ライフサイエンスコーパス: Lys

1 Lys 48-linked polyubiquitin chains signal for protein de

2 Lys(129) mutation to glutamate or arginine led to misfol

3 Lys-63-ubiquitination activates the TGFbeta-activated ki

4 Lys-rich sequences (EK3 (AEEEKKK) and EK2R1 (AEEEKRK)) b

5 tations Arg-126-Gln, Asp-49-Asn, and Arg-126-Lys, we inferred that a crystallographic water acts as a

6 The reference agonist [Nle(14),Lys(40)(Ahx-DOTA)NH2]Ex-4 demonstrated the highest affin

7 he reference GLP-1 receptor agonist [Nle(14),Lys(40)(Ahx-DOTA-(68)Ga)NH2]Ex-4.

8 B(29)-Lys-cholyl-insulin and B(1)-Phe-cholyl-insulin, both wer

9 was no evidence for the absorption of B(29)-Lys-cholyl-insulin when infused into the ileum, B(1)-Phe

10 th key lysine residues in ER-alpha (Lys-299, Lys-302, and Lys-303), which is likely to prevent ubiqui

11 a transgene exogenously expressing histone 3 Lys-36 to Met mutation (K36M) acts in a dominant-negativ

12 (12),Nle(21,38),C(alpha)MeLeu(27,40),Glu(30),Lys(33)]-acetyl-h /r-CRF(9-41)}.

13 ubstrate-linked Ub chains containing Lys-63, Lys-48, and Lys-11 linkages (Lys-63 > Lys-48 > Lys-11).

14 n and substrate analogs) identified Arg(64), Lys(269), and Tyr(309) as key catalytic residues of VioA

15 to the WHO recommendations, having e.g. 4.8% Lys, 2.7% Met+Cys, and 7.7% Phe+Tyr.

16 tified three transmembrane residues (Val-86, Lys-93, and Asn-258) that form a putative barrier to ion

17 s, binding of NT[8-13] analogues harboring a Lys(11) exhibited higher affinity toward the hNTS1-R212E

18 We identify a Lys-Gly-Glu (KGE) integrin-binding motif in the FVIIa pr

19 ral studies show that catalysis depends on a Lys-Tyr-Asn-Tyr tetrad that emerged adjacent to a comput

20 hin the transporter cavity by pivoting about Lys-436 leading to net transport from the outer to the i

21 4 showing high activity against the abundant Lys- and Arg-rich protein, myosin.

22 demonstrated that substrates containing ACC/Lys(DNP) exhibit 7 to 10 times higher sensitivity than c

23 We therefore propose that the ACC/Lys(DNP) pair can be considered a novel and sensitive sc

24 Point mutations identified two amino acids (Lys-98 and Asp-100 in LRRC8A and equivalent residues in

25 FPheK reacted with adjacent Lys, Cys, and Tyr residues in thioredoxin in high yields

26 ridges with key lysine residues in ER-alpha (Lys-299, Lys-302, and Lys-303), which is likely to preve

27 ged residues Asp-997, Glu-998, Arg-1000, and Lys-1001 in M10, participating in this bonding network,

28 cluding the side chains of Arg 6, His 11 and Lys 32 as potentially important in the FS50 NaV1.5 inter

29 ing to residues 14-24, containing Arg-14 and Lys-17.

30 h the positively charged residues Arg-14 and Lys-17.

31 residues in the NCAM Ig2 domain (Arg-156 and Lys-162) and the EphA3 CRD (Glu-248 and Glu-264).

32 or NODAGA chelators at positions Lys(27) and Lys(40) and labeled with (68)Ga and (125)I-BH-Ex(9-39)NH

33 nd NODAGA chelators at positions Lys(27) and Lys(40) of Ex(9-39)NH2 resulted in a distinct loss of af

34 residues in ER-alpha (Lys-299, Lys-302, and Lys-303), which is likely to prevent ubiquitination at t

35 ked Ub chains containing Lys-63, Lys-48, and Lys-11 linkages (Lys-63 > Lys-48 > Lys-11).

