either directly (via oxygen sensi

112 ring flooding) is directly sensed by the Cys-Arg/N-end rule pathway of ubiquitin-mediated proteolysis

113 hydrolysis upon contact with ptDNA and RFC-D Arg-101 serving as a brake that confers specificity for

114 ighly active, selective MOR antagonist, c[-d-Arg-Phe-Lys-Dmt-] (1) ("cyclodal"), with subnanomolar bi

115 eceptor (MOR) agonist [Dmt(1)]DALDA (H-Dmt-d-Arg-Phe-Lys-NH2 (9; Dmt = 2',6'-dimethyltyrosine) result

116 contrast, our systematic SAR studies on [des-Arg(7)]Dyn A analogues found that Arg(7) is not a key re

117 In addition, it was also found that [des-Arg(7)]Dyn A(1-9)-NH2 is a minimum pharmacophore and its

118 vides an easy and sensitive method to detect Arg visually.

119 A di-Arg motif and a long sequence motif within the transmemb

120 Site-directed (Arg-to-Ala) mutagenesis of this cleavage site abolished

121 ary charged residues in the NCAM Ig2 domain (Arg-156 and Lys-162) and the EphA3 CRD (Glu-248 and Glu-

122 The tetrapeptide His-DPhe-Arg-Trp or tripeptide DPhe-Arg-Trp replaced the Arg-Phe-

123 agonist potency at the mMC4R, c[Pro-His-DPhe-Arg-Trp-Asn-Ala-Phe-DPro] and c[Pro-His-DPhe-Arg-Trp-Dap

124 Arg-Trp-Asn-Ala-Phe-DPro] and c[Pro-His-DPhe-Arg-Trp-Dap-Ala-DPro], and may be further developed to g

125 an the melanocortin tetrapeptide Ac-His-DPhe-Arg-Trp-NH2.

126 apeptide His-DPhe-Arg-Trp or tripeptide DPhe-Arg-Trp replaced the Arg-Phe-Phe sequence in the AGRP ac

127 These tumors acquire ectopic Arg for survival, and depleting this source by Arg-deple

128 Metabolizing pro-EGF Arg(1023) to citrulline with recombinant polypeptide arg

129 herefore, these tumors require extracellular Arg for growth.

130 Finally, Arg(245) is crucial for binding the substrate carboxylat

131 The linear concentration range for Arg assay in the final reaction mixture varies for ADI-O

132 entify for the first time a pivotal role for Arg-dependent polyamine production during Plasmodium's h

133 Competence of SlCAT2 for Arg transport was demonstrated measuring uptake of [(3)H

134 uced peptides similar to those expected from Arg-C proteolysis, yet with fewer missed and nonspecific

135 iments indicate that NO is not produced from Arg but via conversion of nitrite by the nitrate reducta

136 bility to variations from a C:G base pair (G-Arg interaction) to a G:C base pair (C-Asp interaction).

137 ndirectly via Src-mediated Abl-related gene (Arg) activation, leading to actin polymerization in inva

138 d negatively charged residues (either Glu(-)/Arg(+), Asp(-)/Arg(+), or Glu(-)/Lys(+)).

139 la (RA), Arg-Pro (RP), Arg-Glu (RE), and Glu-Arg (ER); and two non-arginyl dipeptides: Asp-Asp (DD) a

140 cofactor, bound adjacent to a conserved Glu-Arg-Glu/Asp ionic network in the enzyme's active site.

141 alysis was highly dependent on an intact Glu-Arg-Glu network, as only Glu --> Asp substitutions retai

142 xperiments indicate a clear role for the Glu-Arg-Glu network in both catalysis and oxidative maturati

143 intermediates but is independent of the Glu-Arg-Glu network.

144 -2(CFTERD3) (where CFTERD is Cys-Phe-Thr-Glu-Arg-Asp) was developed for chymase detection.

