ライフサイエンスコーパス: PTM

1 PTM and PTN feature varying diterpene-derived ketolides

2 PTM site sequence analysis from C. glutamicum OMP and ot

3 PTMs and tubulin isotype diversity act as a "tubulin cod

4 PTMs can induce a range of effects, from local stabiliza

5 PTMs can occur on proteins at any time in their lifespan

6 Citrulline, a PTM implicated in epigenetic and immunological function,

7 anslational modifications (PTMs), creating a PTM code that controls the function of proteins in space

8 herapy group who received radiotherapy for a PTM) and tiredness or lethargy (36 [39%] in the immediat

9 We show that methylation is a PTM of dynamic microtubules and that the histone methylt

10 ADP-ribosylation is a PTM, in which ADP-ribosyltransferases use nicotinamide a

11 es proteolytic cleavage in the vicinity of a PTM to yield peptides for sequencing.

12 These results highlight the potency of a PTM-binding protein to regulate DNA accessibility and un

13 Such a PTM is the formation of succinimide (Snn) in a protein t

14 The only serious adverse event related to a PTM or radiotherapy was development of a painful PTM wit

15 ith deferred radiotherapy (given only when a PTM developed) in a suitably powered trial.

16 ed sensitivity for quantifying low-abundance PTMs, requiring the use of affinity reagents for enrichm

17 Most lysine mono-methylation and acetylation PTMs are either symmetrically distributed on old and new

18 and its DUB partner allows erasure of active PTMs and the de novo transition of a transcriptionally a

19 centrations of acyl-CoAs affect histone acyl-PTM abundances by both enzymatic and non-enzymatic mecha

20 ve a dose-dependent increase in histone acyl-PTM abundances in response to acyl-CoA supplementation i

21 ce of acyl-CoAs and their corresponding acyl-PTMs.

22 ectrometry to accurately quantify eight acyl-PTMs in vivo and after in vitro enzymatic assays.

23 acyl post-translational modifications (acyl-PTMs) have been discovered, of which the functional sign

24 In addition, PTMs can be induced or removed on changes in cellular en

25 Among its advantages, PTM allows the measurement of small volumes, which was r

26 horylation partially account for the altered PTMs in APC mutants, suggesting that APC mutants affect

27 ovide detailed primary sequence analysis and PTM site localization of therapeutic monoclonal antibody

28 cal tools cannot efficiently examine ASV and PTM events simultaneously, which limits understanding of

29 n peptides, increasing sequence coverage and PTM localization by combining sequential ETD and HCD fra

30 ssors, coactivators, DNA-binding factors and PTM modifying enzymes.

31 also associations with binding partners and PTMs that divide the MT cytoskeleton into functionally d

32 protein functions and cellular pathways, and PTMs of mutant Htt are likely important modulators of HD

33 association between nucleosome stability and PTMs across cell types, differentiation state and throug

34 l of 21 core histones, histone variants, and PTMs in primary, immortalized, and transformed cells.

35 orted structures of context-independent anti-PTM antibodies in complex with the corresponding PTM.

36 t-translational modification, abbreviated as PTM, refers to the change of the amino acid side chains

37 Because PTMs are catalyzed by enzymes, the toxicity-modulating H

38 enesis by antagonizing the crosstalk between PTMs involving HIF1alpha protein degradation.

39 ocesses, and the potential crosstalk between PTMs, that together regulate the intricate lives of thes

40 ndly shaped by regulatory interplays between PTMs.

41 alyze protein carbamylation, as monitored by PTM of protein lysine residues into N()-carbamyllysine (

42 comparing the following outcomes in SOTR by PTM status: (1) all-cause mortality, (2) cancer-specific

43 ied peptides, respectively, were affected by PTMs, with a total of 277 and 282 sequences showing deam

44 n of plant metabolic enzymes and pathways by PTMs and their cross talk are summarized.

45 sociation between pretransplant skin cancer, PTM, death, and graft failure.

