ライフサイエンスコーパス: DPC

1 DPC conjugates to a 10-mer peptide were bypassed with nu

2 DPC imaging of an FeRh sample with HF-etched substrate r

3 DPCs are bulky lesions that interfere with the progressi

4 DPCs can be removed by the proteolytic activities of the

5 DPCs containing full-length proteins (11-28 kDa) or a 23

6 DPCs frequently occur in cells, either as a consequence

7 DPCs yielded ~20-fold lower RANKL expression but >2-fold

8 ular studies confirm the formation of PARP-1 DPCs during alkylating agent-induced base excision repai

9 muM(-1) MMS) and in human cells (7.8 +/- 1.2 DPC per 10(6) nt mM(-1) MMS).

10 cross-link in both purified DNA (6.0 +/- 0.6 DPC per 10(6) nt muM(-1) MMS) and in human cells (7.8 +/

11 A DPC on the lagging strand template only transiently stal

12 A DPC on the leading strand template arrests the replisome

13 Accordingly, either a DPC tolerance mechanism or a DPC repair pathway is essen

14 ed multiscale simulations of C99(15-55) in a DPC surfactant micelle and POPC lipid bilayer in order t

15 C99(15-55) in a DPC surfactant micelle possesses a "GG kink," in the TM

16 een proposed that the protein component of a DPC is proteolytically degraded, giving rise to smaller

17 The existence of a DPC protease in higher eukaryotes is inferred from data

18 hanisms until the recent identification of a DPC-processing protease in yeast.

19 ingly, either a DPC tolerance mechanism or a DPC repair pathway is essential for C. albicans to maint

20 Cs, yielding a RANKL/OPG ratio of 41:1 (ABCs:DPCs).

21 gnancies but no data are yet available about DPC.

22 Little was known about DPC-specific repair mechanisms until the recent identifi

23 SPRTN accomplishes DPC processing through a unique DNA-induced protease act

24 livers of Sprtn hypomorphic mice accumulate DPCs containing Topoisomerase 1 covalently linked to DNA

25 Additionally, DPC formation and transformation processes were experime

26 ntaining medium did not significantly affect DPC growth; however, GDNF dose-dependently increased via

27 in two maximal distinct clusters, DPC-1 and DPC-3, respectively, reflecting their previous TCE class

28 5-55) homodimer in POPC membrane bilayer and DPC surfactant micelle environments were performed using

29 rturbed DNA replication fork progression and DPC repair.

30 he molecular mechanism underlying RJALS, and DPCs are contributing to accelerated aging and cancer.

31 When assessing DPC transformation in the environment, results can be no

32 d, and the single-crystal structures of Li[B(DPC)(oxalato)] and Li[P(DPC)3] have been determined.

33 ed to prepare a series of lithium salts Li[B(DPC)(oxalato)], Li[B(DPC)2], Li[B(DPC)F2], and Li[P(DPC)

34 s of lithium salts Li[B(DPC)(oxalato)], Li[B(DPC)2], Li[B(DPC)F2], and Li[P(DPC)3].

35 salts Li[B(DPC)(oxalato)], Li[B(DPC)2], Li[B(DPC)F2], and Li[P(DPC)3].

36 Balding DPCs had higher levels of catalase and total glutathione

37 Balding DPCs secreted higher levels of the negative hair growth

38 The complex between DPC and water is only metastable, and even at 3 K the ca

39 the amino terminal tail are involved in both DPC formation and beta-elimination steps.

40 In addition, both B. breve DPC 6330 and B. breve NCIMB 702258 supplementation resul

41 L/6 mice (n = 8 per group) received B. breve DPC 6330 or B. breve NCIMB 702258 (10(9) microorganisms)

42 P = 0.06) in mice supplemented with B. breve DPC 6330 than in mice supplemented with B. breve NCIMB 7

43 Replication blockage by DPC did not produce damaged forks or detectable amounts

44 that prevents inadvertent CMG destruction by DPC proteases, and they reveal CMG's remarkable capacity

45 Ductal pancreatic carcinoma (DPC) is a deadly disease with an incidence of 9 cases in

46 imens derived from 1:2, 1:6 and 1:10 beta-CD:DPC molar ratios exhibited degree of substitution values

47 eta-cyclodextrin:diphenyl carbonate (beta-CD:DPC; 1:2, 1:6 and 1:10).

