ライフサイエンスコーパス: Lys

1 Lys (K) 63-linked ubiquitination modulated by Ube2v1 exp

2 Lys(234) is one of the residues present in class A beta-

3 Lys-149 is conserved in a narrow part of branch B, and T

4 Lys-27-Met mutations in histone 3 genes (H3K27M) charact

5 Lys-SDE2Ct constitutes a short-lived physiological subst

6 We show that UBA(Cez) binds Lys(11)-, Lys(48)-, Lys(63)-, and Met(1)-linked ubiquitin chains i

7 LC-MS/MS analysis revealed that Lys-12, Lys-23, Lys-96, and Lys-226 in apoA-I are modified by ON

8 e to simple mixtures of lysate and CpG-1826 (Lys-Mix) in both Py230 and Py8119 orthotopic syngeneic m

9 MS/MS analysis revealed that Lys-12, Lys-23, Lys-96, and Lys-226 in apoA-I are modified by ONE ketoam

10 Mutations in Ser-23, Lys-148, and Arg-321 uncoupled adenosine triphosphatase

11 Histone 3 Lys 27 trimethylation (H3K27me3)-mediated epigenetic sil

12 we examined the role of the murine histone 3 Lys-27 (H3K27) methyltransferases EZH1 (enhancer of zest

13 eased occupancy of ETS1, p300, and histone 3 Lys-27 acetylation (H3K27Ac) at the BCL-xL promoter.

14 tivation through the action of the histone 3 Lys-4 and Lys-36 methyltransferase PRDM9 to ensure succe

15 MA residues 25 and 26 or residues 29 and 31: Lys->Arg (KR) (25/26KR and 29/31KR) and Lys->Thr (KT) (2

16 The AREL1 HECT domain assembled Lys(33)-, Lys(48)-, and Lys(63)-linked polyubiquitin chains.

17 ses the conformational flexibility of Arg-4, Lys-5 and Gln-6 of BCL11B.

18 show that UBA(Cez) binds Lys(11)-, Lys(48)-, Lys(63)-, and Met(1)-linked ubiquitin chains in vitro, e

19 -118 and Lys-129), helicase domain (Lys-525, Lys-639, and Lys-725), and C terminus (Lys-800).

20 Included in this binding site are Ile-92, Lys-97, and Glu-99, which are entirely or mostly specifi

21 anslation elongation factor EF-Tu carrying a Lys-5 trimethylation, incorporated by the methyltransfer

22 ignal recognition particle pathway through a Lys-rich C-terminal domain.

23 ectly juxtapose an aryl-fluorosulfate with a Lys residue that is located within the binding pocket of

24 some stalling occurs at in-frame cognate AAA Lys codons.

25 hesized proteins away from those rich in AAA Lys codons toward those harboring few or no AAA codons.

26 des containing the proteinaceous amino acids Lys, Arg, or His adjacent to backbone ester bonds genera

27 consecutive positively charged amino acids (Lys/Arg).

28 The additional Lys residue was introduced by substituting residue locat

29 quasi-DET, engineered AvLOx with additional Lys residue was designed.

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

31 ves after Arg, whereas trypsin cleaves after Lys/Arg.

32 and ubiquitin-modification sites by MS after Lys-C digestion and K-epsilonGG-peptide enrichment.

33 er protease, calpain, which cleaves Rb after Lys 810.

34 a a peptide bond between residues Ile(1) and Lys(32).

35 ol complex identified Phe(59), Tyr(101), and Lys(134) as contacting the 4-hydroxyphenyl moiety of the

36 yet at the same time to include Ser-112 and Lys-119, homologous to TGF-beta2 Ile-92 and Lys-97, on t

37 eplacing two of these residues, Lys-1155 and Lys-1230, in the GAP-related domain of IQGAP1 (termed IQ

38 in's sequence on the N terminus (Lys-118 and Lys-129), helicase domain (Lys-525, Lys-639, and Lys-725

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

40 Surprisingly, we found that His-152 and Lys-187 alanine-substituted variants maintain a similar

41 tical tRNA-interacting residues, His-152 and Lys-187, in the context of human Thg1 (hThg1).