46 Certain PTMs' contribution to epigenetics has been extensively e

47 A well-characterized PTM involves in the removal and re-ligation of the C-ter

48 he presently available data on characterized PTMs of key BER proteins, the functional consequences of

49 nd comprise what is termed a "tubulin code." PTMs of histones comprise an analogous "histone code," a

50 growth factors, the outcome of combinational PTM codes on histones and coregulators is profoundly sha

51 ry-based assays, we focus on the most common PTMs-phosphorylation and O-GlcNAcylation-and investigate

52 Unraveling this complex PTM code is one of the great challenges in molecular bio

53 r selective detection of proteins containing PTMs are still lacking.

54 antibodies in complex with the corresponding PTM.

55 reveals those patients with mTBI who develop PTM, and inversely correlates with TTR.

56 and a 3.2 increased likelihood of developing PTM.

57 anisms involving crosstalk between different PTMs.

58 suggesting that the inheritance of different PTMs is regulated distinctly.

59 ore histones, the establishment of different PTMs on individual "sister" histones in the same nucleos

60 tion research and its emergence as a dynamic PTM occurring on histone and non-histone proteins.

61 cation (PTM), we have exploited a eukaryotic PTM to recombinantly synthesize lipid-polypeptide hybrid

62 6 individual histone PTMs and 30 co-existing PTMs were fully quantified with high confidence.

63 owed increasing concentration of fluorescent PTM towards the lens centre in accord with the increased

64 Finally, current research approaches for PTM study will be discussed and compared, including limi

65 confounders were used to calculate risk for PTM, death and graft failure in recipients with pretrans

66 The centerpiece technology for PTM site identification, mass spectrometry (MS), require

67 Nearly all functional PTMs are found on the N-terminal histone domains (tails)

68 e study not only uncovers a novel functional PTMs of Bmi-1 but also reveals a unique oncogenic role o

69 olytic digest products promise a generalized PTM site-mapping strategy based on a toolbox of such mut

70 zogony and late gametocytes; heterochromatic PTMs mark early gametocytes.

71 f the data revealed a highly dynamic histone PTM landscape during life cycle development, with a set

72 an define significant differences in histone PTM patterns in submillimetric layers of three-dimension

73 n measurements suggest that a single-histone PTM can define regions of the genome that are not regula

74 igh-throughput study of histones and histone PTMs across the cell cycle and the study of subpopulatio

75 iation between proteomic changes and histone PTMs in response to HSP90 inhibitor treatment in bladder

76 comprehensive analyses of associated histone PTMs.

77 eosomal context, that is, asymmetric histone PTMs, are difficult to analyze.

78 A substantial association between histone PTMs and stage-specific transition provides insights int

79 entify and functionally characterise histone PTMs in 8 distinct life cycle stages of P. falciparum pa

80 Euchromatic histone PTMs are abundant during schizogony and late gametocytes

81 aw materials needed for studying how histone PTMs regulate chromatin biochemistry.

82 46 individual histone PTMs and 30 co-existing PTMs were fully quantified with

83 500 individual histone PTMs were identified of which 106 could be stringently v

84 uestion the distribution of multiple histone PTMs on old versus new histones in synchronized human ce

85 ife cycle development, with a set of histone PTMs (H3K4ac, H3K9me1 and H3K36me2) displaying a unique

86 drug localization and regulation of histone PTMs after drug treatment.

87 how *NO exposure links modulation of histone PTMs to gene expression changes that promote oncogenesis

88 rate insights into the importance of histone PTMs to the entire asexual and sexual developmental cycl

89 determine the levels of histones or histone PTMs in each stage of the cell cycle.

90 emonstrating the ability to quantify histone PTMs linked to specific chromatin factors in parallel wi

91 ity to comprehensively link specific histone PTMs with specific chromatin factors would be an importa

92 We show that histone PTMs can be grouped into three categories according to t

93 Importantly, 15 of these histone PTMs are novel for Plasmodia (e.g. H3K122ac, H3K27me3, H

94 recent advances in our understanding of how PTMs and regulatory enzymes control the signaling activi

95 ein records, allowing researchers to see how PTMs change across different contexts.

96 indings advance our understanding of the Htt PTM code and its role in HD pathogenesis.

97 yzed by enzymes, the toxicity-modulating Htt PTMs identified here may be promising therapeutic target

98 re new, including seven 11-deoxy-16R-hydroxy-PTM congeners.

