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 has a triplet ground state in all of the solvents co

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

4 DPC localization of CD43 and RhoGDP dissociation inhibit

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

6 DPCs extracted from rat incisors positive for CD44, alka

7 DPCs frequently occur in cells, either as a consequence

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

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

10 It is found that the lifetime of (1)DPC is extended in acetonitrile, benzene, tetrahydrofura

11 A DPC on the lagging strand template only transiently stal

12 A DPC on the leading strand template arrests the replisome

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

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

15 r repair in which the polypeptide chain of a DPC is first reduced by proteolysis prior to NER.

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

20 gnancies but no data are yet available about DPC.

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

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

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

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

25 Although DPCs are biologically important and eight amino acids ha

26 AG3340 and DPC-A37668 administered by oral gavage at doses of 3, 10

27 Ro-31-9790, AG3340, and DPC-A37668 had no effect on normal development of the ra

28 rious selectivities (Ro-31-9790, AG3340, and DPC-A37668) was investigated in a rat model of retinopat

29 5-55) homodimer in POPC membrane bilayer and DPC surfactant micelle environments were performed using

30 3340 (MMP-2- and -9-selective inhibitor) and DPC-A37668 (MMP-2-selective inhibitor) resulted in 65% a

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

32 anscription/translation complexes blocked at DPCs.

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

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

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

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

37 ng DPC grow slower in vitro than non-balding DPC.

38 Premature senescence of balding DPC in vitro in association with expression of p16(INK4a

39 Loss of proliferative capacity of balding DPC was associated with changes in cell morphology, expr

40 sion of p16(INK4a)/pRB suggests that balding DPC are sensitive to environmental stress and identifies

41 and confirmed previous reports that balding DPC grow slower in vitro than non-balding DPC.

42 Balding DPCs had higher levels of catalase and total glutathione

43 Balding DPCs secreted higher levels of the negative hair growth

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

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

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

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

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

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

50 and 21, the protein surface was protected by DPC.

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

52 ate mechanisms of AGA, we cultured DP cells (DPC) from balding and non-balding scalp and confirmed pr

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

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

55 y to use autologous dental progenitor cells (DPCs) to form organized periodontal tissues on titanium

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

57 D) peptides, will bind to dental pulp cells (DPCs) and modulate their differentiation.

58 egration engineering with dental pulp cells (DPCs) by testing a hypothesis that DPCs generate mineral

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

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

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

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

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

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

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

66 mately localized to the distal pole complex (DPC).

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

68 raction with the dystrophin protein complex (DPC).

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

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

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

72 BRCA/FANC pathway is essential to counteract DPCs caused by aliphatic monoaldehydes.

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

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

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

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

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

78 well documented that DNA-protein crosslinks (DPC) likely play an important role with regard to the ge

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

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

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

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

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

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

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

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

87 that rat periodontal ligament (PDL)-derived DPCs can be used to bioengineer PDL tissues on titanium

88 We developed DPC-AJ1951, a 14 amino acid peptide that acts as a poten

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

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

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

92 rates has been studied with diphenylcarbene (DPC) and para-biphenyltrifluoromethylcarbene (BpCCF 3) b

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

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

95 e (DMPC) vesicles and dodecylphosphocholine (DPC) micelles as membrane mimetics.

96 stigated in water and dodecylphosphocholine (DPC) micelles by NMR spectroscopy.

97 environments, SDS and dodecylphosphocholine (DPC) micelles.

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

99 g the two proteins in dodecylphosphocholine (DPC) detergent micelles, a system that preserves the nat

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

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

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

103 ptides solubilized in dodecylphosphocholine (DPC) micelles, we found that the first analogue, MSI-78,

104 onstituted LL-37 into dodecylphosphocholine (DPC) micelles and determined its three-dimensional struc

105 ere incorporated into dodecylphosphocholine (DPC) micelles, and the reduction of amide signal intensi

106 tterionic detergent n-dodecylphosphocholine (DPC).

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

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

109 ogical behaviors, the dodecylphosphocholine (DPC) micelle-bound conformations of bifunctional peptide

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

111 k progression and the inability to eliminate DPCs.

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

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

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

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

116 veloped two plasmid-based in vivo assays for DPC repair.

117 DNA replication-coupled metalloprotease for DPC repair.

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

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

120 n and thus protects proliferative cells from DPC toxicity.

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

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

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

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

125 -called differential phase contrast imaging (DPC).

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

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

128 anic solvent (75%/25%, acetone/water) and in DPC micelles.

129 on to the compound-specific conformations in DPC micelles.

130 differs from the antiparallel dimer found in DPC micelles and may be stabilized by its strong amphipa

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

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

133 cated at the 9q 31.1-3 locus that is lost in DPC at high frequency.

134 Solution NMR experiments of M2TM in DPC micelles indicate that drug binding causes significa

135 ociation constant of approximately 120 nM in DPC micelles.

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

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

138 of the human and rat IAPP(1-19) peptides in DPC micelles.

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

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

141 emonstrate a role for the 26 S proteasome in DPC repair.

142 With the protein in DPC (dodecylphosphocholine) micelles, we used manganous

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

144 nalysis of the structural dynamics of SLN in DPC micelles shows this polypeptide to be partitioned in

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

146 ferent from a recently reported structure in DPC micelles where bending of the two beta-strands was o

147 promoted RANKL expression in ABCs and OPG in DPCs.

148 s not hypersensitive to either aza-C-induced DPC formation or streptolydigin, indicating that Mfd is

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

150 ated that GDNF counteracted TNFalpha-induced DPC cytotoxicity, suggesting that GDNF may be cytoprotec

151 er transcriptional blockage by aza-C-induced DPCs.