42 ted that double-CEL glycations at Lys-16 and Lys-28 of Abeta1-42 had the most profound impact on the

43 Substitutions of Lys-20 and Lys-31 to Ala in the FABP1 helical cap affected neither

44 31: Lys->Arg (KR) (25/26KR and 29/31KR) and Lys->Thr (KT) (25/26KT and 29/31KT).

45 Interestingly, Lys(326) and Lys(328) are among the documented acetylated residues.

46 mptively target highly reactive Lys(326) and Lys(328), also resulted in less inhibited F-actin-Tpm, i

47 residues on actin, particularly Lys(326) and Lys(328), are predicted to form critical electrostatic i

48 hrough the action of the histone 3 Lys-4 and Lys-36 methyltransferase PRDM9 to ensure successful doub

49 3D-homology model predicted that Glu-47 and Lys-50 are facing the central cavity of the protein.

50 single or double substitutions of Glu-47 and Lys-50 do not restore GlcNAc glycoconjugates.

51 ptake; and (iii) substitutions of Glu-47 and Lys-50 dramatically alter kinetic parameters, consistent

52 ECT domain assembled Lys(33)-, Lys(48)-, and Lys(63)-linked polyubiquitin chains.

53 gstrom resolution, revealing the Lys(62) and Lys(191) locations.

54 ubiquitinated SMAC, primarily on Lys(62) and Lys(191) We solved the crystal structure of the tetramer

55 129), helicase domain (Lys-525, Lys-639, and Lys-725), and C terminus (Lys-800).

56 ast, Ala substitution of Lys-57, Glu-77, and Lys-96, located in the loops adjacent to the ligand-bind

57 portal region, including Lys-57, Glu-77, and Lys-96.

58 g SMAD family member 3 (SMAD3) and Lys-9 and Lys-56 in histone 3.

59 Lys-119, homologous to TGF-beta2 Ile-92 and Lys-97, on the inside of the fingers.

60 covalent linkage of ubiquitin to Lys(92) and Lys(94) of UBE2N via Gln(40).

61 is revealed that Lys-12, Lys-23, Lys-96, and Lys-226 in apoA-I are modified by ONE ketoamide adducts.

62 and O side chains of His, Cys, Glu, Asp, and Lys residues.

63 -16 (Abeta-CEL16), Lys-28 (Abeta-CEL28), and Lys-16 and -28 (Abeta-CEL16&28).

64 complex topological relationship of DOPA and Lys as well as the interfacial adhesive roles of other a

65 due to cross-linking between Asn or Gln and Lys side chains.

66 the ion-selectivity filter, whereas Glu and Lys are in positions to accept and release Na(+) ions vi

67 However, the betaA-betaB loop Asn-55-His and Lys-57-Ser substitutions in the pS3-subunit improved car

68 Arg, Ornithine and Lys were identified as substrates.

69 cluding the degree of polyubiquitination and Lys-48 versus Lys-63 linkages.

70 ng the BMAL1-TAD, parts of the G-region, and Lys(537) Tethering the small compound 1-10 in the MLL-bi

71 acetylating SMAD family member 3 (SMAD3) and Lys-9 and Lys-56 in histone 3.

72 ng the negative charge of the substrate, and Lys(143) acts as both the catalytic base and the catalyt

73 on modifies binding of RHBDL4 to p97/VCP and Lys(63)-linked ubiquitinated proteins.

74 s are rich in charged residues (such as Arg, Lys, and Glu) with potential ion pairs across adjacent t

75 ectroscopy, of substituting key charged Arg, Lys, Glu, and Asp residues by Gly or His.

76 nsisting of a high percentage (>75%) of Arg, Lys, and Glu residues, are exceptions to this rule but h

77 H) domains contain a high percentage of Arg, Lys, and Glu residues.

78 Mutation of Shank3 residues (949)Arg-Arg-Lys(951) to three alanines disrupts CaMKII binding in vi

79 etween the suramin sulfonated groups and Arg/Lys residues play critical roles in the binding of suram

80 ubiquitination of Tat by both WT as well as Lys-48-ubiquitin, which has only a single lysine residue

81 The peptides were rich in Glu, Asp, Lys, Gly and Leu, and also exhibited diverse bioactiviti

82 The AREL1 HECT domain assembled Lys(33)-, Lys(48)-, and Lys(63)-linked polyubiquitin cha

83 sphorylation-dependent, chromatin-associated Lys-SDE2Ct degradation upon UVC damage.