99 prioritizing both known and newly identified PTMs for further studies to determine the functional rel

100 e characteristic 11S,16S-ether ring found in PTM.

101 No significant difference was seen in PTM incidence in the immediate and deferred radiotherapy

102 the caveat that rapid disease progression in PTMs was strongly associated with lack of anti-SIV Ab.

103 of the most frequently observed PTMs, the K-PTM, namely, the modification occurring at lysine (K), c

104 apped PTMs represented only 5 % of all known PTMs.

105 domain modifications, found by mapping known PTMs onto RRM domain alignments and structures.

106 It represents the first multi-label PTM predictor ever established.

107 metrics indicate that the first multi-label PTM predictor is very promising and encouraging.

108 thod has ever been developed for multi-label PTM types.

109 established to identify various single-label PTM types and their occurrence sites in proteins, no met

110 These models allow us to locate PTMs within initiation factor complexes and to highlight

111 intestine collected from pigtailed macaques (PTMs) and African green monkeys (AGMs) that experience d

112 ntrasted pathogenic (in pig-tailed macaques [PTMs]) and nonpathogenic (in African green monkeys [AGMs

113 We further showed that Ser-ADPr is a major PTM in cells after DNA damage and that this signalling i

114 Posttransplant malignancy (PTM) is one of the leading causes of late death in kidne

115 ents (SOTR) with a pretransplant malignancy (PTM) are at increased risk for cancer recurrence.

116 ectively), we created new databases that map PTMs to their locations inside or outside of PPIRs.

117 For the three mapped PTM databases which had sufficient numbers of modificati

118 The mapped PTMs represented only 5 % of all known PTMs.

119 erapy to prevent procedure-tract metastases (PTMs) in malignant pleural mesothelioma remains controve

120 In contrast, most di- and tri-methylation PTMs are enriched on old histones, suggesting that the i

121 Particle-tracking microrheology (PTM) is a widely accepted means of determining the visco

122 injury (mTBI) with posttraumatic migraines (PTMs) and those without PTMs on the basis of analysis of

123 gh oxidative posttranslational modification (PTM) of proteins in asthmatic airways through a process

124 (ADPr) is a posttranslational modification (PTM) of proteins that controls many cellular processes,

125 ant histone post-translational modification (PTM) for manipulating chromatin structure and regulating

126 ion of this post-translational modification (PTM) from complex biological samples by shotgun proteomi

127 a dominant post-translational modification (PTM) in Alzheimer's disease (AD) and related tauopathies

128 of the tau post-translational modification (PTM) landscape.

129 This post-translational modification (PTM) of hnRNP E1 promotes its dissociation from a 3' unt

130 The post-translational modification (PTM) of proteins by endogenous reactive chlorine, nitrog

131 analysis, a post-translational modification (PTM) of tyrosine sulfation to this neuropeptide was reso

132 lation is a post-translational modification (PTM) process, in which small ubiquitin-related modifier

133 ication and post-translational modification (PTM) profiling of targeted protein in biofluid.

134 us types of post translational modification (PTM) sites.

135 on of their post-translational modification (PTM) status are therefore required in order to fully und

136 terogeneous post-translational modification (PTM) that plays an essential role in biological regulati

137 jor form of post-translational modification (PTM) that regulates diverse cellular processes.

138 a prevalent post-translational modification (PTM) used by the cell to reversibly regulate protein fun

139 bind to the post-translational modification (PTM), hypusine, with minimal dependence on flanking amin

140 an-specific post-translational modification (PTM), on ribosomes and define its direct substrates.

141 ure through post-translational modification (PTM), we have exploited a eukaryotic PTM to recombinantl

142 tunable by post-translational modification (PTM).

143 nd covalent post-translational modification (PTM).

144 ne type- or posttranslational modification- (PTM-) specific antibodies and automated, quantitative im

145 ges histone posttranslational modifications (PTM) by directly inhibiting the catalytic activity of Jm

146 atures and post-translational modifications (PTM) and thereby minimize the risk of being clinically m

147 roscopy as post-translational modifications (PTM) of Trp and Arg amino acid residues.

