ライフサイエンスコーパス: covalent modification

1 y via small molecule allosteric effectors or covalent modification.

2 e enhanced by kinase activation or oxidative covalent modification.

3 loss, which is a characteristic signature of covalent modification.

4 immobilized to the graphene surface via non-covalent modification.

5 vidence that His-50 is the main site of this covalent modification.

6 r positive allosteric modulator activity via covalent modification.

7 notion that the electrophile, DMF, acts via covalent modification.

8 from screening campaigns modulate GLP-1R by covalent modification.

9 rted interference of different unanticipated covalent modifications.

10 y the molecular mechanism underlying ordered covalent modifications.

11 equently regulated through posttranslational covalent modifications.

12 ure GFP containing the desired site-specific covalent modifications.

13 primarily by recognizing sequence motifs or covalent modifications.

14 Upon this ROS-dependent, reversible, covalent modification, a marked decrease in its catalyti

15 omponents, structure, chromatin folding, and covalent modifications across the human cell cycle.

16 genomic enhancers and promoters, but also by covalent modifications added to both chromatin and RNAs.

17 By contrast, the various covalent modifications added to RNAs, termed epitranscri

18 Covalent modification adding acetyl groups to the C term

19 made in recent years to understand how these covalent modifications affect cell identity and function

20 duction is predominantly involved in protein covalent modification after exposure in vivo to styrene

21 e indeed substrates for CaMKII and that this covalent modification alters the expression of cell surf

22 nyl diazirine and alkyne moieties that allow covalent modification and enrichment of kinases, respect

23 The accumulation of 2AA leads to covalent modification and inactivation of several enzyme

24 species, deregulation of Ca(2+) homeostasis, covalent modification and oxidation of proteins, lipid p

25 epoxide and aziridines and demonstrate their covalent modification and time-dependent inhibition of G

26 Histone covalent modifications and 26S proteasome-mediated prote

27 nce silencing) through modulation of histone covalent modifications and association of silencing fact

28 Chromatin proteins undergo covalent modifications and form complexes that encode a

29 failed to protect inactivation of GAPDH, its covalent modification, and translocation to the nucleus.

30 inal microvascular cells is inhibited by its covalent modifications, and this activates multiple path

31 Allostery and covalent modification are major means of fast-acting met

32 Combinations of histones carrying different covalent modifications are a major component of epigenet

33 Hydrogen-bonding promoted covalent modifications are finding useful applications i

34 ins and has the advantage that the resulting covalent modifications are irreversible, thus permitting

35 While a number of covalent modifications are known to occur on histone tai

36 These stable, heritable, covalent modifications are largely associated with the r

37 losteric regulation, product inhibition, and covalent modification as well as alterations in gene tra

38 nisms of bacteria, while phages have evolved covalent modifications as a counterdefense mechanism to

39 he first report that identifies H2O2-induced covalent modifications as an essential component for the

40 A, CaMKII) and postsynaptic (Ca(2+), CaMKII) covalent modifications, as well as both presynaptic and

41 ted photocatalytic process that introduces a covalent modification at a C(sp(3))-H bond in the methyl

42 ed tryptic peptides have shown evidence of a covalent modification at the N-terminus and a noncovalen

43 Covalent modification at two conserved cysteine residues

44 ferent time points during folding introduces covalent modifications at solvent accessible side chains

45 ovative technique for incorporating multiple covalent modifications at specific sites in covalently c

46 ctivation of the nucleotide that involves no covalent modification but only electrostatic polarizatio

47 lling activity of the target protein through covalent modification, but accumulating evidence points

48 The covalent modification by (2-(trimethylammonium)ethyl) me

49 and can be irreversibly inactivated through covalent modification by a mechanism-based inhibitor, wh

50 system, protein substrates are degraded via covalent modification by a polyubiquitin chain.

51 erall activity or function but allows direct covalent modification by a small-molecule probe containi

52 Owing to their covalent modification by cholesterol and palmitate, Hedg

53 rimary human T cells that are susceptible to covalent modification by electrophilic small molecules.