84 ng defined CEL modifications on Abeta1-42 at Lys-16 (Abeta-CEL16), Lys-28 (Abeta-CEL28), and Lys-16 a

85 e demonstrated that double-CEL glycations at Lys-16 and Lys-28 of Abeta1-42 had the most profound imp

86 fibril formation, whereas CEL glycations at Lys-16 of Abeta1-42 delayed fibril formation.

87 Single-CEL glycations at Lys-28 of Abeta1-42 had the least impact on fibril forma

88 rimethylates heat shock protein 8 (Hspa8) at Lys-561 to enhance its stability.

89 , we confirmed that a Schiff base linkage at Lys-255 is critical for substrate binding and isomerizat

90 f FAM173A is required for ANT methylation at Lys-52 to occur.

91 ought KMT responsible for ANT methylation at Lys-52, and point out the functional significance of Lys

92 the attachment of polyubiquitin moieties at Lys-132 in p53.

93 We found that methylation occurs at Lys-52 of ANT, which was previously reported to be trime

94 acetylated by the acetyltransferase p300 at Lys-566 and deacetylated by sirtuin1 (SIRT1).

95 ts E3-ligase-dependent polyubiquitination at Lys 3584 (referred to as Ub-DMD) and its subsequent prot

96 We show that UBA(Cez) binds Lys(11)-, Lys(48)-, Lys(63)-, and Met(1)-linked ubiquiti

97 SPT, and a negative control were digested by Lys-C and followed by HILIC-MS analysis.

98 er Lys residues, implying that the catalytic Lys may act as a proton donor in catalysis.

99 pocket forming a salt bridge with catalytic Lys, which can be tested in selective inhibitor design.

100 They catalyze Lys ubiquitination of themselves and other proteins and

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

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

103 ations on Abeta1-42 at Lys-16 (Abeta-CEL16), Lys-28 (Abeta-CEL28), and Lys-16 and -28 (Abeta-CEL16&28

104 3 and in rat CD147 by the positively charged Lys-73.

105 nal function in the clearance of circulating Lys-type peptidoglycan, revealing a mechanism that keeps

106 , is sufficiently small to allow conglutinin Lys-343 access to the bound ligand, whereas Asp-320 lies

107 Replacement of a conserved Lys residue with Ala abolished the in vitro RNA-binding

108 one of the transported H(+) to the conserved Lys-300 residue, a salt bridge partner of Asp-163.

109 parison of adhesion of dipeptides containing Lys and either DOPA (KY) or phenylalanine (KF) shows tha

110 e that preferentially hydrolyzes crosslinked Lys-type peptidoglycan fragments.

111 is with a naturally-occurring contracted Cys-Lys-Cys-His (CKCH) heme-binding motif, which is encoded

112 Distinct l- and d-Lys adsorption behaviours on the H-ZSM-5 framework have

113 for the enantiomeric difference in l- and d-Lys adsorption.

114 pite demonstrating the approach for l- and d-Lys over MFI zeolites at an atomistic resolution, the di

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

116 Mozamide A contains l-Val, d-Lys, and l-Ile (instead of d-Val, l-Lys, and l-allo-Ile)

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

118 y a heteromeric receptor complex of distinct Lys motif (LysM)-type transmembrane receptors named NOD

119 inus (Lys-118 and Lys-129), helicase domain (Lys-525, Lys-639, and Lys-725), and C terminus (Lys-800)

120 ciated with AD patients and occurs at either Lys-16 or Lys-28 of Abeta1-42.

121 lyzing formation of a gamma-glutamyl-epsilon-Lys (Gln40(Ub)-Lys92(Ube2N)) isopeptide crosslink using

122 s suggest that actin acetylation, especially Lys(328), modulates muscle contraction via disrupting in

123 d by increased nuclear gammaH2AX expression, Lys(382)-p53 acetylation, and genomic instability.

124 sition the N-terminal sequence to facilitate Lys-5 modification.