36 RRK2 promoted the deacetylation of Lys-5 and Lys-12 on histone H4, causing repression of gene transcr

37 demonstrated that two of these, Lys-565 and Lys-663, coordinate ATP in the active site.

38 ere inserted as surrogates of the Trp(7) and Lys(8) residues in the biologically relevant Trp-Lys-Tyr

39 gagement of CR4 by Lys-88, CR5 by Arg-76 and Lys-80, and CR6 by Lys-69, with the strongest interactio

40 strates, and accepts substrates with Arg and Lys in P1 and does not require Ca(2+) for activity.

41 hat is regulated by proteolytic cleavage and Lys-63-polyubiquitination.

42 ces (SAHs), are rich in Arg (R), Glu (E) and Lys (K) residues, and stabilized by multiple salt bridge

43 crosslinks could be formed between FPheK and Lys residue of two interacting proteins, including the h

44 motifs YRYRQ and RYESK are the best Gln and Lys substrates of KalbTG, respectively.

45 ctivity but stimulated activation of Glu and Lys forms of plasminogen by alphaFXIIa.

46 romote salt-bridge formation between Glu and Lys/Arg.

47 ining nucleophilic sidechains (Cys, His, and Lys) and selected proteins (bovine and human hemoglobin

48 ing amino acids Ala, Asn, Gln, His, Ile, and Lys at positions equivalent to 782 and/or 786 in Fn-bind

49 derably increased the expression of MIB2 and Lys-63-linked ubiquitination of GABAB receptors.

50 Arg, Ornithine and Lys were identified as substrates.

51 Among the studied antagonists, [Lys(40)(NODAGA-(nat)Ga)NH2]Ex(9-39) showed the lowest IC

52 a-peptide/beta-peptoid hybrid Lau-((S)-Aoc)-(Lys-betaNphe)6-NH2 (F2M2), showing comparable potency in

53 g dependence of the potency on a basic (Arg, Lys) exocyclic residue that addressed the S1' binding po

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

55 nge columbic interactions between basic (Arg/Lys) residues located N-terminally to the phosphorylated

56 oes not alter the sCT fibrillary core around Lys(11) but makes changes to Val(8) on the exterior side

57 side-chains and charged hydrophilic (such as Lys) side-chains in a peptide sequence determines the or

58 E2 paralogs of the Ubc4/5 clade to assemble Lys(63)-linked polyubiquitin chains.

59 gation to the protein degradation-associated Lys-48-linked ubiquitin-chains.

60 3 and of the BRD domain for H3 acetylated at Lys(14) (H3K14ac), the exact mode of H3 binding by BAZ2B

61 T1 activity is low, and SIRT3 acetylation at Lys(57) inhibits its deacetylase activity and promotes p

62 We identified acetylation at Lys-36 in histone H3 (H3K36ac) as a new chromatin modifi

63 ll ordered break in the polypeptide chain at Lys(147), resulting in a large conformational rearrangem

64 at Arg(162) was not required for cleavage at Lys(158) or regulation of chemerin bioactivity.

65 Dimethylation at Lys-36 on histone H3 (H3K36me2) is associated with activ

66 0-dependent activating acetylation of p65 at Lys-310, contributing to NF-kappaB transcriptional activ

67 novel acetylation-phosphorylation switch at Lys-321/Ser-324 that coordinately regulates tau polymeri

68 integrin alpha and beta-subunits; the basic Lys or Arg side chain hydrogen bonds to the alphaIIb-sub

69 he design of new NT analogues bearing basic (Lys, Orn) or acid (Asp or Glu) function.

70 utual, methylene-bridged cross-links between Lys(158) and Cys(245) residues.

71 l of AMSH-STAM to show how the complex binds Lys(63)-linked ubiquitin chains and cleaves at the dista

72 bioactive gamma-turn conformation of the Bip-Lys-Tyr tripeptide in Urocontrin ([Bip(4)]URP), which mo

73 e that binding involves engagement of CR4 by Lys-88, CR5 by Arg-76 and Lys-80, and CR6 by Lys-69, wit

74 Lys-88, CR5 by Arg-76 and Lys-80, and CR6 by Lys-69, with the strongest interactions to CR5 and CR6.

75 -proteolytic ubiquitin signaling mediated by Lys(63) ubiquitin chains plays a critical role in multip

76 o digestion with either Asp-N, Arg-C, Glu-C, Lys-C, or Lys-N.