148 ffected by post-translational modifications (PTM).

149 Posttranslational modifications (PTMs) affecting E2 function and stability have been demo

150 fluenced by posttranslational modifications (PTMs) and assisted by a number of co-chaperone proteins.

151 ces tubulin posttranslational modifications (PTMs) and stabilizes dynamic microtubules (MTs) by reduc

152 Posttranslational modifications (PTMs) are key contributors to chromatin function.

153 ylation and posttranslational modifications (PTMs) in histones, are important factors in determining

154 and histone posttranslational modifications (PTMs) in single cells.

155 Posttranslational modifications (PTMs) of tubulin specify microtubules for specialized ce

156 Posttranslational modifications (PTMs) regulate protein functions and interactions.

157 by multiple posttranslational modifications (PTMs), creating a PTM code that controls the function of

158 Protein posttranslational modifications (PTMs), including acetylation, methylation, phosphorylati

159 l-conserved posttranslational modifications (PTMs), including O-mycoloylation, pyroglutamylation, and

160 Mapping posttranslational modifications (PTMs), which diversely modulate biological functions, re

161 to protein posttranslational modifications (PTMs).

162 of protein post-translational modifications (PTMs) across sample cohorts is a prerequisite for functi

163 Post-translational modifications (PTMs) affect protein function, localization, and stabili

164 Post-translational modifications (PTMs) allot versatility to the biological functions of h

165 HIF1alpha post-translational modifications (PTMs) and HIF1alpha-induced tumor angiogenesis remains t

166 ow histone post-translational modifications (PTMs) are inherited through the cell cycle remains poorl

167 Post-translational modifications (PTMs) control and regulate many protein functions and ce

168 iants, and post-translational modifications (PTMs) in antibody-derived therapeutics.

169 nd histone post-translational modifications (PTMs) in bladder carcinoma in response to HSP90 inhibiti

170 uantifying post-translational modifications (PTMs) in full-length proteins is a challenge, especially

171 to detect post-translational modifications (PTMs) in human MDDCs due to chronic alcohol exposure.

172 on protein post-translational modifications (PTMs) in mammals, protein glycosylation has been observe

173 ce of many post-translational modifications (PTMs) is not well understood.

174 Post-translational modifications (PTMs) of alpha/beta-tubulin are believed to regulate int

175 Post-translational modifications (PTMs) of histones regulate chromatin structure and funct

176 icing, and post-translational modifications (PTMs) of the proteins (proteoforms).

177 by various post-translational modifications (PTMs) on histone proteins in the nucleosome and by nucle

178 gnals into post-translational modifications (PTMs) on histones and coregulators such as corepressors,

179 occurring post-translational modifications (PTMs) on proteins induced by physiological signals and r

180 individual post translational modifications (PTMs) on the biological activities of antibodies, even w

181 those with post-translational modifications (PTMs) or small molecules.

182 Post-translational modifications (PTMs) produce significant changes in the structural prop

183 (ASVs) and post-translational modifications (PTMs) reportedly tied to central nervous system maturati

184 gulated by post-translational modifications (PTMs) resulting in a robust yet 'tunable' cytokine respo

185 to dynamic post-translational modifications (PTMs) that cooperatively modulate the chromatin structur

186 Post-translational modifications (PTMs) that occur in the PPIR can either interfere with o

187 nenzymatic post-translational modifications (PTMs) that result in a very small mass change of the elu

188 ve protein post-translational modifications (PTMs) when suitable element-tags are designed and specif

189 ., histone post-translational modifications (PTMs), in the layers of the HCT116 colon carcinoma MCTS.

190 atabase of post-translational modifications (PTMs), ProteomeScout, we found that RRM domains are also

191 lized with post-translational modifications (PTMs), substituted with histone variants, and even lacki

192 rated with post-translational modifications (PTMs), such as glutamylation of tubulin tails.

193 Post-translational modifications (PTMs), such as phosphorylation, acetylation and glycosyl

194 ulation of post-translational modifications (PTMs), which are not dependent on beta-catenin transcrip

195 iption and post-translational modifications (PTMs).

196 including post-translational modifications (PTMs).

197 ations and post-translational modifications (PTMs).

