ライフサイエンスコーパス: Arg

1 Arg significantly affected the concentrations of 16 meta

2 Arg significantly increased plaque ADS activity (P = 0.0

3 Arg(Nap) can be incorporated into peptides with sterical

4 Arg, Ornithine and Lys were identified as substrates.

5 Arg-161 in the active site of CblC suppressed the NO(2)C

6 nnose receptor C type 1) MRC1+, (arginase 1) Arg+ macrophages in the tumor microenvironment.

7 orated into the peptide macrocycles c[Pro(1)-Arg(2)-Phe(3)-Phe(4)-Xaa(5)-Ala(6)-Phe(7)-dPro(8)], wher

8 Moreover, Galpha(13) Arg-200 mutants induced oncogenic transformation in vitr

9 The simulations suggested that an Asp-156-Arg-39-Tyr-202 triad creates a hydrogen-bonded network t

10 e oncogenic GOF mechanisms of p53 codon 158 (Arg(158)) mutation, a DBD mutant found to be prevalent i

11 ocket on Stx2A1 and interacted with Arg-172, Arg-176, and Arg-179, which were previously shown to be

12 pose that IGF-1 Glu-58 interacts with IGF-1R Arg-704 and belongs to IGF-1 site 1, a finding supported

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

14 We found that Tyr 96, Glu 201, Arg 204, and Trp 234 in the presumptive active site of J

15 e conserved catalytic site residues Lys-249, Arg-270, and His-271 resulted in activity loss.

16 r selective antagonist arodyn (Ac[Phe(1,2,3),Arg(4),d-Ala(8)]dynorphin A(1-11)-NH(2)) by ring closing

17 xtracellular N terminus of PAR(2) at Asn(30) Arg(31), proximal to the canonical trypsin activation si

18 As an intact Glu-343/Arg-378 bridge is the default state in unbound ETS1 and

19 rs the loss of a distal salt bridge (Glu-343/Arg-378) via a large side-chain motion that compromises

20 bstitutions of the tri-arginine patch Arg-42-Arg-44 or the R44K cancer-associated mutation in caspase

21 NAD(+)-binding site revealed that Phe(727), Arg(757), and Arg(780) are essential for NAD(+) hydrolys

22 s, the most active being those with 16 and 8 Arg residues.

23 d-Aza-Thr(8),Arg(10)-teixobactin exhibits 2-8-fold greater antibiotic

24 phic structure of N-Me-d-Gln(4),d-aza-Thr(8),Arg(10)-teixobactin reveals an amphipathic hydrogen-bond

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

26 Mutation of Shank3 residues (949)Arg-Arg-Lys(951) to three alanines disrupts CaMKII bindi

27 identified three arginine residues (Arg-97, Arg-277, and Arg-303) that are important for both enzyme

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

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

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

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

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

33 ligands, derived from the hexapeptide acetyl-Arg-Tyr-Arg-Leu-Arg-Tyr-NH(2) (1), reported to be a Y(4)

34 of trans-acting Tyr(290) against cis-acting Arg(349) compels Arg(349) to maintain proper conformatio

35 different substrates; thrombin cleaves after Arg, whereas trypsin cleaves after Lys/Arg.

36 h previously reported Gly -> Xaa (Xaa = Ala, Arg, or Val) vEDS substitutions within a high-affinity i

37 sB effectors of ECL both contain Pro-Ala-Ala-Arg (PAAR) repeat domains, which bind the beta-spike of

38 avage of S generates a polybasic Arg-Arg-Ala-Arg carboxyl-terminal sequence on S1, which conforms to

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

40 The PDZ binding motif (PBM) and an Arg-rich motif upstream of PBM conserved in TARPs bind t

41 es RC bearing several amino acid changes, an Arg in place of the native Leu at L185-positioned over o

42 observed that all sensitive viruses have an Arg residue at the P4 position of the cleavage site betw

43 We present the first structure of an Arg-AA9, LsAA9B, a naturally occurring protein from Lent

44 catalytic triad and unconventionally uses an Arg residue in the formation of an oxyanion hole.