77 acceptor site for the formation of canonical Lys-48-linkages.

78 ecific cross-linking of RNA to the catalytic Lys of FemXWv but not to related transferases recognizin

79 analog JR11 (Cpa-c[d-Cys-Aph(Hor)-d-Aph(Cbm)-Lys-Thr-Cys]-d-Tyr-NH2), an antagonist with selectivity

80 cid and JR11 = Cpa-c(dCys-Aph(Hor)-dAph(Cbm)-Lys-Thr-Cys)-dTyr-NH2)) for PET imaging.

81 cid and JR11 = Cpa-c(dCys-Aph(Hor)-dAph(Cbm)-Lys-Thr-Cys)-dTyr-NH2)), a novel radiolabeled sst recept

82 TA-JR11; DOTA-[Cpa-c(DCys-Aph(Hor)-DAph(Cbm)-Lys-Thr-Cys)-DTyr-NH2]) labeled with (177)Lu, (90)Y, and

83 (TCIs) based on our previously reported Cbz-Lys scaffold.

84 electrostatic bridge with positively charged Lys-89, mutation of which has been shown previously to d

85 Further replacement of the charged Lys-5 by neutral Gln to resemble Fyn (Src-S3C/S6C/K5Q) r

86 embles substrate-linked Ub chains containing Lys-63, Lys-48, and Lys-11 linkages (Lys-63 > Lys-48 > L

87 d the hD4R mutant that lacked 17 cytoplasmic Lys, Ser, and Thr residues was nearly insensitive to bor

88 udy suggested that a trans conformation at D-Lys(2)-Xxx(3) is crucial for these cyclic peptides to ma

89 mu-opioid receptor ligand, analogs H-Tyr-c[D-Lys-Xxx-Tyr-Gly] were synthesized and their biological a

90 ) was conjugated to the targeting peptide [d-Lys(6)]-GnRH, generating SAN1GSC.

91 ptical antipode) of cyclodal, c[-Arg-d-Phe-d-Lys-d-Dmt-] (2), also turned out to be a selective MOR a

92 ly charged induce a not previously described Lys-146 lift.

93 DOTA-conjugated GRPr antagonist, HZ220 (DOTA-Lys(IRDye 650)-PEG4-[D-Phe(6), Sta(13)]-BN(6-14)NH2), by

94 (6), Sta(13)]-BN(6-14)NH2), by reacting DOTA-Lys-PEG4-[D-Phe(6), Sta(13)]-BN(6-14)NH2 (HZ219) with IR

95 that binding of Ac-CoA to hMOF likely drives Lys-274 autoacetylation for subsequent cognate substrate

96 endent ubiquitination on the pex12-1 ectopic Lys residue.

97 Several surface-exposed Lys residues are present in IL-1beta, but not in IL1RN.

98 remarkable selectivity for cleaving extended Lys-48-linked polyubiquitin chains.

99 gradation; however, the structural basis for Lys 48 selectivity remains largely unknown.

100 5 for ligand binding but is not critical for Lys-155 because of the inherent flexibility of its side

101 that a K268M mutant, which is defective for Lys-274 chemical acetylation in the context of a K274-pe

102 The present work identifies a key role for Lys(66) in the regulation of PTEN expression and provide

103 ould change the 558-encoding amino acid from Lys to Asn (K558N).

104 ic processing, mature HMR, which begins from Lys-58, retains its biochemical properties in phytochrom

105 ssible pathway by which proton transfer from Lys 73 to Ser 130 can occur.

106 ved from endogenous readthrough, namely Gln, Lys, or Tyr at UAA or UAG PTCs and Trp, Arg, or Cys at U

107 minases (MTGs) catalyze the formation of Gln-Lys isopeptide bonds and are widely used for the cross-l

108 r pairs compared to Asp(-)/Arg(+) and Glu(-)/Lys(+).

109 ther Glu(-)/Arg(+), Asp(-)/Arg(+), or Glu(-)/Lys(+)).