125 Fmoc-Lys(Fmoc)-Asp exhibits the lowest CGC and highest mechan

126 ein, a minimalistic, de novo dipeptide, Fmoc-Lys(Fmoc)-Asp, as an hydrogelator with the lowest CGC ev

127 Conductive composite gels composed of Fmoc-Lys(Fmoc)-Asp and a conductive polymer exhibit excellent

128 1, CDE-096, confirming an important role for Lys-207 in the interaction of PAI-1 with LRP1 and of the

129 the predisposition of patients carrying FXII-Lys/Arg309 to angioedema after trauma, and reveal a regu

130 ine substitutions for Thr(309) in FXII (FXII-Lys/Arg309).

131 In mice given human FXII-Lys/Arg309, induction of thrombin generation by infusion

132 Here, we show that FXII-Lys/Arg309 is susceptible to cleavage after residue 309

133 ge after its ubiquitin-like domain generates Lys-SDE2Ct, the C-terminal SDE2 fragment bearing an N-te

134 enesis of His583 to Ala, Asp, Asn, Glu, Gln, Lys, Phe, Tyr, and Trp showed that although both the Cu(

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

136 vealed associations with features such as H3 Lys-27 methylated histones (H3K27me3) and accessible DNA

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

138 COMPASS protein family catalyzes histone H3 Lys 4 (H3K4) methylation and its members are essential f

139 ociating with SET1 (COMPASS) is a histone H3 Lys-4 methyltransferase that typically marks the promote

140 toplasmic and nuclear mono-methylation of H3 Lys 9 (H3K9) at the expense of broad losses in histone d

141 His, Lys, Arg, or Pro residues prohibit cleavage when found a

142 C in addition to other residues such as His, Lys, and Cys, providing very good structural resolution.

143 Heme 2 reduction triggers a switch from His/Lys ligation (E(m) , -129 mV) to His/Met (E(m) , +266 mV

144 e rates of interconversion are such that His/Lys ligation would be retained during turnover.

145 our low-spin hexa-coordinated hemes with His/Lys (heme 1), His/Cys (heme 2), and two His/His ligation

146 Histone Lys demethylase KDM3C demonstrates anti-inflammatory eff

147 Histone Lys-specific demethylases (KDMs) play a key role in many

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

149 His-165-apoA-I Lys-93, apoA-I His-154-apoA-I Lys-105, apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys

150 cross-link adducts of apoA-I His-165-apoA-I Lys-93, apoA-I His-154-apoA-I Lys-105, apoA-I His-154-ap

151 apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys-30-apoE His-227.

152 on, and thus removal of a positive charge in Lys, abrogates binding of cyt c to negatively charged CL

153 that the N-terminal BMAL1 G-region including Lys(537) forms elongated extensions emerging from the bu

154 he loops around the portal region, including Lys-57, Glu-77, and Lys-96.

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

156 ts: the complex formation with the inhibitor Lys(32) in the trypsin S1 pocket, the inhibitor C-termin

157 Interestingly, Lys(326) and Lys(328) are among the documented acetylate

158 te and its polyubiquitylation at an internal Lys residue without substrate's dissociation into the bu

159 ng selected Ca(2+)-ligands or by introducing Lys residues in the membrane-binding loops had variable,

160 s gingivalis is a keystone pathogen, and its Lys-gingipain (Kgp) virulence factor is involved in the

161 s-154-apoA-I Lys-105, apoA-I His-154-apoA-IV Lys-149, and apoA-II Lys-30-apoE His-227.

162 aquinone derivatives with the N(alpha)Fmoc-l-Lys and ethynyl group were synthesized from the isolated

163 with both the ethynyl and the N(alpha)Fmoc-l-Lys groups showed an antioxidant activity-enhancing effe

164 Aloe-emodin derivative with N(alpha)Fmoc-l-Lys shows the highest inhibition values by 94.11 +/- 0.1

165 l-Val, d-Lys, and l-Ile (instead of d-Val, l-Lys, and l-allo-Ile) and is a hydroxylated brunsvicamide

166 y CPT1C as a new regulator of anterograde LE/Lys transport in response to malonyl-CoA changes, and gi

167 bition of malonyl-CoA synthesis decreases LE/Lys abundance at the axon terminal, and shortens axon le

168 C (CPT1C) senses malonyl-CoA and enhances LE/Lys anterograde transport by interacting with the endopl

169 transport of late endosomes or lysosomes (LE/Lys) is crucial for proper axon growth.