145 t position 177, Gln/Glu at position 180, Gly/Arg at position 239, and Pro/Ser at position 280.

146 Tyr, and His)/amide (Asn and Gln)/Guanidine (Arg)) side-chains and charged hydrophilic (such as Lys)

147 t was demonstrated measuring uptake of [(3)H]Arg in proteoliposomes which was trans-stimulated by int

148 ed at lower efficiency with respect to [(3)H]Arg.

149 y reading the H3-Lys-4 trimethylation and H3-Arg-8 asymmetric dimethylation marks.

150 PRMT7-mediated monomethylation of histone H4 Arg-17 regulates PRMT5 activity at Arg-3 in the same pro

151 any evidence for PRMT7-catalyzed histone H4 Arg-3 methylation.

152 18 [Ac-Arg-Arg-(pI)DPhe-Tic-NH2], 1 [Ac-His-Arg-(pI)DPhe-Tic-NH2], and 41 [Ac-Arg-Arg-(pI)DPhe-DNal(

153 However, Arg-rich de novo sequences (ER3 (AEEERRR) and EK1R2 (AEE

154 For both ASP and AGRP, the hypothesized Arg-Phe-Phe pharmacophores are on exposed beta-hairpin l

155 tryptophan and substrate analogs) identified Arg(64), Lys(269), and Tyr(309) as key catalytic residue

156 ues within the GDP-binding pocket identified Arg(93) as playing a key role in the nucleotide interact

157 fic stop codon recognition by RFs identified Arg-213 as a crucial residue on Escherichia coli RF2 for

158 female (not male) mice deficient in Arg-II (Arg-II(-/-)) are protected from age-associated glucose i

159 Arginase-II (Arg-II), the type-II L-arginine-ureahydrolase, is highly

160 how that female (not male) mice deficient in Arg-II (Arg-II(-/-)) are protected from age-associated g

161 of part of the active site, particularly in Arg-316 and Phe-318, to achieve the correct geometry for

162 ing single alpha-helices (SAHs), are rich in Arg (R), Glu (E) and Lys (K) residues, and stabilized by

163 peptide was completely symmetrical, rich in Arg and Trp residues, and able to adopt a native RTD-1-l

164 ed Ld lipid domains increased beta1-integrin-Arg-Gly-Asp-peptide affinity and valency, thus implicati

165 dothelial cells, BA increased beta1-integrin-Arg-Gly-Asp-peptide affinity by 18% with a transition fr

166 perturbing a ctenophore-specific interdomain Arg-Glu salt bridge that is notably absent from vertebra

167 Interestingly, Arg-213 is highly conserved in RF2 and substituted by Il

168 ation of a charged residue at the interface (Arg-103) weakens the interface significantly, whereas ef

169 somes which was trans-stimulated by internal Arg or ornithine.

170 nanocarrier for the co-delivery of GOx and l-Arg, a novel glucose-responsive nanomedicine (l-Arg-HMON

171 lyzing the C5 hydroxylation of l-arginine (l-Arg) driven by the oxidative decarboxylation of 2OG to f

172 rated acidic H2 O2 can oxidize l-Arginine (l-Arg) into NO for enhanced gas therapy.

173 f the generated ferryl species to catalyze l-Arg hydroxylation.

174 on the metal face opposite to that facing l-Arg, thus requiring reorientation of the generated ferry

175 , a novel glucose-responsive nanomedicine (l-Arg-HMON-GOx) has been for the first time constructed fo

176 Subsequent addition of l-Arg resulted in compression of the active site, a confor

177 Binding of 2OG in the absence of l-Arg resulted in predominantly monodentate metal coordina

178 ygenases, is facilitated by the binding of l-Arg which leads to an altered positioning of the carboxy

179 berate 5 and cathepsin K cleavage of the Leu-Arg-PABA element will liberate alendronic acid.

180 ed by their conserved N-terminal Arg-Xaa-Leu-Arg (RxLR) motif.