110 and plasma of UCP3 Tg mice (e.g., Asp, Glu, Lys, Tyr, Ser, Met) were significantly reduced after an

111 trogen hydrolase domain containing a Cys-Glu-Lys catalytic triad.

112 conformations, and are more dynamic than Glu-Lys.

113 s-48, and Lys-11 linkages (Lys-63 > Lys-48 > Lys-11).

114 ys-63, Lys-48, and Lys-11 linkages (Lys-63 > Lys-48 > Lys-11).

115 Uptake of [(3)H]Ornithine and [(3)H]Lys was also detected at lower efficiency with respect t

116 key regulator for monoubiquitination at H2A Lys-119 as both knockdown and deletion of USP7 results i

117 s an important role in the regulation of H2A Lys-119 monoubiquitination.

118 structural data suggests that a Ser(84)-H2O-Lys(114) hydrogen-bonding network in human serine racema

119 RD4 acetyltransferase activity on histone H3 Lys (K) 122, demonstrating that RSV infection activates

120 nts of VIN3 and trimethylation of Histone H3 Lys 27 at the FLC locus without invoking the increased e

121 histone modifications, including histone H3 Lys 27 monomethylation (H3K27me1), imparted by ATXR5 and

122 4 activity is anticorrelated with histone H3 Lys 9 dimethylation (H3K9me2) levels at AtMu1c Double mu

123 Reduction in acetylation of histone H3 Lys-27 accompanies loss of FoxO1 and FoxA1/A2 binding.

124 binding to di- and trimethylated histone H3 Lys-36 and that this binding is important for NuA4 occup

125 own to bind di- and trimethylated histone H3 Lys-36 stimulated by Eaf3.

126 C) resulted in a complete loss of histone H3 Lys-36 trimethylation (H3K36me3).

127 H3 and H4 tails, only acetylation of the H3 Lys(14) substantially decreased binding to several Impor

128 SPIN1 and masks its ability to engage the H3-Lys-4 trimethylation activation mark.

129 age the tail of histone H3 by reading the H3-Lys-4 trimethylation and H3-Arg-8 asymmetric dimethylati

130 ondensin activity or affected for histone H4 Lys-16 deacetylation are impaired, at least in part, for

131 For example, basic residues (Arg, His, Lys) increase peptide retention when located closer to t

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

133 cysteine (His-Cys) and histidine-lysine (His-Lys) in addition to histidine-histidine (His-His) cross-

134 Surprisingly, His378Arg/Lys variants do not degrade in light despite maintaining

135 Histone Lys-to-Met (K-to-M) mutations act as gain-of-function mu

136 evealed that VRS3 encodes a putative histone Lys demethylase with a conserved zinc finger and Jumonji

137 nt to the critical and specific role of hMOF Lys-274 autoacetylation in hMOF stability and cognate su

138 A mutational scan of hMOF Lys-274 reveals that all amino acid substitutions of thi

139 substrate ubiquitin chain contain homogenous Lys(63)-linkages.

140 H-Dmt-d-Arg-Aba-beta-Ala-Arg-Tyr-Tyr-Arg-Ile-Lys-NH2) to mice resulted in potent and long lasting ant

141 uitin mutants or GABAB1 mutants deficient in Lys-63-linked ubiquitination prevented glutamate-induced

142 or the transport activity of NhaA, including Lys-300, a residue that has recently been proposed to ca

143 ermore, mass spectrometry analysis indicated Lys-72 as an acetylation site in the ERK1 N terminus, ad

144 be non-K48; among them, the most abundant is Lys 63 (K63)-linked polyUb chains that do not tag substr

145 the MARCKS-ED has further revealed that its Lys and Phe residues play an essential role in how MARCK

146 ly upon genetic incorporation of N--acetyl-l-Lys (AcK), and subsequent enzymatic deacetylation in the

147 Besides l-Lys, recombinant ALD1 transaminates l-methionine, l-leuc

148 ggest that the biosynthesis of 2,3-DP from l-Lys is the major in vivo function of ALD1.

149 at ALD1 transfers the alpha-amino group of l-Lys to acceptor oxoacids.