48 Dermal papilla cells (DPCs) located in the hair bulb are the main site of andr

49 Dermal papilla cells (DPCs) taken from male androgenetic alopecia (AGA) patien

50 sues were engineered from dental pulp cells (DPCs) and assessed as a device for pulp regeneration.

51 enic differentiation from dental pulp cells (DPCs) in vitro.

52 Human dental pulp cells (DPCs), adherent cells derived from dental pulp tissues,

53 g diode (LED) exposure on dental pulp cells (DPCs).

54 otrophic factor (GDNF) on dental pulp cells (DPCs).

55 -matched rat dental pulp (dental pulp cells [DPCs]) and alveolar bone (alveolar bone cells [ABCs]) we

56 TN can elicit proteolytic activity; cleaving DPC substrates and itself.

57 HLA-DP alleles into 3-DP peptidome clusters (DPC).

58 separated in two maximal distinct clusters, DPC-1 and DPC-3, respectively, reflecting their previous

59 g T-cell uropod and the distal pole complex (DPC) opposite the immunological synapse via association

60 The dystrophin protein complex (DPC), composed of dystrophin and associated proteins, is

61 raction with the dystrophin protein complex (DPC).

62 e structural mimics of N7-guanine-conjugated DPCs were generated by reductive amination reactions bet

63 ndently as dapsone-phytochemical conjugates (DPCs) based on azo-coupling reaction.

64 es by combining differential phase contrast (DPC) magnetic imaging with in situ heating.

65 In contrast, DPC neurons coded the stimulus patterns as broader categ

66 atterns, the primate dorsal premotor cortex (DPC) neurons exhibit a complex repertoire of coding dyna

67 tracts that recapitulate replication-coupled DPC proteolysis, we show that DPCs can be degraded by SP

68 esents a specialized DNA replication-coupled DPC repair pathway essential for DNA replication progres

69 -functionalized AGT proteins formed covalent DPC but no other types of nucleobase damage when incubat

70 generally, these data suggest that covalent DPC lesions contribute to the cytotoxic and mutagenic ef

71 e are impaired in the resolution of covalent DPCs in vivo.

72 ease is essential for DNA-protein crosslink (DPC) repair and DNA replication in vertebrate cells.

73 DNA-protein crosslink (DPC), the covalent linkage of proteins with DNA, is one

74 racterized hurdle, DNA-protein crosslinking (DPC), by insertion sequence (IS)-mediated copy number va

75 DNA-protein crosslinks (DPC) arise from a wide range of endogenous and exogenous

76 replication-blocking DNA-protein crosslinks (DPC).

77 ces the formation of DNA-protein crosslinks (DPCs) and causes DNA replication and transcriptional str

78 genomic DNA, such as DNA-protein crosslinks (DPCs) and tight nucleoprotein complexes, can block repli

79 DNA-protein crosslinks (DPCs) are bulky lesions that interfere with DNA metaboli

80 DNA-protein crosslinks (DPCs) are caused by environmental, endogenous, and chemo

81 DNA-protein crosslinks (DPCs) are highly toxic DNA lesions that threaten genomic

82 Covalent DNA-protein crosslinks (DPCs) are toxic DNA lesions that interfere with essentia

83 ring or drug-induced DNA-protein crosslinks (DPCs) interfere with key DNA transactions if not repaire

84 The cytotoxicity of DNA-protein crosslinks (DPCs) is largely ascribed to their ability to block the

85 DNA-protein crosslinks (DPCs) represent a severe threat to the genome integrity;

86 -1) and Wss1 resolve DNA-protein crosslinks (DPCs), including Topoisomerase-DNA adducts, during DNA r

87 resolving cytotoxic DNA-protein crosslinks (DPCs)- a function that had only been attributed to the m

88 ved in the repair of DNA-protein crosslinks (DPCs).

89 a mutants accumulate DNA-protein crosslinks (DPCs).

90 evealed that FGF2 priming protected cultured DPCs from hydrogen-peroxide-induced cell death and incre

91 em dienone photorearrangement-cycloaddition (DPC) reaction of novel cyclohexadienone substrates tethe

92 Desphenylchloridazon (DPC), the main metabolite of the herbicide chloridazon (

93 on, and degradation of desphenylchloridazon (DPC), the major degradation product of the herbicide chl

94 lt was complexed with 1,5-diphenylcarbazone (DPC) and extracted into the DMBA phase.