54 and several nucleophilic side chains undergo covalent modification by ethyl diazoacetate (EDA).

55 a) accessibility of substituted cysteines to covalent modification by methanesulfonate reagent depend

56 One potential mechanism involves covalent modification by reactive carbonyls of apolipopr

57 ed to activate IKs channels depends on their covalent modification by small ubiquitin-like modifier (

58 Covalent modification by small ubiquitin-related modifie

59 was identified as the residue that undergoes covalent modification by the 12,13-epoxide group of trip

60 pectrometry identified Cys475 as the site of covalent modification by the active metabolite.

61 bitory flavonoids to alpha-synuclein and the covalent modification by the flavonoid quinone led to th

62 rate, protected L393C, I397C, and T400C from covalent modification by the MTS reagents.

63 eic acid, and the structural consequences of covalent modification by these two inhibitors are fundam

64 Recognition of histone covalent modifications by chromatin-binding protein modu

65 UV-activated aromatic azide, mapping of the covalent modifications by liquid chromatography-tandem m

66 ation by one tail shock involves presynaptic covalent modifications by protein kinase A (PKA) and Cam

67 and/or multiple sites of post-translational covalent modification can be modeled using reaction rule

68 The kinetics of covalent modification can be monitored spectroscopically

69 redox-sensitive cysteine residues that, upon covalent modification, can allosterically regulate kinas

70 Thus, covalent modification chemistry occurs already prior to

71 ved complex, which is a prerequisite for the covalent modification chemistry to occur.

72 n of methionine residues is reversible, this covalent modification could also function as a mechanism

73 or one or both forms of the substrate of the covalent modification cycle affected the steady-state ou

74 by the out-of-equilibrium properties of the covalent modification cycle controlling Cdk1 activity.

75 esult in subsensitive responses, even if the covalent modification cycle displays significant ultrase

76 ream target on the signaling properties of a covalent modification cycle, an example of retroactivity

77 roperties of an upstream signal transduction covalent modification cycle.

78 Covalent modification cycles (systems in which the activ

79 Here, we analyze the properties of covalent modification cycles and ligand/receptor interac

80 Covalent modification cycles are basic units and buildin

81 nt spatial aspects of signal transduction in covalent modification cycles by starting with a basic te

82 the systematic understanding of signaling in covalent modification cycles, pathways, and networks in

83 Such covalent modification cycles, triggered by transcription

84 Among different covalent modifications found on p53 the most controversi

85 Histone tail covalent modifications have been extensively studied, bu

86 Here we identify a distinct function of this covalent modification in controlling the later proteolyt

87 best satisfied by including a mutation and a covalent modification in the C-terminal part, and the as

88 ylation is one of the most prevalent protein covalent modifications in eukaryotes and is mediated by

89 l mono-acetylation at LYS-16, which is a key covalent modification, induces a significant reorganizat

90 Such covalent modifications involve extensive preparative and

91 Regulation by covalent modification is a common mechanism to transmit

92 sible inhibitor scaffold to demonstrate that covalent modification is not a requirement for activity

93 idopsisthaliana) the isothiocyanate provokes covalent modification (K4me3, K9ac) of histone H3 in the

94 indicate that FAT10 not only plays a role in covalent modification, leading its substrates to proteas

95 However, how covalent modification leads to channel opening and, impo

96 st that dynamic counterbalance by reversible covalent modification may be a general strategy for cont

97 Together, our results suggest covalent modification may be used to stabilize the GLP-1

98 ARP-1 and -2 are regulated by DNA breaks and covalent modifications, mechanisms of PARG regulation ar

99 is report improves the repertoire of peptide covalent modification methods by exploiting the syntheti

100 olvent at ambient temperatures suggests that covalent modification might be involved in the Golgi-alt

101 proteins continuously undergo non-enzymatic covalent modifications (NECMs) that accumulate under nor

102 cules and form adducts known as nonenzymatic covalent modifications (NECMs).