45 Subsequent mutation of Tyr(117) and Arg(273) led to diminished binding and activation of XCR

46 ts involving Glu(4) of XCL1 and Tyr(117) and Arg(273) of XCR1.

47 Mutations in Ser-23, Lys-148, and Arg-321 uncoupled adenosine triphosphatase and Rca activ

48 rom the ER, a salt bridge between Asp-17 and Arg-57 is essential.

49 A1 and interacted with Arg-172, Arg-176, and Arg-179, which were previously shown to be critical for

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

51 p of the substrate was bound by Arg(265) and Arg(307) .

52 hree arginine residues (Arg-97, Arg-277, and Arg-303) that are important for both enzyme activity and

53 sis revealed that two arginines, Arg-332 and Arg-521, are key specificity determinants of BT0997 in t

54 two arginine isotopologues (Arg-(15)N(4) and Arg-D(4), differs by 36 mDa).

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

56 h of positive charge consisting of Lys-5 and Arg-17.

57 onfirmed that the side chains of Gln-623 and Arg-661 play important roles in mediating PI(4,5)P(2)-in

58 g site revealed that Phe(727), Arg(757), and Arg(780) are essential for NAD(+) hydrolysis by TNT.

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

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

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

62 cine (coded by GGX), Ser (coded by AGY), and Arg (coded by CGX and AGZ).

63 e carboxyl group of allosteric effectors and Arg-120 of Eallo; however, structural studies show some

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

65 ng between the suramin sulfonated groups and Arg/Lys residues play critical roles in the binding of s

66 protonate the Ala-enamine intermediate, and Arg-56 facilitates catalysis by hydrogen bonding with th

67 o-base substitutions, in contrast to Leu and Arg, of which codons are mutually exchangeable by a sing

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

69 The methylation states of Lys and Arg represent a particularly challenging set of targets

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

71 n which we replaced seven C-terminal Lys and Arg residues with Ala and added a Cys residue at either

72 eight possible methylation states of Lys and Arg that can be recognized selectively.

73 eader protein that binds RNA through RRM and Arg-Gly-Gly (RGG) motifs.

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

75 Here, we review evidence that Trp and Arg catabolism contributes to inflammatory processes tha

76 Processes that induce Trp and Arg catabolism in the TME remain incompletely defined.

77 Cells catabolizing Trp and Arg suppress effector T cells and stabilize regulatory T

78 arginase 1 (ARG1), which catabolize Trp and Arg, respectively, respond to inflammatory cues includin

79 ut no function has been demonstrated for any Arg-AA9.

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

81 Arginase (Arg) 1 is expressed by hematopoietic (e.g., macrophages)

82 e amino acids tryptophan (Trp) and arginine (Arg) is a common TME hallmark at clinical presentation o

83 identification of histidine (His), arginine (Arg), lysine (Lys), aspartate (Asp), glutamate (Glu) and

84 cids, three of them-leucine (Leu), arginine (Arg), and serine (Ser)-are encoded by six different codo

85 l plaque in response to the use of arginine (Arg: 1.5% arginine, fluoride-free) or fluoride (F: 1,100

86 NP granule dynamics, in particular arginine (Arg)-methylation and phosphorylation.

87 h the use of molecular precursors (arginine (Arg) and ethylenediamine (EDA)) and making use of microw

88 lting from trypsin digestion, with arginine (Arg) or lysine (Lys) at the C-terminus, can be analyzed

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

90 inaceous amino acids (lysine, Lys; arginine, Arg; and histidine, His), along with nonproteinaceous an

91 rmatic analysis revealed that two arginines, Arg-332 and Arg-521, are key specificity determinants of

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

93 omains are rich in charged residues (such as Arg, Lys, and Glu) with potential ion pairs across adjac

94 ied enrichment of histone 3 dimethylation at Arg-8 (H3(Me2)R8) in the promoter regions of miR33b, miR

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

96 using a ParA with an alanine substitution at Arg(351), a residue previously predicted to participate

97 subsites of the cathepsin protease, and (b) Arg(19) which forms cation-pai interactions with Trp(291

98 onships (SAR) of a dipeptide library bearing Arg alpha-ketobenozothiazole (kbt) warheads as novel inh

99 iant altered a communication pathway between Arg-293 and the serine loop by reducing its dynamicity.