95 The interactions between diphenylcarbene DPC and the halogen bond donors CF3I and CF3Br were inve

96 Diphenylcarbene (DPC) generated by high-intensity laser photolysis of dip

97 Diphenylcarbene (DPC) shows a triplet ground-state lying approximately 3

98 derivatized with 1,5-diphenylcarbohydrazide (DPC) and finally detected by a miniaturized fiber optic

99 Here, CSIA provided evidence of two distinct DPC transformation processes: one shows significant chan

100 ination to give DPCs containing cleaved DNA (DPC(cl)).

101 environments, SDS and dodecylphosphocholine (DPC) micelles.

102 d bilayers as well as dodecylphosphocholine (DPC) micelles.

103 as well as correlated dodecylphosphocholine (DPC) micelle binding and membrane-induced peptide confor

104 uct was determined in dodecylphosphocholine (DPC) micelles by solution NMR spectroscopy.

105 mCp) reconstituted in dodecylphosphocholine (DPC) micelles exhibits much greater resistance to trypsi

106 NMR studies in dodecylphosphocholine (DPC) micelles suggested that the N-terminal half of the

107 tterionic detergent n-dodecylphosphocholine (DPC).

108 isolate EUH1480) in n-dodecylphosphocholine (DPC).

109 The propensity of dodecylphosphocholine (DPC), a detergent widely utilized in NMR studies of memb

110 ctivity for DOPC over dodecylphosphocholine (DPC) was also observed, and computer modeling studies sh

111 ealistic field scenario, showing that during DPC formation, (13)C/(12)C ratios of DPC were depleted i

112 O recommended concentration 0.01% mg/kg each DPC for 12 weeks, and the host-toxicity testing of the a

113 Here, we describe that the efficient DPC disassembly requires Ddi1, another conserved predict

114 aminated or dirty abdominal wounds to either DPC or PC.

115 k progression and the inability to eliminate DPCs.

116 easurements of both exogenous and endogenous DPCs in a structurally specific manner.

117 l tissues examined, suggests that endogenous DPCs may be responsible for increased risks of bone marr

118 Cells deficient in SPRTN protease exhibit DPC-induced replication stress and genome instability, m

119 ethod for measuring endogenous and exogenous DPCs presents a new perspective for the potential health

120 We found that exogenous DPCs readily accumulated in nasal respiratory tissues bu

121 ssor of smt3 (Wss1), WSS1A, is essential for DPC repair in Arabidopsis (Arabidopsis thaliana).

122 DNA replication-coupled metalloprotease for DPC repair.

123 hat there are three independent pathways for DPC repair in Arabidopsis.

124 Here we define the pathways for DPC repair in plants.

125 The time to first review for DPC was provided at between 2 and 5 days postoperatively

126 inc 3 and BRCT sub-domains is sufficient for DPC formation.

127 al-seepage water indicated that newly formed DPC could be distinguished from "old" DPC by the differe

128 n and thus protects proliferative cells from DPC toxicity.

129 er genotoxic stress conditions that generate DPCs and that the catalytic metalloprotease domain of Ca

130 rmation followed by beta-elimination to give DPCs containing cleaved DNA (DPC(cl)).

131 ihydroxy-1,4-phenylene)bis(phosphonate) (H2 -DPC), has been used to prepare a series of lithium salts

132 plains the remarkable stability of the HMCES DPC, its resistance to strand cleavage and the proteolys

133 We derived immortalized human DPC lines from balding (BAB) and non-balding (BAN) scalp

134 Surprisingly, if DPC is generated in amorphous water ice at 3 K, it is pr

135 -called differential phase contrast imaging (DPC).

136 In contrast, immortalized DPCs have high resemblance to intact dermal papilla.

137 The absence of RTEL1 impairs DPC proteolysis, suggesting that CMG must bypass the DPC

138 vidence that partial loss of Spartan impairs DPC repair and tumor suppression.

139 HLA-DP alleles categorized in DPC-2 shared certain similar peptide-binding motifs with

140 first investigation of the role of CaWss1 in DPC tolerance in C. albicans.

141 se results suggest that temporal dynamics in DPC reflect the underlying cognitive processes of this t

142 that the TMD and JM region are an ?-helix in DPC micelles, whereas residues S212-D224 at the N-termin

143 m that inferred from an NMR investigation in DPC, implying that in this detergent, the protein struct

144 tight homodimer (K(d) approximately 7 nM) in DPC micelles.

145 The loss of thermal transition observed in DPC confirms that the protein is no longer properly fold

146 ct bond formation between ortho positions in DPC, referred to as ortho,ortho' coupling.