103 we use particle-based simulation to study a covalent modification network in which the activating co

104 to CXCL12, indicates the importance of this covalent modification not only in marking receptors for

105 The apparent covalent modifications occurred in the cytoplasm within

106 features found on known druggable sites and covalent modification of a bystander tyrosine residue pr

107 ective inhibitor of the Ag85 complex through covalent modification of a cysteine residue proximal to

108 ctive metabolite (AM) of clopidogrel and the covalent modification of a cysteinyl residue of human cy

109 ional constraints to dramatically accelerate covalent modification of a distal, poorly nucleophilic l

110 Covalent modification of a drug with a peptide moiety ha

111 Postsynthetic covalent modification of a metal-organic framework (MOF)

112 s of NO are mediated by S-nitrosylation, the covalent modification of a protein cysteine thiol by an

113 Catalyzing the covalent modification of aliphatic amino groups, such as

114 Pathways for HA iodination include covalent modification of aromatic-type rings by I(2) / H

115 these findings, it can be proposed that the covalent modification of beta-lactoglobulin functions as

116 iarylphosphines has been employed for direct covalent modification of biomolecules with probes in the

117 Reversible inactivating covalent modification of BiP is believed to contribute t

118 Acute hyperglycaemia causes covalent modification of CaMKII by O-linked N-acetylgluc

119 Thus, SUMOylation is a covalent modification of caveolins that influence the re

120 CIATED NEDD8-DISSOCIATED1 participate in the covalent modification of CULLIN1 by RELATED TO UBIQUITIN

121 Likewise, the covalent modification of Cys residues at selected positi

122 group acts as inhibitor of catBoNT/A through covalent modification of Cys(165).

123 We conclude by demonstrating that covalent modification of Cys118 on Ras leads to a novel

124 Conclusive evidence for the covalent modification of Cys181 is provided from enzyme

125 2-oxo-clopidogrel inactivates CYP2B6 through covalent modification of Cys475.

126 ccurs through an unusual mechanism involving covalent modification of cysteine residues clustered wit

127 ctivate both insect and vertebrate TRPA1 via covalent modification of cysteine residues in the amino-

128 immunosuppressive activity is related to the covalent modification of cysteine residues in the human

129 bit the protein-protein interactions through covalent modification of cysteine residues within the RG

130 genases, as well as posttranslationally, via covalent modification of cysteine residues.

131 d by a variety of reactive irritants via the covalent modification of cysteine residues.

132 Activation of hPLCbeta3 by U73122 required covalent modification of cysteines as evidenced by the o

133 hilic agents activate these channels through covalent modification of cytosolic cysteine residues, th

134 The turnover process utilizes covalent modification of D244, requiring two transition-

135 Covalent modification of DNA and histones, also termed e

136 ion-molecule proton transfer reactions, and covalent modification of DNA anions using trimethylsilyl

137 as been demonstrated that DNA methylation, a covalent modification of DNA that can regulate gene expr

138 tional modifications of nuclear proteins and covalent modification of DNA, result in potent regulatio

139 city is believed to occur mainly through its covalent modification of DNA, resulting in the formation

140 -MS) is the method of choice for analysis of covalent modification of DNA.

141 visible light, which induces ligand loss and covalent modification of DNA.

142 ores, a surprising tolerance for substantial covalent modification of each antibiotic, and a potentia

143 were evaluated for each of the proteins: (1) covalent modification of electron-rich amino acids (asse

144 a robust mechanism tuning TRPV1 activity via covalent modification of evolutionarily conserved cystei

145 ma membrane and is activated by H(2)O(2) via covalent modification of extracellular cysteine residues

146 Covalent modification of flaxseed protein isolate by phe

147 Covalent modification of graphene by organic diazonium s

148 these reagents are particularly effective at covalent modification of His-tags, which are common moti

149 imicrobial effector genes, also required the covalent modification of histone H3 at gene promoters.