198 gh histone post-translational modifications (PTMs).

199 ication of post-translational modifications (PTMs).

200 quence and post-translational modifications (PTMs); however, large-scale production in cell culture o

201 aging parameters on the sensitivity of muOCT-PTM by performing theoretical and numerical analyses, wh

202 requires very small fluid quantities, muOCT-PTM could also be generally applied to interrogate the v

203 alyzed our efforts to evolve MS-grade mutant PTM-directed proteases.

204 taptmO5 mutant SB12036 that accumulated nine PTM and PTN congeners, seven of which were new, includin

205 ase of spontaneously occurring, nonenzymatic PTMs.

206 As one of the most frequently observed PTMs, the K-PTM, namely, the modification occurring at l

207 roup at C-16, is crucial for the activity of PTM.

208 iotherapy (same dose given within 35 days of PTM diagnosis).

209 ikelihood ratios for mTBI and development of PTM.

210 rm is broadly applicable to the discovery of PTM sites that are amenable to chemical labeling, as wel

211 The unique mass spectral features of PTM-dependent proteolytic digest products promise a gene

212 The 5-year cumulative incidence of PTM in patients with and without a pretransplant skin ca

213 The primary outcome was the incidence of PTM within 7 cm of the site of pleural intervention with

214 nd developing effective drugs, prediction of PTM sites in proteins have currently become a hot topic

215 transplant skin cancer had increased risk of PTM (sub-HR [SHR], 2.60; 95% CI, 2.27-2.98), and posttra

216 nity labeling approach broadens the scope of PTM detection by chemical means and may facilitate the d

217 ng homogenously modified IDPs for studies of PTM-mediated IDP regulatory mechanisms.

218 terial activities, albeit lower than that of PTM, indicating that the ether ring, or minimally the st

219 ch ones can accommodate two or more types of PTM, which ones only one, and which ones none?

220 sting that APC mutants affect other types of PTM.

221 nhibition of MT dynamics and accumulation of PTMs are driving factors for the induction of tau-mediat

222 nding of the (combinatorial) consequences of PTMs, is needed to convert this growing wealth of data i

223 niques to unravel the location and extent of PTMs in the chloroplast ATP synthase (cATPase) purified

224 or outside of PPIRs for the vast majority of PTMs, a machine learning strategy was used to generate p

225 our knowledge, the first genome-wide maps of PTMs in cccDNA-containing chromatin from de novo infecte

226 Alterations of selected numbers of PTMs of Htt fragments have been shown to modulate Htt ce

227 Here we examine the role of PTMs and the tubulin code in the ciliary specialization

228 In this review we examine the roles of PTMs in both parasite-specific and conserved eukaryotic

229 Virtually all proteins are targets of PTMs.

230 tive proteome studies identified 14 types of PTMs with 93 marks on the core histones, including 34 no

231 ed asymmetrically with two distinct types of PTMs.

232 e biological processes that are dependent on PTM regulation of IDPs.

233 ve PTMs is expected to undergo more than one PTM in cells stimulated with growth factors, the outcome

234 This assay can be extended to other PTM biosignatures by conjugation of other affinity ligan

235 ween HIF1alpha protein methylation and other PTMs in regulating tumor angiogenesis.

236 ones serves as a regulatory switch for other PTMs, and connects chromatin remodeling complexes into g

237 or radiotherapy was development of a painful PTM within the radiotherapy field that required hospital

238 Here, by performing PTM with high-resolution micro-optical coherence tomogra

239 Platensimycin (PTM) and platencin (PTN) are highly functionalized bacte

240 s consisting of a polychlorotriphenylmethyl (PTM) electron-acceptor moiety linked to an electron-dono

241 The two fully processed PTM analogues showed antibacterial activities, albeit lo

242 curate quantitation and discovery of protein PTMs in complex biological systems without the requireme

243 The PTM database is a compendium of public PTM data, coupled with user-uploaded experimental data.

244 protein with multiple residues for putative PTMs is expected to undergo more than one PTM in cells s

245 As a result, PTM is a selective inhibitor for FabF/FabB, while PTN is

246 ys in primary neurons, we identified several PTMs whose alteration can block neuronal toxicity and pr

247 the functional relationship between specific PTMs and protein-protein interactions.