150 enuated in the receptor variants that lacked Lys or Ser/Thr residues, and the hD4R mutant that lacked

151 e of Gln residues, in contrast to the larger Lys and Arg residues in yeast and plant orthologs.

152 This includes a Leu-Lys-Ile-Pro sequence (residues 125-128 of AKAP79) that o

153 n synthetases, Ala-, Arg-, Asp-, Asn-, Leu-, Lys- and TyrRS, appear to associate with ES7.

154 taining Lys-63, Lys-48, and Lys-11 linkages (Lys-63 > Lys-48 > Lys-11).

155 This loop features a lysine (Lys(129)) likely occupying the S1 specificity pocket and

156 he fluorophore and 2,4-dinitrophenyl-lysine (Lys(DNP)) as the quencher.

157 bidopsis (Arabidopsis thaliana), the lysine (Lys) aminotransferase AGD2-LIKE DEFENSE RESPONSE PROTEIN

158 When lysine (Lys) residues of the hD4R are substituted with arginine

159 mologous proteins, namely cationic lysozyme (Lys) and anionic alpha-lactalbumin (aLac), both of which

160 ified electrodes, a model protein, lysozyme (Lys), was selected as the biological agent to be immobil

161 al 7-methoxy-coumarin-4-yl acetic acid (MCA)/Lys(DNP) substrates; thus, substantially lower amounts o

162 ere we show that Mind bomb-2 (MIB2)-mediated Lys-63-linked ubiquitination of the GABAB1 subunit at mu

163 The level of modified Lys(541) ranged from 2.6 to 4.8%.

164 ught to characterize the effects of mutating Lys-300 of NhaA to amino acid residues containing side c

165 In addition, a nonsense RB1 mutation (Lys-->STOP) from 1 child was also identified from the AH

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

167 3S10ph often associates with the neighboring Lys-9 di- or tri-methylations, they are not required for

168 mbrane antigen (PSMA) inhibitor Glu-NH-CO-NH-Lys(Ahx) using the (68)Ga chelator HBED-CC (PSMA(HBED))

169 ein, we investigated the use of Glu-NH-CO-NH-Lys(Ahx)-HBED-CC ((68)Ga-PSMA-HBED-CC) for this purpose.

170 n of (68)Ga-labeled DOTATOC and Glu-NH-CO-NH-Lys(Ahx)-HBED-CC (PSMA-HBED-CC) intended for clinical st

171 evaluate the detection rate of Glu-NH-CO-NH-Lys-(Ahx)-[(68)Ga(HBED-CC)] ((68)Ga-PSMA ligand; PSMA is

172 Glu-NH-CO-NH-Lys-(Ahx)-[(68)Ga(HBED-CC)] ((68)Ga-PSMA-11) is a PET tr

173 was to evaluate the accuracy of Glu-NH-CO-NH-Lys-(Ahx)-[(68)Ga(HBED-CC)] PET compared with morphologi

174 e metabolically stable peptide sequence NLys-Lys-Pro-Tyr-Tle-Leu suitable for PET imaging.

175 MDP-Lys(L18), norAbuMDP-Lys(B30), norAbuGMDP-Lys(L18), norAbuGMDP-Lys(B30), B30 norAbuMDP, L18 norAbu

176 DP-Lys(B30), norAbuGMDP-Lys(L18), norAbuGMDP-Lys(B30), B30 norAbuMDP, L18 norAbuMDP) are designed and

177 rgdorferi, and lipophilic analogue norAbuMDP-Lys(B30) as adjuvant, are shown to provoke OspA-specific

178 30 norAbuGMDP, norAbuMDP-Lys(L18), norAbuMDP-Lys(B30), norAbuGMDP-Lys(L18), norAbuGMDP-Lys(B30), B30

179 -L18 norAbuGMDP, N-B30 norAbuGMDP, norAbuMDP-Lys(L18), norAbuMDP-Lys(B30), norAbuGMDP-Lys(L18), norAb

180 al to discover unexpected and possibly novel Lys and Arg modifications.