181 rgininyl-para-aminophenylmeth ylalcohol (Leu-Arg-PABA).

182 te salt-bridge formation between Glu and Lys/Arg.

183 Moreover, Arg-II is mainly expressed in acinar cells and is upregu

184 We mutated Arg-84, Arg-88, and Arg-101 in the ATPase-active B, C, a

185 ng the size or charge conservative mutations Arg-126-Gln, Asp-49-Asn, and Arg-126-Lys, we inferred th

186 ional in silico digestion with either Asp-N, Arg-C, Glu-C, Lys-C, or Lys-N.

187 ary to trypsin, such as Glu-C, Asp-N, Lys-N, Arg-C, LysargiNase has been reported.

188 mity to the MMP-9 zymogen cleavage site near Arg-106, which is distinct from the catalytic domain.

189 cted peptides containing Arg or Arg-Asn, not Arg-Met, with a 0 or +1 charge, significantly reduced pl

190 um of isolated acinar cells from old WT (not Arg-II(-/-)) mice contains higher TNF-alpha levels than

191 explain the increased propensity of de novo Arg-rich SAHs to aggregate.

192 degrons (N-degrons), including arginine (Nt-Arg).

193 system and autophagy through its binding Nt-Arg and other N-degrons.Soluble misfolded proteins that

194 The binding of Nt-Arg and synthetic ligands to ZZ domain facilitates disul

195 a basic surface including the side chains of Arg 6, His 11 and Lys 32 as potentially important in the

196 sessing the precise chemical contribution of Arg side chains to protein function and pharmacology has

197 e new ZnLATP-AgNPs assay allows detection of Arg down to 200+/-15nM, provides an easy and sensitive m

198 iseases and therefore selective detection of Arg in biological fluids has an enormous impact on disea

199 ere developed for the selective detection of Arg, the colorimetric method has an advantage over these

200 for the selective colorimetric detection of Arg.

201 a, the product of the enzymatic digestion of Arg by ADI, reacts with OPA and forms in the presence of

202 ular, compensated for the negative effect of Arg at the i-2 position.

203 two PpMS monomers through the interaction of Arg-742 and Asp-113 is essential for catalytic activity

204 Kinetics of Arg and Ach transport were performed from which Km value

205 aused rapid and preferential modification of Arg(117) in FADD.

206 e malaria parasite through the modulation of Arg uptake and polyamine synthesis.

207 This promiscuous nature of Arg helps explain the increased propensity of de novo Ar

208 horylation leads to charge neutralization of Arg(24), a residue crucial for MCa agonist activity.

209 useful intermediates for the preparation of Arg-Gly-Asp (RGD)-based cyclopentapeptides (cRGD) with n

210 downward arrow, and requires the presence of Arg(198) at P1 and a combination of two other basic resi

211 s further validated by the quantification of Arg in supplement tablets.

212 With the hypothesis that replacement of Arg-213 and Asp-143 with the corresponding RF1 residues

213 Substitution of Arg-72, Tyr-190, Arg-234, or Glu-282 reduced LigY activi

214 hat ligand binding triggers translocation of Arg-143 from the membrane interface into the membrane to

215 Inclusion of (Arg)9 or TAT(57-57) CPPs further modified the translatio

216 he reliance of neurotransmitter receptors on Arg side chains and highlight the exceptional capacity o

217 y neurotransmitter receptors often relies on Arg residues in the binding site, leading to the assumpt

218 d aorta, selected peptides containing Arg or Arg-Asn, not Arg-Met, with a 0 or +1 charge, significant

219 C:G base pairs H-bond with conserved His or Arg residues in ZnF8, ZnF9, and ZnF11, and the consensus

220 in alpha and beta-subunits; the basic Lys or Arg side chain hydrogen bonds to the alphaIIb-subunit, a

221 anti-Valpha24 Abs depends on whether Ser or Arg is encoded.

222 ) with a higher affinity compared with other Arg-Gly-Asp binding integrins.