170 e transfer of Kinesin-1 from protrudin to LE/Lys.

171 e identified a single conserved surface Lys (Lys-127) residue as well as active-site interactions of

172 n-like modifier (SUMO) proteins to a lysine (Lys) residue on target proteins, enhances EZH2 transcrip

173 of histidine (His), arginine (Arg), lysine (Lys), aspartate (Asp), glutamate (Glu) and cysteine (Cys

174 stereospecific bindings of l- and d-lysine (Lys) in achiral MFI zeolites.

175 y, adhesive synergy between flanking lysine (Lys, K) and 3,4-Dihydroxyphenylalanine (DOPA, Y) residue

176 in digestion, with arginine (Arg) or lysine (Lys) at the C-terminus, can be analyzed using the HECD m

177 cationic proteinaceous amino acids (lysine, Lys; arginine, Arg; and histidine, His), along with nonp

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

179 The BMAL1(K537Q) mutation mimicking Lys(537) acetylation, however, did not affect the KIX-bi

180 Moreover, Lys-149 in the -4 subsite interacted with the galactosyl

181 The resulting nanostructures (Lys-SNAs) enhance the codelivery of adjuvant and antigen

182 age, 64.2 y old) who underwent Glu-NH-CO-NH-Lys-(Ahx)-[(68)Ga(HBED-CC)] ((68)Ga-PSMA11) PET/MRI for

183 s to identify the compound [(68)Ga]Ga-NODAGA-Lys(Cy5**)-AEEAc-[Me-Arg(8),Tle(12)]-NT(7-13) as the one

184 Circadian acetylation of Lys(537) within the G-region enhances repressive BMAL1-T

185 Herein, we study adhesion of Lys and DOPA-containing peptides to organic and inorgani

186 His), along with nonproteinaceous analogs of Lys harboring fewer methylene groups in their side chain

187 binding site, with the charged side chain of Lys-203 replacing the second bound ion.

188 Pyruvate interacts with the side chain of Lys-43 and with the peptide backbone of Ser-328 and Gly-

189 Size-exclusion chromatography of Lys-C-digested native DMBT1 showed that only high-Mw fra

190 ins a patch of positive charge consisting of Lys-5 and Arg-17.

191 one (TPQ) capable of inducing deamination of Lys e-amino groups and formation of the carbonylated pro

192 inimally perturbed, however, the dynamics of Lys and Thr residues, located primarily in the imperfect

193 the cellular and physiological functions of Lys-63 (K63)-linked ubiquitin chains, although they are

194 aenorhabditis elegans Interestingly, lack of Lys-43 methylation caused aberrant incorporation of ATPS

195 found that METTL21C catalyzes methylation of Lys-943 of AARS1 (AARS1-K943me) both in vitro and in viv

196 ere, we introduced single point mutations of Lys-428 in the CTE of Rca-alpha from wheat (Triticum aes

197 f PAI-1 with LRP1 and of the orientations of Lys-207, -88, and -80 for the interaction of uPA:PAI-1 c

198 uggest a chemical basis for the selection of Lys, Arg, and His over other cationic amino acids for in

199 We have recently reported a series of Lys-covalent agents targeting the BIR3 domain of the X-l

200 and point out the functional significance of Lys-52 methylation in ANT.

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

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

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

204 Substitution of Lys-428 with Arg dramatically altered ADP inhibition, in

205 In contrast, Ala substitution of Lys-57, Glu-77, and Lys-96, located in the loops adjacen

206 Substitutions of Lys-20 and Lys-31 to Ala in the FABP1 helical cap affect

207 ngineering, we report that trimethylation of Lys-27 at histone H3 (H3K27me3), a marker of heterochrom

208 mammalian cells abrogated trimethylation of Lys-43 in ATP synthase c-subunit (ATPSc), a modification

209 catalyzes the demethylation of histone H3 on Lys 4 (H3K4), which results in the repression of gene ex

210 degron-mediated polyubiquitylation of p53 on Lys-132 had functional consequences, with cells in which

211 AREL1 ubiquitinated SMAC, primarily on Lys(62) and Lys(191) We solved the crystal structure of

212 h AD patients and occurs at either Lys-16 or Lys-28 of Abeta1-42.