150 Covalent modification of histones by protein arginine me

151 Covalent modification of histones is a fundamental mecha

152 Covalent modification of histones on chromatin is a dyna

153 a may produce certain of its effects through covalent modification of host proteins.

154 vated by electrophilic compounds through the covalent modification of intracellular cysteine residues

155 chimeras and the assessment of the effect of covalent modification of introduced Cys at the domain-do

156 ust have two distinct binding sites, because covalent modification of its free cysteines with N-ethyl

157 Mutagenesis studies showed that covalent modification of just Cys81 is sufficient to inh

158 l products that modify Keap1 does not detect covalent modification of Keap1 by some highly reversible

159 es that decrease NRF2-ubiquitination through covalent modification of KEAP1 cysteine residues, but su

160 Covalent modification of LC3 and GABARAP proteins to pho

161 DNA methylation, the only known covalent modification of mammalian DNA, occurs primarily

162 Cytosine methylation is the major covalent modification of mammalian genomic DNA and plays

163 Postsynthetic covalent modification of metal-organic frameworks (MOFs)

164 xposure irreversibly inhibits respiration by covalent modification of mitochondrial cytochrome oxidas

165 How the covalent modification of mRNA ribonucleotides, termed ep

166 genome by altering the epigenome, including covalent modification of nucleosomal histones.

167 y elements and germline transcription in the covalent modification of nucleosomes at Ag receptor loci

168 ion of ATP hydrolysis is irreversible due to covalent modification of P-gp.

169 We identify covalent modification of p300 by the dicarbonyl metaboli

170 that 3-HPAA inactivation did not result from covalent modification of PGHS-2 or damage to the heme mo

171 PUVA increases the order of lipid phases by covalent modification of phospholipids, thereby inhibiti

172 soluble precursors, products and lipids, and covalent modification of phosphorylation, while in vivo

173 Covalent modification of primary amine groups in multipl

174 nactivated after one turnover because of the covalent modification of Pro-1.

175 periment with Cg10062 does not result in the covalent modification of Pro-1.

176 Covalent modification of protein by drugs may disrupt se

177 The covalent modification of protein substrates by ubiquitin

178 However, the questions of whether covalent modification of proteins by IsoLGs are subject

179 hr phosphorylation is the primary reversible covalent modification of proteins in eukaryotes.

180 nsduction mechanisms: protein binding, and a covalent modification of proteins termed protein pyropho

181 ed ROS generation, site-specific, reversible covalent modification of proteins, particularly oxidatio

182 rylhydrazone approach for the chemoselective covalent modification of QDs that is compatible with neu

183 When bound to Rab1, LidA interfered with the covalent modification of Rab1 by phosphocholination or A

184 rolled environments, or functionalization or covalent modification of reagents.

185 analogues were potent inhibitors, effecting covalent modification of recombinant Cal1 catalytic doma

186 CDK inhibitor THZ1 identified dose-dependent covalent modification of several unexpected kinases, inc

187 lts suggest the feasibility of DNA-catalyzed covalent modification of side chains of large protein su

188 ROS are modulated in large part through the covalent modification of specific cysteine residues foun

189 Targeted covalent modification of surface-exposed lysines is chal

190 vatize the triazine with an electrophile for covalent modification of target proteins, an alkyne as a

191 ences indicate that distal damage occurs via covalent modification of the 5'-adjacent dG, but there i

192 fomycin, which specifically inhibits MurA by covalent modification of the active site residue Cys-115

193 active-site directed manner consistent with covalent modification of the active site.

194 ment of NHS from NHS esters with concomitant covalent modification of the arginine residue.

195 Covalent modification of the Cys residues with a structu

196 c acetal groups are installed through direct covalent modification of the dextran.

197 Reversible covalent modification of the DNA via N3 of adenine occur

198 d coronavirus 3CLpro inhibitors that act via covalent modification of the enzyme, 16-(R) is a noncova

199 n turn acts as a suicide inhibitor of SPT by covalent modification of the essential catalytic lysine.