100 four classes of integrins: collagen-binding, Arg-Gly-Asp (RGD)-binding, laminin-binding, and leukocyt

101 erivative with a fluorescent side-chain, Boc-Arg(Nap)-OH, was prepared by palladium(0)-catalyzed coup

102 ed by palladium(0)-catalyzed coupling of Boc-Arg-OH with a 4-bromonaphthalimide.

103 carboxyl group of the substrate was bound by Arg(265) and Arg(307) .

104 ation of the serine-rich loop is mediated by Arg-293 of CRY1, identified as a rare CRY1 SNP in the En

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

106 During catalysis, Arg(169), Tyr(185), and Tyr(187) are responsible for neu

107 Cationic Arg or Lys side chains lining the S4 helix move through

108 MR spectroscopy, of substituting key charged Arg, Lys, Glu, and Asp residues by Gly or His.

109 an invariably conserved, positively charged Arg that is believed to enhance interaction of the negat

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

111 t GP70, we identified the positively charged Arg-130 as the binding site.

112 Tyr(290) against cis-acting Arg(349) compels Arg(349) to maintain proper conformation of Walker A.

113 een of MICU1 identifies two highly-conserved Arg residues that might contact the DIME-Asp.

114 In addition, the conserved Arg-215 plays a critical role in substrate specificity,

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

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

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

118 compassed by protein degradation via the Cys/Arg branch of the N-degron pathway-part of the PROTEOLYS

119 nic acid, triggering degradation via the Cys/Arg branch of the N-degron pathway.

120 nsing of oxygen availability through the Cys/Arg N-degron pathway functions alongside ROS production

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

122 u-/delta-opioid agonist tetrapeptide H-Dmt-d-Arg-Aba-beta-Ala-NH(2) (KGOP01) was fused to NT(8-13) an

123 gm) and 38 (c(Bua-Cpa-Thi-Val-Asn-Cys)-Pro-d-Arg-NEt(2)) have been selected for clinical development

124 n five or six positively charged residues (d-Arg, d-Lys, d-Orn, l-Dab, or l-Dap) on the polar face to

125 -PDX or the pharmacologic inhibitor Decanoyl-Arg-Val-Lys-Arg-chloromethylketone repressed PD-1 and ex

126 hat, a vicious positive feedback loop of des-Arg(9)-bradykinin- and bradykinin-mediated inflammation

127 R proteins on their intrinsically disordered Arg-Ser (RS) domains, mobilizing them from storage speck

128 nking residue Val-339, unlike the equivalent Arg-343 in the homologous human surfactant protein D, is

129 herefore, these tumors require extracellular Arg for growth.

130 Y180A/M183A (open conformation), but not FAK/Arg(454) (kinase-dead), augmented Rab5-GTP levels in FAK

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

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

133 s generated in greater amounts with the GlcN-Arg caramels.

134 ues through Michael addition, including Gln, Arg, and Asn, which are inaccessible to existing chemica

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

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

137 ched between two neighboring glycines (a Gly-Arg-Gly, or "GRG," sequence).

138 The Gly -> Arg substitution destabilized CMP-alpha(2)I side-chain i

139 sidues 25 and 26 or residues 29 and 31: Lys->Arg (KR) (25/26KR and 29/31KR) and Lys->Thr (KT) (25/26K

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

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

142 odeling and mutagenesis of AKR1A1 identified Arg-312 as a key residue mediating the specific interact

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

144 n the HCN1 structure analysis, we identified Arg(237) and Gly(239) residues on the S2 of the VSD that

145 ing site-directed mutagenesis, we identified Arg-8 of subunit e as a critical residue in mediating in

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

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

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

149 ified cancer-associated hotspot mutations in Arg-200 of Galpha(13) (encoded by GNA13) as potent activ

150 12/13) pathway alterations were mutations in Arg-200 of Galpha(13), which we validated to promote YAP

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

152 Thus, the Ca(2+)-independent, Arg-containing NrfA from G. lovleyi represents a new sub

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

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

155 cally labeled by two arginine isotopologues (Arg-(15)N(4) and Arg-D(4), differs by 36 mDa).