213 of Glu-83 in subunit g (gGlu-83) with Ala or Lys destabilized the digitonin-extracted F-ATP synthase,

214 Cationic Arg or Lys side chains lining the S4 helix move through this "g

215 the conserved residues Gln(758) (Q motif) or Lys(785) (I motif) of both motifs, all variants still bo

216 doxin, Met-SO formation, phosphorylation, or Lys acetylation, but we currently only understand the fu

217 Both in human cells and in rat organs, Lys-52 was exclusively trimethylated, indicating that th

218 an abnormally lower pKa compared with other Lys residues, implying that the catalytic Lys may act as

219 vely charged residues on actin, particularly Lys(326) and Lys(328), are predicted to form critical el

220 lly, a minimalistic self-assembling peptide, Lys-Tyr-Tyr (KYY) with strong propensity to form supramo

221 mposed of Val, Pro, Tyr, Met, Leu, Trp, Phe, Lys and Glu.

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

223 ion, to presumptively target highly reactive Lys(326) and Lys(328), also resulted in less inhibited F

224 thened its noncatalytic activity in reducing Lys-63 polyubiquitylation of its target protein TRAF3 (T

225 Viperin is also implicated in regulating Lys-63-linked polyubiquitination of interleukin-1 recept

226 ted agents that targeted a relatively remote Lys residue with respect to the target's binding site, t

227 To that end, we replaced Lys-300 with Gln, either alone or together with the simu

228 ing an acetylation-mimic mutation at residue Lys-280 (K280Q), we evaluated whether this substitution

229 Finally, we determined ATG3 residue Lys-243 as an LC3B modification site.

230 substitution of the SNO-CoA-binding residue Lys-127 minimally affected the GSNO-reducing activity of

231 o1 uses an evolutionarily conserved residue, Lys(185) This residue interacted with the phosphate grou

232 that substitution of the equivalent residue, Lys-305, of a related Na(+)/H(+) antiporter, NapA from T

233 sitively charged patches comprising residues Lys-32 to Lys-58.

234 ons of the conserved catalytic site residues Lys-249, Arg-270, and His-271 resulted in activity loss.

235 We also noted that residues Lys-101, Trp-103, and Glu-184 are crucial for proteolyti

236 en MGO and nucleophilic amino acid residues (Lys, Arg and Cys) and naringenin in milk.

237 93 cells, we identified six lysine residues (Lys-556, -1155, -1230, -1465, -1475, and -1528) as ubiqu

238 found that replacing two of these residues, Lys-1155 and Lys-1230, in the GAP-related domain of IQGA

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

240 s of a beta-arrestin binding domain (Ala-Ser-Lys) within the intracellular C terminus of 5-HT(2A)R se

241 LR2 signaling was induced with Pam(3)Cys-Ser-Lys(4), and the role of ERK signaling was interrogated p

242 Most substrates contain a C-terminal Ser-Lys-Leu (SKL) sequence that is recognized by the recepto

243 lpha/epsilon-amino group of one of the seven Lys residues of lycosin-I, generating eight different li

244 ubiquitin in proximity to the acceptor site Lys-48.

245 ation K24G, which alters the activation site Lys in T7 trypsinogen, abolished autoactivation while ac

246 e Asp residues preceding the activation site Lys revealed that mutation D22A accelerated CTSB-mediate

247 es, we identified a single conserved surface Lys (Lys-127) residue as well as active-site interaction

248 ariant in which we replaced seven C-terminal Lys and Arg residues with Ala and added a Cys residue at

249 at the epsilon-NH(2) group of the C-terminal Lys with isotopically labeled acetyl-alanine; (3) thiol

250 KDEL receptor, which recognises a C-terminal Lys-Asp-Glu-Leu (KDEL) sequence.

251 dependent recognition of a carboxyl-terminal Lys-Asp-Glu-Leu (KDEL) signal by the KDEL receptor.

252 terminal SDE2 fragment bearing an N-terminal Lys residue.

253 -525, Lys-639, and Lys-725), and C terminus (Lys-800).