200 resulting in partial oxidation, reduction or covalent modification of the graphene sheets.

201 In 3, covalent modification of the interacting proteins procee

202 S inactivation of reduced 2-KPCC occurs with covalent modification of the interchange thiol (Cys(82))

203 Covalent modification of the membranes was achieved by r

204 Covalent modification of the metastable helicates preven

205 oelectron spectroscopy (XPS) demonstrate the covalent modification of the nanoparticle surface with t

206 In this paradigm, covalent modification of the NP with cell-targeting moti

207 potency through a reversible or irreversible covalent modification of the nucleophile Ser241 in the u

208 e proteases was probed using mutagenesis and covalent modification of the obtained cysteine mutants w

209 Covalent modification of the pi-electron basal planes of

210 ne quinone, dilution-independent, suggesting covalent modification of the protein by the catecholamin

211 Covalent modification of the proteome by SUMO is critica

212 Covalent modification of the specific cysteine residue(s

213 crease in fluorescence quantum yield and not covalent modification of the SWCNT or scavenging of reac

214 th tritylium tetrafluoroborate resulted in a covalent modification of the terminal O-atom, and cleava

215 The covalent modification of therapeutic biomolecules has be

216 Mutation and covalent modification of these residues have charge-depe

217 f the acetylenic group of 9EP and subsequent covalent modification of Thr 302.

218 To characterize the effect of covalent modification of Thr302, tBPA-modified P450 2B4

219 subject to irreversible photodamage through covalent modification of tryptophans (Trps) and other UV

220 In summary, covalent modification of TSC2 by iNOS-derived NO is asso

221 CCG-4986 inhibits RGS4 function through the covalent modification of two spatially distinct cysteine

222 ersensitivity reactions that can result from covalent modification of unintended targets.

223 tryptic peptide anions is consistent with a covalent modification of unprotonated primary amines (i.

224 We have investigated the potential use of covalent modification of VSV with polyethylene glycol (P

225 nhibitor of eukaryotic transcription through covalent modification of XPB, a subunit of the general t

226 ependent redox changes can mediate transient covalent modifications of cysteine thiols to modulate th

227 Epigenetic information encoded in covalent modifications of DNA and histone proteins regul

228 The epigenetic mechanisms involve covalent modifications of DNA and histones, which affect

229 etazoan gene expression includes coordinated covalent modifications of DNA and its associated histone

230 Covalent modifications of histone proteins have profound

231 DNA methylation and covalent modifications of histone tails contribute to ch

232 Covalent modifications of histones have an established r

233 Covalent modifications of histones integrate intracellul

234 Covalent modifications of histones, such as acetylation,

235 epigenetic regulation by DNA methylation and covalent modifications of histones.

236 Covalent modifications of intracellular proteins, such a

237 g RNAs that form ribonucleoproteins to guide covalent modifications of ribosomal and small nuclear RN

238 The epigenome includes covalent modifications of the DNA and its associated pro

239 s process is dynamically regulated by direct covalent modifications of the polymerase that synthesize

240 n structure that include DNA methylation and covalent modifications of the proteins that bind DNA.

241 g process of SV40 Vp1 by stimulating certain covalent modifications of Vp1 or by recruiting certain c

242 at least partly achieved through changes in covalent modifications on DNA and histones.

243 The structure explains how covalent modifications on H4K16 and H3K79 regulate forma

244 Upon exposure to anthropogenic chemicals, covalent modifications on the genome can drive developme

245 Covalent modifications on therapeutic proteins are tradi

246 such as allyl isothiocyanate (AITC) through covalent modification or activated by noncovalent agonis

247 sting change in receptor molecules, either a covalent modification or conformation that enhances thei

248 altering contacts at this A1-C2 junction by covalent modification or increasing hydrophobicity incre

249 ctionality to the monomer structures through covalent modification, or through the use of new thermod

250 Covalent modification provides a mechanism for modulatin

251 This covalent modification redirects the de-excitation pathwa

252 figurations that are regulated by reversible covalent modifications, referred to as epigenetic marks.