223 LK2 variants, with a major preference for P1-Arg.

224 basic residues at either P2 (Lys(197)), P6 (Arg(193)), or P8 (Lys(191)) positions.

225 antigen possessed a P7-Leu instead of the P7-Arg residue, but nevertheless was accommodated within th

226 he" motif with respect to the classical "Phe-Arg" melanocortin signaling motif, which results in phar

227 accommodate a variable base, whereas PRDM9a Arg(764) recognizes a conserved guanine.

228 a reported AGRP macrocyclic scaffold (c[Pro-Arg-Phe-Phe-Asn-Ala-Phe-DPro]) were explored with 14-com

229 nce in the AGRP active loop derivative c[Pro-Arg-Phe-Phe-Xxx-Ala-Phe-DPro], where Xxx was the native

230 Gly) and two positively charged domains (Pro-Arg-Gly) at both N- and C-termini.

231 e a HyaA-R193L variant to disrupt a proposed Arg-His cation-pi interaction in the secondary coordinat

232 inyl dipeptides: Ala-Arg (AR), Arg-Ala (RA), Arg-Pro (RP), Arg-Glu (RE), and Glu-Arg (ER); and two no

233 e pore profile at the gate formed by residue Arg-187.

234 l modeling pointed to a key role for residue Arg-135 in binding and properly positioning the l-THA an

235 (C), we predicted that MYO1C(35) NTR residue Arg-21 would engage in a specific interaction with post-

236 Moreover, we show that TolA residue Arg-325 involved in one of the two salt bridges is criti

237 cleaves APP at a specific arginine residue (Arg-102) both in vitro and in cells.

238 n the ECL2 of hNTS2 or with a basic residue (Arg(212)) at the same position in hNTS1.

239 ions of the functionally equivalent residue (Arg-165) in the prokaryotic Kir channel KirBac1.1 also s

240 actions with the positively charged residues Arg-14 and Lys-17.

241 For example, basic residues (Arg, His, Lys) increase peptide retention when located c

242 B1 glycosylated two GAPDH arginine residues, Arg(197) and Arg(200), and that these two residues were

243 ces of TRBV4-1 revealed two unique residues, Arg(30) and Tyr(51), as critical in conferring CD1c-rest

244 s template contains a sequentially reversed "Arg-(pI)DPhe" motif with respect to the classical "Phe-A

245 results suggested that the common high risk Arg-325 variant is hyperactive, and thus may be targeted

246 s: Ala-Arg (AR), Arg-Ala (RA), Arg-Pro (RP), Arg-Glu (RE), and Glu-Arg (ER); and two non-arginyl dipe

247 Ser/Arg-rich (SR) proteins are essential nucleus-localized s

248 Leu-81 and Leu-148, autolytic cleavage site Arg-122, and restoration of the missing disulfide bridge

249 of the epidermal growth factor receptor-Src-Arg kinase cascade is known to be a critical trigger for

250 d methoxychlor inhibited cortisol-stimulated Arg and TAT gene expression.

251 is more helical and thermo-stable suggesting Arg increases stability.

252 ), has been in clinical trials for targeting Arg auxotrophic tumors by Arg starvation therapy.

253 An Ala mutation of the distal C-terminal Arg-354 or Ser-357, which forms a consensus phosphorylat

254 ctors, defined by their conserved N-terminal Arg-Xaa-Leu-Arg (RxLR) motif.