147 (yAAC3) toward cardiolipins is preserved in DPC, thereby suggesting that DPC is a suitable environme

148 26S proteasome, implying its broader role in DPC repair.

149 cally relevant specific pore-binding site in DPC micelles, which was not observed with a different de

150 We further investigated yAAC3 solubilized in DPC and in the milder dodecylmaltoside with thermal-shif

151 promoted RANKL expression in ABCs and OPG in DPCs.

152 or the proteasome, which act as independent DPC proteases.

153 not likely responsible for red-light-induced DPC activity.

154 ast, potential contributions of drug-induced DPCs are poorly understood.

155 ious methods to measure formaldehyde-induced DPCs were incapable of discriminating between endogenous

156 finding that endogenous formaldehyde-induced DPCs were present in all tissues examined, suggests that

157 imeter study with CSIA enabled insights into DPC transformation in the field that are superior to tho

158 the conditions of matrix isolation at 25 K, DPC reacts with single water molecules embedded in solid

159 (unlabeled) and exogenous ((13)CD2-labeled) DPCs.

160 di1 is recruited to a persistent Top1cc-like DPC lesion in an S phase-dependent manner to assist in t

161 NCPs is initiated by DNA-protein cross-link (DPC(un)) formation followed by beta-elimination to give

162 capable of forming a DNA-protein cross-link (DPC) by covalently attaching to the AP site.

163 A HMCES DNA-protein cross-link (DPC) intermediate is thought to shield the AP site from

164 n method to quantify DNA-protein cross-link (DPC).

165 o formation of such DNA-protein cross-links (DPC), and their impact on cellular functions, have remai

166 DNA-protein cross-links (DPCs) are bulky DNA lesions that form both endogenously

167 DNA-protein cross-links (DPCs) are exceptionally bulky, structurally diverse DNA

168 Covalent DNA-protein cross-links (DPCs) impede replication fork progression and threaten g

169 nd cross-links, and DNA-protein cross-links (DPCs).

170 Patient-matched DPCs from balding and occipital scalp were cultured at a

171 In contrast, SPRTN-mediated DPC degradation does not require DPC polyubiquitylation

172 We screened 40 laser-microdissected DPC samples and 6 pre-invasive lesions for 9 microsatell

173 These model DPCs were subjected to in vitro replication in the prese

174 ross all studies using a fixed-effect model, DPC significantly reduced the chance of SSI (odds ratio,

175 In vitro studies with human and mouse DPCs treated with calcium hydroxide (CH) or mineral trio

176 monoepoxides produce cytotoxic and mutagenic DPC lesions within chromosomal DNA.

177 Because of their bulky nature, DPCs pose severe threats to genome stability, but previo

178 At 21% O2, DPCs showed flattened morphology and a significant reduc

179 ered carbohydrate-derived porous carbons (OC-DPCs) were first functionalized with thiol groups (-SH)

180 The Au-SH-OC-DPCs showed a good voltammetric performance in the elect

181 The Au-SH-OC-DPCs were applied for the fabrication of a new electroch

182 The Au-SH-OC-DPCs were characterized by CHN analysis, transmission el

183 dle oxidative stress compared with occipital DPCs.

184 First, surface application of DPC enabled studying its degradation in the absence of C

185 us limitations that preclude applications of DPC for ultra-high spatial resolution imaging, where the

186 of KLF4 protein was found in 86.8% cases of DPC (33/38).

187 insight into the biological consequences of DPC formation, we generated DNA-reactive protein reagent

188 related genes, suggesting that deficiency of DPC from balding scalps in fostering vascularization aro

189 The unique family of DPC-specific proteases Wss1/SPRTN targets DPC protein mo

190 This study investigated the fate of DPC by combining concentration-based methods with compou

191 Hydrolysis of DPC(cl) produces a DNA single strand break (SSB).

192 sm or exogenous agents, but the mechanism of DPC repair is not completely understood.

193 e integrity; however, the main mechanisms of DPC repair were only recently elucidated in humans and y

194 tope analysis (delta(13)C and delta(15)N) of DPC by liquid chromatography-isotope-ratio mass spectrom

195 ith a limit of precise analysis of 996 ng of DPC on-column.

196 y GC-IRMS after derivatization of >100 ng of DPC with 160-fold excess of (trimethylsilyl)diazomethane

197 Smaller numbers of DPC lesions and reduced levels of cell death were observ

198 S micelles and a single helix in presence of DPC.

199 nealing, the formal C-X insertion product of DPC is observed.