248 One of the most studied PTMs is the oxidation of susceptible residues but other

249 Studying PTMs by NMR spectroscopy is a promising method to analyz

250 protein modification of peptide substrates, PTMs of individual histones, and the relative abundance

251 is especially important to search for subtle PTMs in proteins.

252 One such PTM is lysine succinylation, which is regulated by sirtu

253 mall molecule inhibitors developed to target PTM writers.

254 fic proteases are available towards targeted PTMs.

255 We further employ FLEXITau to define the tau PTM landscape present in AD post-mortem brain.

256 The PTM database is a compendium of public PTM data, coupled

257 The PTM unit can be switched between the nonradical and radi

258 for the biosynthetic divergence between the PTM and PTN diterpene-derived ketolides.

259 s in E. coli and genetic manipulation in the PTM-PTN dual overproducer Streptomyces platensis SB12029

260 cluster, partitions the biosynthesis of the PTM and PTN diterpene-derived ketolides.

261 We now report investigation of the PTM cassette through the construction of diterpene produ

262 Unraveling of the PTM code, i.e. a predictive understanding of the (combin

263 We previously determined that the PTM cassette, consisting of five genes found in the ptm,

264 ical activities of antibodies, even when the PTM levels are relatively low.

265 c antibody (Ab) production was higher in the PTMs than in AGMs, with the caveat that rapid disease pr

266 d to identify interacting subunits and their PTMs and the structural techniques that allow the archit

267 ironmental and longitudinal effects on their PTMs.

268 The effects of each of these PTM alteration constructs were tested on cell toxicity u

269 These PTMs included previously described sites such as serine

270 These PTMs therefore play key roles in regulating the BER path

271 istones, and the relative abundance of these PTMs as a function of subcellular location.

272 Relative quantification of these PTMs in hemoglobin extracted from blood samples shows th

273 rmalisation of the emission spectra of these PTMs to the fluorescence intensity of Trp, to determine

274 Collectively, it seems that these PTMs have evolved in the Corynebacteriales order and bey

275 We show a correlation between this PTM and levels of Akt2 and its activated form, phosphory

276 sing the possibility that appearance of this PTM in higher eukaryotes represents an evolutionary subs

277 DP-ribosylation and the consequences of this PTM on substrates.

278 of Snn were used to detect and quantify this PTM in the model protein lysozyme, the biotherapeutic fi

279 get proteins (Ser-ADPr) and showed that this PTM is specifically made by PARP1/HPF1 and PARP2/HPF1 co

280 Thus, PTMs are likely to be key regulators of developmental tr

281 constituting the largest effect of a tubulin PTM on motor function observed to date.

282 Nobly, the underlying PTMs regulation of Bmi-1 is poorly known.

283 system for further studies on understanding PTM crosstalk.

284 hese models are the first to predict whether PTMs are located inside or outside of PPIRs, as demonstr

285 performed in 74 patients with mTBI (57 with PTM, 17 without PTM).

286 scrimination between patients with mTBI with PTM and those without PTM (AUC = 0.85; P < .001).

287 Patients with mTBI with PTM had significantly lower SE (P < .001) but not mean F

288 o malignancies exist between recipients with PTM and those without PTM.

289 Similarly, recipients with PTM were 3 times more likely to die of cancer (pooled HR

290 Recipients with PTM were at increased risk of all-cause mortality compar

291 eful selection of transplant recipients with PTM.

292 t peptides resolved by any method, some with PTM contributing just 0.25% to the mass.

293 ciation of all-cause mortality and SOTR with PTM did not vary by transplanted organ.

294 patients with mTBI (57 with PTM, 17 without PTM).

295 use mortality compared to recipients without PTM (pooled hazard ratio [HR], 1.51; 95% confidence inte

296 atients with mTBI with PTM and those without PTM (AUC = 0.85; P < .001).

297 etween recipients with PTM and those without PTM.

298 and between patients with and those without PTM.

299 transplantation compared with those without PTM.

300 traumatic migraines (PTMs) and those without PTMs on the basis of analysis of fractional anisotropy (