255 es on [des-Arg(7)]Dyn A analogues found that Arg(7) is not a key residue and even deletion of the res

256 We report that Arg-593, a residue located in the E4 loop near the TRPC5

257 Instead, our data show that Arg contributes crucially to ligand sensitivity via a hy

258 ing the Potential Mean Force, we showed that Arg is prone to direct binding onto the NP surface, whil

259 ion of available sequence data suggests that Arg-135 may have originated for l-THA-like beta-eliminat

260 Computer modeling suggests that Arg-593 may cross-bridge the E3 and E4 loops, forming th

261 The Arg-degrading recombinant protein, pegylated arginine de

262 The Arg-Gly-Gly repeats within the low-complexity region are

263 The Arg/Ser substitution also influenced Ag recognition as d

264 Here we report that CED-3 caspase and the Arg/N-end rule pathway cooperate to inactivate the LIN-2

265 n here to be targeted for degradation by the Arg/N-end rule pathway in naa10Delta cells include Kar4,

266 rapidly destroyed in naa10Delta cells by the Arg/N-end rule pathway, which recognized a C terminus-pr

267 range of permissive lipid compositions, the Arg-325 variant consistently exhibited accelerated zinc

268 Cyclic peptides containing the Arg-Gly-Asp (RGD) sequence have been shown to specifical

269 l and physiological in vivo evidence for the Arg(838) substitutions in RetGC1 being the culprit behin

270 To investigate the role of the Arg residues, one or two arginines were replaced by Ala.

271 n homeostasis, a strong up-regulation of the Arg/N-end rule pathway in the absence of NatA, and showe

272 -acetylase but also by overexpression of the Arg/N-end rule pathway in wild-type cells.

273 To investigate the impact of the Arg/N-end rule pathway on the proteome of etiolated seed

274 nts are previously unknown substrates of the Arg/N-end rule pathway.

275 -Trp or tripeptide DPhe-Arg-Trp replaced the Arg-Phe-Phe sequence in the AGRP active loop derivative

276 Our data suggest that the Arg that is taken up is primarily metabolized by the arg

277 Numerous SAR studies have revealed that the Arg(7) residue is essential for KOR activity.

278 ollectively, these results indicate that the Arg/Ser encoded at the third CDR3beta residue can effect

279 This Arg-Asp conformational switch allows identical ZF module

280 We identified a conserved Thr-Arg motif that orients the sialic acid moiety and is req

281 lation and asymmetric dimethylation at three Arg residues.

282 l incorporation of the isosteric, titratable Arg analog, canavanine, into a neurotransmitter receptor

283 Resistance to Arg starvation is often developed through reactivation o

284 n silico modeling validated that this Ser-to-Arg mutation could alter the structure of the CDR3beta l

285 ticle ensemble exhibited selectivity towards Arg by showing distinguishable colour change from yellow

286 at AGA codons due to deficiencies in a tRNA(Arg)UCU tRNA and GTPBP2, a mammalian ribosome rescue fac

287 Targeting tRNA(Arg)(UCU) with an antisense oligonucleotide replicated e

288 Gln, Lys, or Tyr at UAA or UAG PTCs and Trp, Arg, or Cys at UGA PTCs.

289 Oxidation of Ala-Ala-Ala-Tyr-Arg (AAAYR) produces a mixture of cation radicals involv

290 -141 fragment of hemoglobin (Thr-Ser-Lys-Tyr-Arg), a small (653Da) and hydrophilic antimicrobial pept

291 cell migration by targeting integrins, using Arg-Gly-Asp (RGD) peptide-functionalized gold nanorods.

292 t remains unclear how the high risk variant (Arg-325), which is also a higher frequency (>50%) allele

293 nsitivity via a hydrogen bond network, where Arg interacts both with agonist and with a conserved Thr

294 on to the kinase domain, a process for which Arg-204 is important.

295 exist in a dimer-like configuration in which Arg-742 of a monomer forms a salt bridge with Asp-113 of

296 otrimer, thereby forming hydrogen bonds with Arg(104) in the adjacent subunit.

297 on in alphaENaC that substituted Cys479 with Arg (C479R).

298 te formation, stabilized by interaction with Arg-126, which is itself modulated by its respective int

299 Substituting Lys with Arg (or vice versa) in the naturally-occurring myosin-6

300 asic substrates, and accepts substrates with Arg and Lys in P1 and does not require Ca(2+) for activi