200 Furthermore, the slow rate of DPC repair provided evidence for the persistence of DPCs

201 during DPC formation, (13)C/(12)C ratios of DPC were depleted in (13)C relative to CLZ, while (15)N/

202 The most common site of DPC formation in DNA following treatment with bis-electr

203 y strong complexes with the singlet state of DPC, but only weakly interact with triplet DPC.

204 results in a switching of the spin state of DPC, the singlet complexes becoming more stable than the

205 gher excited state (most likely S2 or T1) of DPC, because it is not observed at all under thermolysis

206 Defective SPRTN-dependent clearance of DPCs is the molecular mechanism underlying RJALS, and DP

207 a central player in proteolytic cleavage of DPCs.

208 he structural and biological consequences of DPCs have not been fully elucidated due to the complexit

209 Cultures of DPCs expressed GDNF as well as its receptors, GFRalpha1

210 base excision repair (BER) and formation of DPCs is enhanced by a PARP inhibitor.

211 duced cell death and increased the number of DPCs in the SCI rat spinal cord even 7 weeks after trans

212 air provided evidence for the persistence of DPCs.

213 promotes cell survival and proliferation of DPCs and suggest that GDNF may play a multifunctional ro

214 metalloprotease SPRTN in S phase removal of DPCs, but how SPRTN is targeted to DPCs during DNA repli

215 ines a minor backup pathway in the repair of DPCs.

216 formed DPC could be distinguished from "old" DPC by the different isotopic signatures of the two DPC

217 similar peptide-binding motifs with DPC-1 or DPC-3 alleles, but significant differences were observed

218 urface membrane levels of utrophin and other DPC proteins, including beta-dystroglycan, alpha-syntrop

219 l structures of Li[B(DPC)(oxalato)] and Li[P(DPC)3] have been determined.

220 alato)], Li[B(DPC)2], Li[B(DPC)F2], and Li[P(DPC)3].

221 er DNA with dCTP opposite the 10-mer peptide DPC revealed that this bulky lesion can be accommodated

222 tile, proteolysis-based mechanism of S phase DPC repair that avoids replication fork collapse.

223 In a dose-dependent fashion, Polbeta-DPC were detected in MDA-MB-231 human cells treated with

224 Nonoxidative agents did not generate Polbeta-DPC.

225 ed with TPZ or Cu(OP)2 also incurred Polbeta-DPC.

226 or drug tirapazamine (TPZ; much more Polbeta-DPC under 1% O2 than under 21% O2) and even more robustl

227 te dL in DNA led to the formation of Polbeta-DPC in vivo.

228 the genotoxic potential of oxidative Polbeta-DPC and the biological pressure to repair them.

229 cision DNA repair pathway: oxidative Polbeta-DPC depended on the Ape1 AP endonuclease, which generate

230 Oxidative Polbeta-DPC had an unexpectedly short half-life ( approximately

231 ot blot approach to detect oxidative Polbeta-DPC in vivo.

232 mary somatosensory (S1) and dorsal premotor (DPC) cortex while trained monkeys reported whether the t

233 Widely used monolayer-cultured primary DPCs in hair-related studies often lack dermal papilla c

234 dicated that 653-nm LED irradiation promoted DPC responses relevant to tissue repair, and this is lik

235 ions suggest that FGF2 priming might protect DPCs from the post-trauma microenvironment in which DPCs

236 We use Xenopus egg extracts to recapitulate DPC repair in vitro and show that this process is couple

237 followed by retrograde pulpectomy to remove DPCs and immediate replantation into the extraction sock

238 Loss of SPRTN results in failure to repair DPCs and hypersensitivity to DPC-inducing agents.

239 late SPRTN chromatin accessibility to repair DPCs and maintain genomic stability and a healthy lifesp

240 If not repaired, DPCs can induce toxicity and mutations.

241 TN-mediated DPC degradation does not require DPC polyubiquitylation but instead depends on nascent st

242 Proteasome recruitment requires DPC polyubiquitylation, which is partially dependent on

243 Wss1 function distinctly in vivo to resolve DPCs.

244 the importance of the topsoil for retaining DPC.

245 dy shows that 3D self-assembled scaffoldless DPC engineered tissues can regenerate a vital dental pul

246 d in the root canals containing scaffoldless DPC engineered tissues was vascular, as characterized by

247 dative stress on balding and occipital scalp DPCs.