156 e reported that both SLC7A2 expression and L-Arg availability are decreased in colonic tissues from i

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

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

159 the semi-essential amino acid L-arginine (L-Arg), which has been implicated in wound repair.

160 are heme-based monooxygenases that convert l-Arg to l-citrulline and nitric oxide (NO), a key signali

161 Strategies to enhance L-Arg availability by supplementing L-Arg and/or increasin

162 functions as a dimer and produces NO from l-Arg and NADPH in a tetrahydrobiopterin (H(4)B)-dependent

163 to function in nitrogen assimilation from l-Arg.

164 y by supplementing L-Arg and/or increasing L-Arg uptake could represent a therapeutic approach in IBD

165 l-NMA or N(delta)-hydroxy-N(omega)-methyl-l-Arg (l-HMA).

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

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

168 otein does not confer growth advantages on l-Arg as a nitrogen source.

169 nhance L-Arg availability by supplementing L-Arg and/or increasing L-Arg uptake could represent a the

170 he 26S proteasome, suggesting an even larger Arg/N-degron-targeting complex that contains the proteas

171 from the hexapeptide acetyl-Arg-Tyr-Arg-Leu-Arg-Tyr-NH(2) (1), reported to be a Y(4)R partial agonis

172 ion of 1 resulted in a tetrapeptide (Arg-Leu-Arg-Tyr-NH(2)), being a Y(4)R partial agonist with uncha

173 the hexapeptide H(2)N-(CH(2))(4)-CO-Pro-Leu-Arg-Phe-Gly-Ala-NH-CH(2)-Fc is the optimal probe for cat

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

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

176 ontaining the proteinaceous amino acids Lys, Arg, or His adjacent to backbone ester bonds generally p

177 His, Lys, Arg, or Pro residues prohibit cleavage when found at the

178 t a chemical basis for the selection of Lys, Arg, and His over other cationic amino acids for incorpo

179 O and nucleophilic amino acid residues (Lys, Arg and Cys) and naringenin in milk.

180 pharmacologic inhibitor Decanoyl-Arg-Val-Lys-Arg-chloromethylketone repressed PD-1 and exhausted CTLs

181 secutive positively charged amino acids (Lys/Arg).

182 after Arg, whereas trypsin cleaves after Lys/Arg.

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

184 activity than the corresponding macrolactone Arg(10)-teixobactin.

185 pound [(68)Ga]Ga-NODAGA-Lys(Cy5**)-AEEAc-[Me-Arg(8),Tle(12)]-NT(7-13) as the one with the most promis

186 gnizes the central 5mCpG by forming a methyl-Arg-G triad, and its conformation is constrained by Val2

187 guanidinium occupies the site of a 'missing' Arg side chain found in other fungal species where (i) t

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

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

190 Keratin mutation (Arg-to-Lys/Ala) at the methylation sites, but not the ac

191 )N value reconstruction including delta(15)N(Arg) values better reflect the measured bulk values, as

192 of archaeological cattle collagen delta(15)N(Arg) values confirmed the suitability of this method to

193 d cattle collagen, enabling their delta(15)N(Arg) values to be related to AA biosynthesis.

194 d determine its delta(15)N value (delta(15)N(Arg)) by gas chromatography-combustion-isotope ratio mas

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

196 ere, we report on the development of a novel Arg-specific NMR experiment that detects the methylation

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

198 and found that a critical residue on Nprl2, Arg-78, is the arginine finger that carries out GATOR1's

199 Nt-Asp, binding of resulting (conjugated) Nt-Arg to the UBR1-RAD6 E3-E2 ubiquitin ligase, ligase-medi

200 s, consisting of a high percentage (>75%) of Arg, Lys, and Glu residues, are exceptions to this rule

201 Most genera from the exclusive clades of Arg-containing NrfA proteins are also represented in cla

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

203 e, resulting in displacement and disorder of Arg-120, located at the opening to the active site.