181 s of incubation medium revealed that 2.6% of Lys(541) in HSA was modified when T cells were activated

182 removal of Lys-63 chains and the addition of Lys-48 polyubiquitin.

183 To understand the mechanism for assembly of Lys(48)-linked polyubiquitin degradation signals, we pre

184 e recruitment process through the binding of Lys(63)-linked poly-Ub chains by tandem Ub interacting m

185 ift before and after the covalent bonding of Lys.

186 While characterization of Lys methylation has seen improvements over the past deca

187 fically, LRRK2 promoted the deacetylation of Lys-5 and Lys-12 on histone H4, causing repression of ge

188 viability assay revealed distinct effects of Lys and aLac on IAPP amyloid aggregation, fibril remodel

189 t cortical neurons increased the fraction of Lys-63-linked ubiquitinated GABAB receptors and enhanced

190 nzyme, indicating the critical importance of Lys-300 for optimal NhaA structural stability and functi

191 Accordingly, the interactions of Lys(129) within the S1 pocket are also essential for cor

192 ort on a detailed molecular investigation of Lys-274 autoacetylation of the human MYST protein Males

193 inetics, we found that, although the kcat of Lys(63)-linked ubiquitin chain cleavage was comparable f

194 latforms could bind 335ng/mL and 250ng/mL of Lys for batch and continuous processes, respectively.

195 in the adipose tissue through modulation of Lys(63) ubiquitination events.

196 Inclusion of exon 16 introduces a pair of Lys residues, providing a site for controlled endoproteo

197 phosphorylate Imd, triggering the removal of Lys-63 chains and the addition of Lys-48 polyubiquitin.

198 is and further clarifications of the role of Lys 73 in the acylation mechanism may facilitate the des

199 titration calorimetry supports a key role of Lys-232 in the reaction mechanism.

200 rating the functional and structural role of Lys-300.

201 o ATP, suggesting that acetylation status of Lys-72 may affect ERK1 ATP binding.

202 ate and assess the relative stoichiometry of Lys and Arg modifications (QuARKMod) in complex biologic

203 Biodistribution of [Lys(40)(NODAGA-(68)Ga)NH2]Ex(9-39) showed only 2.2 +/- 0

204 responsive to HDAC6 and that acetylation on Lys-321 (within a KCGS motif) is both essential for acet

205 e demonstrated that METTL12 methylates CS on Lys-395, which is localized in the CS active site.

206 rt that substitution of Gly-4941 with Asp or Lys results in functional channels as indicated by caffe

207 n with either Asp-N, Arg-C, Glu-C, Lys-C, or Lys-N.

208 on of two other basic residues at either P2 (Lys(197)), P6 (Arg(193)), or P8 (Lys(191)) positions.

209 either P2 (Lys(197)), P6 (Arg(193)), or P8 (Lys(191)) positions.

210 lated alpha-peptide/beta-peptoid hybrid Pam-(Lys-betaNspe)6-NH2.

211 gy modeling and suggested that a pro-peptide Lys residue intrudes into the S2 pocket, which is more s

212 tive, selective MOR antagonist, c[-d-Arg-Phe-Lys-Dmt-] (1) ("cyclodal"), with subnanomolar binding af

213 (MOR) agonist [Dmt(1)]DALDA (H-Dmt-d-Arg-Phe-Lys-NH2 (9; Dmt = 2',6'-dimethyltyrosine) resulted in a

214 rearrangements in the ribosome-EF-Tu-GDP-Pi-Lys-tRNA(Lys) complex following GTP hydrolysis by EF-Tu.

215 d with DOTA or NODAGA chelators at positions Lys(27) and Lys(40) and labeled with (68)Ga and (125)I-B

216 on of DOTA and NODAGA chelators at positions Lys(27) and Lys(40) of Ex(9-39)NH2 resulted in a distinc

217 hin the membrane domain (out of 16 potential Lys and Arg sites).

218 ism of action of an unrelated lysis protein, Lys(M), of the Escherichia coli levivirus M (5) .

219 th an intramolecular crosslink to a proximal Lys residue, leading to increased thermal stability.