248 estimates may be confounded by simultaneous DPC formation from CLZ.

249 template, bypasses an intact leading strand DPC.

250 Strikingly, DPCs attenuated osteoclastogenesis when cocultured with

251 In this study, DPCs were treated with fibroblast growth factor-2 (FGF2)

252 Surviving DPCs could increase the availability of neurotrophic fac

253 of DPC-specific proteases Wss1/SPRTN targets DPC protein moieties for degradation, including stabiliz

254 cs provide a much better membrane model than DPC micelles in this system, and that most of the SNARE

255 is preserved in DPC, thereby suggesting that DPC is a suitable environment in which to study membrane

256 cation-coupled DPC proteolysis, we show that DPCs can be degraded by SPRTN or the proteasome, which a

257 These findings suggest that DPCs of the mesenchymal compartment have an innate abili

258 he expression of p16(INK4a), suggesting that DPCs from balding scalp are more sensitive to environmen

259 The DPC is then degraded on DNA, yielding a peptide-DNA addu

260 we identify the metalloprotease SPRTN as the DPC protease acting in metazoans.

261 on, implying that polymerase stalling at the DPC activates SPRTN on both leading and lagging strand t

262 re of the positioning of the receptor at the DPC-water interface.

263 by generating single-stranded DNA beyond the DPC.

264 eolysis, suggesting that CMG must bypass the DPC to enable proteolysis.

265 ions predict that in this second complex the DPC...I distance is shorter than the F3C...I distance, w

266 e, whereas in the first (type I) complex the DPC...I distance is, as expected, longer.

267 y palmitoylation, even in the absence of the DPC.

268 or Br, respectively, are transferred to the DPC carbene center and radical pairs are formed.

269 esults reveal a recruitment of L1CAMs to the DPC to ensure neural integrity is maintained.

270 es T-cell migration and CD43 movement to the DPC while blocking ERM association, showing that CD43 mo

271 FGF2 priming facilitated the DPCs to promote axonal regeneration and to improve locom

272 This DPC formation is specific to the presence of the natural

273 nd to liposomes, even though it does bind to DPC micelles.

274 ordered secondary structure upon binding to DPC micelles, whereas BL6 largely lacks secondary struct

275 e protease activity hypersensitizes cells to DPC trapping agents independently from Wss1 and 26S prot

276 ropose that the Ddi1 protease contributes to DPC proteolysis.

277 lic mutations in SPRTN are hypersensitive to DPC-inducing agents due to a defect in DNA replication f

278 ilure to repair DPCs and hypersensitivity to DPC-inducing agents.

279 ver, the binding affinity of each peptide to DPC micelles was determined, revealing that BL6 displaye

280 xpressing low amounts of Spartan is prone to DPC repair defects and spontaneous tumors is unknown.

281 Here we report that, in response to DPC induction, the deubiquitinase VCPIP1/VCIP135 is phos

282 1 (MUS81) results in a strong sensitivity to DPC-inducing agents.

283 emoval of DPCs, but how SPRTN is targeted to DPCs during DNA replication is unknown.

284 in part, by promoting the resolution of TOP2 DPCs.

285 t that poly-Ub regulates TDP2-catalyzed TOP2-DPC removal, and TDP2 single nucleotide polymorphisms ca

286 Topoisomerase 2 DNA-protein crosslinks (TOP2-DPCs) in a direct-reversal pathway licensed by ZATTZNF45

287 lular exposure to dihydromyricetin triggered DPCs-dependent DNA replication stress in cancer cells.

288 f DPC, but only weakly interact with triplet DPC.

289 the different isotopic signatures of the two DPC sources.

290 the suppression of the growth defects under DPC-inducing conditions.

291 was equivalent in FGF2-treated and untreated DPCs.

292 Randomized clinical trials comparing PC vs DPC were included.

293 We show here that when DPC proteolysis is blocked, the replicative DNA helicase

294 to a carbene-carbene rearrangement, whereby DPC undergoes ring expansion to phenylcycloheptatetraene

295 om the post-trauma microenvironment in which DPCs infiltrate and resident immune cells generate cytot

296 CF3I forms a second complex (type II) with DPC that is thermodynamically slightly more stable.

297 certain similar peptide-binding motifs with DPC-1 or DPC-3 alleles, but significant differences were

298 showed that replication fork collision with DPCs causes their proteolysis, followed by translesion D

299 Within DPC-2, divergence between the alleles was observed based

300 domains from a crystal structure of the YedK DPC.