204 es a loop in Eallo immediately downstream of Arg-120.

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

206 nalysis revealed four separate emergences of Arg-containing NrfA enzymes.

207 talyzes the methylation of the equivalent of Arg(285) in a peptide substrate surrogate, but only in t

208 increases the conformational flexibility of Arg-4, Lys-5 and Gln-6 of BCL11B.

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

210 n RS enzyme implicated in the methylation of Arg-285 in methyl coenzyme M reductase, binds a methylco

211 cs simulations revealed enhanced mobility of Arg(208) in mutants exhibiting H(+) leak.

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

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

214 l (SAH) domains contain a high percentage of Arg, Lys, and Glu residues.

215 Replacement of Arg-177 in PKG1alpha with alanine or methionine also inc

216 king experiments suggested a pivotal role of Arg-635 at the entrance of the binding pocket in HCN2, e

217 Substitution of Arg 289 in Rrp9 to Ala (R289A) specifically reduced clea

218 ith this hypothesis, (i) the substitution of Arg-8 in subunit e (eArg-8) with Ala or Glu or of Glu-83

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

220 promoting phase separation relative to other Arg-rich stretches of sequence, subsequently confirmed b

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

222 The P4 Arg-to-His substitution partially rescues this defect.

223 that substitutions of the tri-arginine patch Arg-42-Arg-44 or the R44K cancer-associated mutation in

224 difference is that CPMPs containing a penta-Arg motif are released efficiently from endosomes, while

225 g a precisely defined, penta-arginine (penta-Arg) motif that traffics readily to the cytosol and nucl

226 (12.2%) when assayed in the presence of Phe-Arg-beta-Napthylamide, with 35 of these 42 possessing at

227 Cleavage of S generates a polybasic Arg-Arg-Ala-Arg carboxyl-terminal sequence on S1, which

228 analogous side chain in RB69 DNA polymerase (Arg-482) and HIV reverse transcriptase (Lys-65) were pre

229 and absence of the fibrin inhibitor Gly-Pro-Arg-Pro.

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

231 In contrast, the putative Arg-Gly-Asp (RGD)-binding alphaPAT-2/betaPAT-3 integrin

232 ritized the missense variant rs147647315 (R (Arg) > H (His)) as the sole causal variant.

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

234 th PI(3)P and that this interaction requires Arg-292.

235 The N terminus of MinD, including residue Arg 3, which is near the ATP-binding site in sequence, i

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

237 ly charged and highly conserved H4c residue, Arg(108), was indispensable and crucial for metabolite t

238 ffects of the most commonly mutated residue, Arg-183, on PP2A function have yet to be fully elucidate

239 that form direct interactions with residues Arg(154) and Ser(158) on the HCND.

240 says, we identified three arginine residues (Arg-97, Arg-277, and Arg-303) that are important for bot

241 beta-hairpin loop composed of six residues (Arg-Phe-Phe-Asn-Ala-Phe) that is imperative for binding

242 Among these residues, Arg-277 appeared to be particularly important for signal

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

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

245 nd cultured neurons, SRPK phosphorylates Ser-Arg motifs in RNF12/RLIM, a key developmental E3 ubiquit

246 finger CCCH-type, RNA binding motif, and Ser/Arg rich 2/Rough endosperm 3 (RGH3).

247 The Ser/Arg (SR)-rich splicing factor (SRSF) protein kinase (SRP

248 y a mass spectrometry and identified the Ser/Arg-like protein REDUCED RED-LIGHT RESPONSES IN CRY1CRY2

249 t unique BMP15 finger residues at this site (Arg(301), Gly(304), His(307), and Met(369)) enable poten

250 addition, specific features of protein-sized Arg/N-degron substrates, including their partly sequenti

251 natural N-terminal His to Arg substitution (Arg-AA9).