220 Here, we demonstrate that Imd is rapidly Lys-63-polyubiquitinated at lysine residues 137 and 153

221 lly, the BRCA1-A complex not only recognizes Lys(63)-linked ubiquitin (K63-Ub) adducts at the damaged

222 Ser/Thr kinase (RIPK) activation by removing Lys-63-linked polyubiquitinated chains from key proteins

223 hich is linked to a peptide/peptoid repeat ((Lys-betaNphe)6-NH2).

224 for the monoubiquitination of H2A at residue Lys-119 (uH2AK119) through its association with the PRC1

225 e role and function of the conserved residue Lys 73 in the catalytic mechanism of class A type beta-l

226 A lysine residue (Lys(1112)) at the C-terminal tail of mGluR1 (a member of

227 nalysis revealed also a key role of residues Lys-74/Ile-76 at the N-terminal of FGF14 in the FGF14.Na

228 n, we describe a method that uses restricted Lys-C enzymatic digestion to increase the average mass o

229 Biochemical and kinetic analysis revealed Lys(147) to be an intramolecular processing site at whic

230 A conserved lysine residue in RGS1 (Lys(259) ) is directly involved in RGS1-PA binding.

231 otent FPR2-selective antagonists (i.e., RhB-(Lys-betaNphe)n-NH2; n = 4-6) are expected to become valu

232 alpha137-141 fragment of hemoglobin (Thr-Ser-Lys-Tyr-Arg), a small (653Da) and hydrophilic antimicrob

233 hat changed the conserved modification site (Lys 32) and abolished post-translational modification.

234 e also identified a region of RBM25 spanning Lys-77 that binds with high affinity to serine- and argi

235 owever in all of our acyl-enzyme structures, Lys 73 is present in two different conformations, in whi

236 In our ligand free structures, Lys 73 is present in a single conformation, however in a

237 Substituting Lys with Arg (or vice versa) in the naturally-occurring

238 We show that although the C'-terminal Lys residue of Wnt3a is critical for its activity and is

239 The finding that Lys(M) inhibits a distinct step in the PG synthesis path

240 We also found that Lys-714 was located within a leucine-rich stretch, which

241 These findings indicate that Lys-63-linked ubiquitination of GABAB1 at multiple sites

242 -like membrane interactions, indicating that Lys-5 in the context of Src-S3C/S6C interferes with its

243 Our results revealed that Lys-776, located in the P-loop of PI3Kalpha, is essentia

244 Here we show that Lys(66) is not required for cellular activity, yet domin

245 We show that Lys(M) inhibits the translocation of the final lipid-lin

246 Our data suggest that Lys(63)-linked polyubiquitination is involved in the lig

247 The Lys mutations reduced, but did not completely abrogate,

248 the absence of a protonatable residue at the Lys-300 position.

249 Modification at the Lys-93 position may alter substrate specificity of lipid

250 t cation-heterocycle interaction between the Lys-155 side chain of the double substitution, R155K/D16

251 eed, we define the acetylation status of the Lys 80 residue located in the DNA-binding domain of HSF1

252 uced the remaining agonistic activity of the Lys mutants.

253 Substitution of the Lys residues to Glu markedly reduced integrin binding of

254 Changes of amino acid sequences outside the Lys(87)-Leu(122) central portion of the molecule either

255 nding of E128K IL-1beta, suggesting that the Lys residues mediate integrin binding.

256 nges induced by weak integrin binding to the Lys mutants.

257 m the addition of two DOPAL molecules to the Lys sidechain amine through their aldehyde moieties and

258 e regulation of the cyclase localizes to the Lys(87)-Leu(122) region.

259 lisation (Gly, Pro, Hyp and Hyl), whilst the Lys content was greater for the WP group, indicating a m

260 mutagenesis demonstrated that two of these, Lys-565 and Lys-663, coordinate ATP in the active site.

261 3A-APC (Lys191-193Ala) mutant in which three Lys residues (KKK191-193) were replaced with alanine, an

262 al manner and are linked exclusively through Lys-63 of Ub.