253 Thr(328)) in the activation loop is the only covalent modification required for kinase activation in

254 for a better understanding of the underlying covalent modifications responsible for the charge differ

255 Overall, examining the spatial dimension of covalent modification reveals that 1), there are importa

256 uding regulation of cotranslational folding, covalent modifications, secretion, and expression level.

257 function at spindle poles by extending from covalent modification sites on PARP-5a and NuMA and bind

258 display many of the attributes of reversible covalent modifications such as protein phosphorylation o

259 Covalent modifications, such as methylation and demethyl

260 can bind either ligand in the absence of any covalent modifications, such as oxidation.

261 o protect their genomes from R-M cleavage by covalent modifications, such as the hydroxymethylation a

262 rotein SidD that hydrolytically reverses the covalent modification, suggesting a tight spatial and te

263 etely protect the beta2M286C suflhydryl from covalent modification, suggesting close steric interacti

264 This contrasts with the well-mixed covalent modification system studied by Goldbeter and Ko

265 sphorylation, ubiquitylation is a reversible covalent modification that regulates the stability, acti

266 onsequences of phosphorylating serine 381, a covalent modification that turns off F-actin bundling ac

267 on-channel signaling to epigenetic chromatin covalent modifications that affect gene expression patte

268 uding UV shadowing and heat annealing, cause covalent modifications that alter folding behavior.

269 eome consists of reversible and irreversible covalent modifications that link redox metabolism to bio

270 In contrast, covalent modifications that may regulate its action afte

271 Control is achieved through several covalent modifications that occur both on DNA and chroma

272 Activation of Nrf2 by covalent modifications that release it from its inhibito

273 small nuclear RNAs (snRNAs) undergo multiple covalent modifications that require guide RNAs to direct

274 The adaptation helices undergo reversible covalent modifications that tune the stimulus-responsive

275 of sequestering reactive metabolites through covalent modification, thereby limiting their exposure t

276 te drugs in this and other systems by simple covalent modification to form lipophilic analogs that re

277 d add quantitation of protein expression and covalent modification to the arsenal of techniques for c

278 lorimetry, and NMR titrations indicated that covalent modifications to a carrier protein modulate dom

279 can differ from its neighbors as a result of covalent modifications to both the DNA and the histone p

280 omatin-modifying enzymes that add or reverse covalent modifications to DNA and histones have a critic

281 Covalent modifications to histones are essential for dev

282 Covalent modifications to histones play important roles

283 have been extended: extra symbols represent covalent modifications to nucleotides, logos with multip

284 These changes include covalent modifications to the DNA and histones as well a

285 Such information exists in the form of covalent modifications to the histone proteins that comp

286 The relevance of these covalent modifications to the several functions ascribed

287 es revealed that LRAT undergoes spontaneous, covalent modification upon incubation with a variety of

288 These data demonstrated that our non-covalent modification was able to alter Ad's interaction

289 The covalent modification was characterized, and we establis

290 The site of covalent modification was mapped to a cysteine residue l

291 Covalent modification was surprising because the accumul

292 ation of target enzymes occurs preferably by covalent modification, which imposes challenges in balan

293 e receptor is a conformational change and/or covalent modification, which then sets in motion a signa

294 pplement the current repertoire for cysteine covalent modification while avoiding some of the limitat

295 findings provide a physiological role for a covalent modification widespread in nature and suggest p

296 ntributed to develop, and which concerns the covalent modification with appropriate molecules to enha

297 Toward these objectives, covalent modification with poly(ethylene glycol) (PEG) h

298 abilized using site-directed mutagenesis and covalent modification with poly(ethylene glycol) chains

299 ated with unintegrated DNAs become marked by covalent modifications, with a delay relative to the tim

300 Our results indicate that covalent modifications within this pocket may alter inte