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

253 The second cluster surrounded Arg(101) on a surface of helix 3.

254 , charge neutralization mutations in TARP_CT Arg-rich motif weakened TARP's condensation with PSD-95

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

256 protein phosphorylation near the N-terminal Arg and the carbohydrate-binding site, for which the pot

257 ediction of the importance of the N-terminal Arg-containing region of this construct for promoting ph

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

259 truncation of 1 resulted in a tetrapeptide (Arg-Leu-Arg-Tyr-NH(2)), being a Y(4)R partial agonist wi

260 RIPK1 are key for ceramide binding and that Arg(258) or Leu(293) residues are involved in the myosin

261 Our results are strong evidence that Arg-AA9s function markedly different from canonical AA9

262 nding to C-S bond cleavage and indicate that Arg-56, His-123, and Cys-364 are critical SufS residues

263 Additional biochemical studies revealed that Arg-65 is critical for activation by facilitating a conf

264 analyses we present data, which suggest that Arg-AA9 proteins could have a hitherto unidentified role

265 P2 on model membrane surfaces suggested that Arg-88 is critical for P2-membrane interactions, in addi

266 The Arg/N-degron pathway targets proteins for degradation by

267 The Arg/N-degron pathway targets proteins for degradation by

268 The Arg/N-end rule and VCP/p97UFD1-NPL4 segregase cooperate

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

270 nt exploration of the vector directed at the Arg-108 residue, leading to the identification of highly

271 previously unappreciated axis connecting the Arg/N-end rule and the p97-mediated proteolysis with the

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

273 ned at low digitonin concentrations from the Arg-8 variants displayed currents of strikingly small co

274 ein transferase 1 (Ate1), a component of the Arg/N-degron pathway of protein degradation.

275 ng UBR1 and UBR2 E3 ubiquitin ligases of the Arg/N-degron pathway.

276 that GR is a physiological substrate of the Arg/N-degron pathway.

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

278 a short-lived physiological substrate of the Arg/N-end rule proteolytic pathway, in which UBR1 and UB

279 of their mRNAs, strongly suggesting that the Arg/N-degron pathway can also modulate translation of sp

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

281 ion of the aromatic triazole moiety with the Arg(356) residue of the receptor is accountable for thes

282 O family display a natural N-terminal His to Arg substitution (Arg-AA9).

283 Resistance to Arg starvation is often developed through reactivation o

284 ovides a therapeutic opportunity specific to Arg(158)-mutp53 tumors utilizing a regimen consisting of

285 d 44; additional escape mutants had a His-to-Arg mutation at amino acid 44 or a duplication of amino

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

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

288 GA) are decoded by two Escherichia coli tRNA(Arg) isoacceptors.

289 ng tRNAs codons read by tRNA(Gln(TTG)), tRNA(Arg(CCG)), and tRNA(Thr(CGT)) These findings collectivel

290 omplete loss of the m3C modification in tRNA-Arg species.

291 were detected; two of them were in the tRNA-Arg and Cell division protein FtsH genes, respectively.

292 derived from the hexapeptide acetyl-Arg-Tyr-Arg-Leu-Arg-Tyr-NH(2) (1), reported to be a Y(4)R partia

293 Substitution of Lys-428 with Arg dramatically altered ADP inhibition, independently o

294 Folded OmpA in NDs was incubated with Arg-C protease, resulting in the digestion of OmpA to me

295 shallow pocket on Stx2A1 and interacted with Arg-172, Arg-176, and Arg-179, which were previously sho

296 n a conformation lacking an interaction with Arg-120.

297 of the P1 Leu(15) in the reactive loop with Arg(15).

298 he metabolic profiles of plaque treated with Arg or F.

299 ere recruited and assigned to treatment with Arg or F for 12 wk.

300 no difference was found when treatment with Arg was compared to F (P = 0.46).