254 ut the protein's sequence on the N terminus (Lys-118 and Lys-129), helicase domain (Lys-525, Lys-639,

255 through distinct C-terminal motifs and that Lys-13 in Sestrin-2 is a putative ubiquitin acceptor sit

256 ctably cleave lignostilbene, indicating that Lys(134) plays a key catalytic role.

257 LC-MS/MS analysis revealed that Lys-12, Lys-23, Lys-96, and Lys-226 in apoA-I are modifi

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

259 ing its N-terminal peptide (encompassing the Lys-5 target site), we generated an EftM homology model

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

261 ovalent complex triggered by cleavage of the Lys(368)-Thr(369) (P2-P1) reactive site bond with a stoi

262 AC to 2.8 angstrom resolution, revealing the Lys(62) and Lys(191) locations.

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

264 These results suggest that the Lys-428 residue is involved in interacting with the gamm

265 his work, we sought to establish whether the Lys-300 residue and its partner Asp-163 are essential fo

266 harged patches comprising residues Lys-32 to Lys-58.

267 positive charge at the interface (Glu(32) to Lys) also lowered the affinity.

268 ha-helical structure extending from Glu-6 to Lys-63.

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

270 ussed as potential prebiotic alternatives to Lys, are ornithine, 2,4-diaminobutyric acid, and 2,3-dia

271 acid substitution on Glu324, or on Asn408 to Lys to increase the positive charge at the rim of the in

272 t catalyses covalent linkage of ubiquitin to Lys(92) and Lys(94) of UBE2N via Gln(40).

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

274 somal dominant PD) through homologous Glu-to-Lys substitutions in alphaSyn's N-terminal region (i.e.

275 Our results showed that the Thr-to-Lys mutation of residue 367 in E protein (E367) plays a

276 Here, we found that the Thr-to-Lys substitution at E367 is a crucial determinant of TMU

277 trongly stimulated OTUB1 DUB activity toward Lys-48-linked diubiquitin.

278 ly enhanced its isopeptidase activity toward Lys-48-linked ubiquitin moieties but also strengthened i

279 ase (Arg-482) and HIV reverse transcriptase (Lys-65) were previously observed to inhibit dNDP incorpo

280 tRNAs, including tRNA(Glu), tRNA(Gly), tRNA(Lys), tRNA(Val), tRNA(His), tRNA(Asp), and tRNA(SeC) to

281 atalyzes methylthiolation of t(6)A37 in tRNA(Lys)(UUU) to ms(2)t(6)A37.

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

283 sRS) is essential for aminoacylation of tRNA(Lys) Higher eukaryotic LysRSs possess an N-terminal exte

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

285 st that gallium 68 ((68)Ga)-labeled Glu-urea-Lys (Ahx)-HBED-CC ligand targeting the prostate-specific

286 ombined gallium 68 ((68)Ga)-labeled Glu-urea-Lys (Ahx)-HBED-CC ligand targeting the prostate-specific

287 the pharmacologic inhibitor Decanoyl-Arg-Val-Lys-Arg-chloromethylketone repressed PD-1 and exhausted

288 her validate aryl-fluorosulfates as valuable Lys-targeting electrophiles, for the design of inhibitor

289 gree of polyubiquitination and Lys-48 versus Lys-63 linkages.

290 The polyubiquitylation of p53 occurred via Lys-48 linkage and involved phosphorylation on p53 at Se

291 ement by covalently tethering rhodopsins via Lys residue side chains.

292 ow that for CTX-M-14 beta-lactamase, whereas Lys(234) is required for hydrolysis of cephalosporins su

293 Substitution of Ser-6 with Lys, but not with Asp, enhanced the ability of Pep8 to i

294 ution of eArg-8 with Glu and of gGlu-83 with Lys rescued digitonin-stable F-ATP synthase dimers.

295 ement of eArg-8 with Glu and of gGlu-83 with Lys restored high-conductance channels indistinguishable

296 es to effectively form covalent adducts with Lys, Tyr, and His residues, given that these agents were

297 es as warheads to form covalent adducts with Lys, Tyr, and His residues.

298 e tumor microenvironment, when compared with Lys-SNAs and simple mixtures of oxidized lysates with Cp

299 the N-acetyl group oxygen and nitrogen with Lys-343 and Asp-320, respectively.

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