263 ion site in the ERK1 N terminus, adjacent to Lys-71, which binds to ATP, suggesting that acetylation

264 ntified a 5-aminopentanol moiety attached to Lys(32) of B. subtilis EF-P that is required for swarmin

265 he beta-strand, possibly through contacts to Lys(18) Thus GAGs significantly modulate sCT fibrillatio

266 y was partially compromised, a single Gln to Lys substitution (2) restored activity equivalent to Tyr

267 bidopsis (Arabidopsis thaliana) pex12 Glu-to-Lys missense allele that conferred severe peroxisomal de

268 he unfolding of LPL; and (2) that its Glu-to-Lys substitution destabilizes its N-terminal alpha-helix

269 far exhibit chemoselective reactivity toward Lys and, particularly, Tyr side chains, and can be used

270 d an expansive interface where trimethylated Lys bound to an unusually extensive aromatic cage in one

271 ked reads originating from AAA-decoding tRNA(Lys)(UUU) were 10-fold enriched over its cellular abunda

272 ation is slower with the s(2)-deficient tRNA(Lys).

273 Elevated tRNA(Lys)UUU levels suppressed the elp3Delta phenotypes and s

274 ements in the ribosome-EF-Tu-GDP-Pi-Lys-tRNA(Lys) complex following GTP hydrolysis by EF-Tu.

275 SC), restricting the pool of free LysRS-tRNA(Lys) Mounting evidence suggests that LysRS is released u

276 c analysis we show that mcm(5)-modified tRNA(Lys) lacking the s(2) group has a lower affinity of bind

277 iently rejected than the fully modified tRNA(Lys).

278 caused by the m.8344A>G mutation in mt-tRNA(Lys), aminoacylated by a Class II aaRS.

279 d mutant human mt-tRNA(Leu(UUR)) and mt-tRNA(Lys), and stabilize mutant mt-tRNA(Leu(UUR)).

280 e mcm(5) or s(2) modification at U34 of tRNA(Lys), tRNA(Glu), and tRNA(Gln) causes ribosome pausing a

281 lta phenotypes, indicating that lack of tRNA(Lys)UUU modifications were responsible.

282 show how the s(2) modification in yeast tRNA(Lys) affects mRNA decoding and tRNA-mRNA translocation.

283 II (UII, 1, H-Glu-Thr-Pro-Asp-c[Cys-Phe-Trp-Lys-Tyr-Cys]-Val-OH) fragment 4-11 were synthesized to e

284 8) residues in the biologically relevant Trp-Lys-Tyr triad.

285 steps were omitted by implementing a trypsin/Lys-C enzyme-immobilized multichannel reactor (MCR) cons

286 ed to bind the minimal FLAG peptide (Asp-Tyr-Lys-Asp) were grafted onto a single-chain variable fragm

287 d (HBED-CC)-based PET tracer (68)Ga-Glu-urea-Lys(Ahx)-HBED-CC ((68)Ga-PSMA-11) to allow accurate intr

288 eting fluorescent dye conjugates of Glu-urea-Lys-HBED-CC was synthesized, and their biologic properti

289 ecific tumor uptake, whereas (68)Ga-Glu-urea-Lys-HBED-CC-AlexaFluor488 (9.12 +/- 5.47 %ID/g) revealed

290 linically relevant candidate (68)Ga-Glu-urea-Lys-HBED-CC-IRDye800CW reinforced a fast, specific enric

291 ng even identical modifications of tRNA(UUU)(Lys) and tRNA(QUA)(Tyr) has the opposite effect of decre

292 surface loop that interacts with Rubisco via Lys-216.

293 al protein in exon definition, but only when Lys-77 is unmethylated.

294 ated RIPK3, which was partially reduced when Lys-264 was mutated.

295 onsistent with a chemical mechanism in which Lys-232 activates a water molecule for catalysis.

296 to direct binding onto the NP surface, while Lys needs to overcome a ~2 kT free energy barrier.

297 DNA readily form Schiff-base conjugates with Lys side chains of nuclear proteins in vitro and in vivo

298 egatively charged headgroup interaction with Lys-436 for transport.

299 Interfering with Lys-63-linked ubiquitination by overexpressing ubiquitin

300 Gly-4941 replacement with Lys resulted in channels having reduced K(+) conductance