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

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

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

155 The CFTR inhibitors DPC, GlyH-101 and CFTRinh-172 all significantly reduced

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

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

158 X foci occurred with DPC formation, and like DPC, persisted after aminoflavone removal.

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

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

161 tructural aspects of DNA-protein cross-link (DPC) formation.

162 minoflavone induced DNA-protein cross-links (DPC) and DNA single-strand breaks (SSB).

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

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

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

166 in the formation of DNA-protein cross-links (DPCs) as a primary genotoxic effect.

167 ine (aza-C) induces DNA-protein cross-links (DPCs) between cytosine methyltransferase and DNA as the

168 DNA-protein cross-links (DPCs) in nucleosome core particles (NCPs), the fundament

169 DNA-protein cross-links (DPCs) present a formidable obstacle to cellular processe

170 rmation of covalent DNA-protein cross-links (DPCs) with repair enzymes such as DNA polymerase beta (p

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

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

173 f the full-length HhaI DNA methyltransferase-DPC yields a substrate that is efficiently removed by a

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

175 ety of detergents, including SDS, DPC, mixed DPC/SDS, and LPPG micelles, indicating that the peptide

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

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

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

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

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

181 dissociation inhibitor, as well as the novel DPC protein Src homology region 2 domain-containing phos

182 However, recruitment of three novel DPC proteins, ezrin binding protein of 50 kDa, Csk bindi

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

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

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

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

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

188 dle oxidative stress compared with occipital DPCs.

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

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

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

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

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

194 hyltransferase, indicating the importance of DPC formation.

195 Aminoflavone induced high levels of DPC and much lower level of SSB than camptothecin, which

196 camptothecin, which induces equal levels of DPC and SSB due to the trapping topoisomerase I-DNA comp

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

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

199 The structures determined in the presence of DPC micelles are compared to available models of 1 or CC

200 R conformational analysis in the presence of DPC micelles.

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

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

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

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

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

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

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

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

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

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

211 Elimination of DPCs is critical for cell survival because their persist

212 t the mechanisms leading to the formation of DPCs in NCPs, and the exact sites of these lesions in ch

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

214 cess for dL lesions that avoids formation of DPCs that would threaten the integrity of DNA and perhap

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

216 air provided evidence for the persistence of DPCs.

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

218 ion of the characteristics and properties of DPCs formed in vivo and will be helpful in identifying b

219 The precise structure of DPCs depended on the nature of the oxidant and cross-lin

220 l injection of 5, 15, and 50 mg/mL AG3340 or DPC-A37668 for 6 days after variable oxygen exposure res

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

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

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

224 Rat PDL DPCs also exhibited differentiative potential characteri

225 proof-of-principle findings suggest that PDL DPCs can organize periodontal tissues in the jaw, at the

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

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

228 been characterized in dodecyl phosphocholin (DPC) micelles by UV-vis, CD spectroscopy, gel electropho

229 tructure in either a dodecyl phosphocholine (DPC) micelle or a dimyristoyl phosphatidylcholine (DMPC)

230 D) and the detergent dodecyl phosphocholine (DPC) were studied using NMR spectroscopy.

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

232 Nonoxidative agents did not generate Polbeta-DPC.

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

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

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

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

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

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

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

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

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

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

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

244 Using paramagnetic probes and protein-DPC nuclear Overhauser effects (NOEs), we define portion

245 ected for clinical development as razaxaban (DPC 906, BMS-561389).

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

247 assay shows that in nontranscribed regions, DPC repair is greater than 60% in 6 h.

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

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

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

251 Wss1 function distinctly in vivo to resolve DPCs.

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

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

254 dative stress on balding and occipital scalp DPCs.

255 d in a variety of detergents, including SDS, DPC, mixed DPC/SDS, and LPPG micelles, indicating that t

256 Strikingly, DPCs attenuated osteoclastogenesis when cocultured with

257 To study DPC repair, we have used DNA methyltransferases to gener

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

259 Surviving DPCs could increase the availability of neurotrophic fac

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

261 For CCK and 1, these comparisons show that DPC micelle associated structures duplicate some importa

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

263 green fluorescent protein demonstrates that DPCs in transcribed genes are also repaired.

264 lp cells (DPCs) by testing a hypothesis that DPCs generate mineralized tissue on titanium.

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

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

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

268 The O(2)-carbonyl is protected as the DPC derivative, and the trityl group is removed.

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

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

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

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

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

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

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

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

277 immunological synapse before movement to the DPC.

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

279 e characterization of trypsin digests of the DPCs.

280 Furthermore, these DPCs are stable for days at 37 degrees C, indicating tha

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

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

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

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

285 s between a G*+ and some amino acids lead to DPC formation in both DNA-peptide and DNA-protein comple

286 s, we hypothesized that DNA CT could lead to DPC formation within NCPs.

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

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

289 vo host cell reactivation assay and a unique DPC indicates that NER has a role in the repair of this

290 ed DNA methyltransferases to generate unique DPC adducts in oligodeoxyribonucleotides or plasmids to

291 To examine the repair of that unique DPC, we have developed two plasmid-based in vivo assays

292 was equivalent in FGF2-treated and untreated DPCs.

293 reen of a small compound collection by using DPC-AJ1951 as the ligand.

294 Randomized clinical trials comparing PC vs DPC were included.

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

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

297 aded calbindin D(9k) does not associate with DPC micelles.

298 sence of Ca(2+), the protein associates with DPC micelles.

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

300 When it interacts with DPC, LL-37 is adsorbed on the surface of the micelle wit

301 Gamma-H2AX foci occurred with DPC formation, and like DPC, persisted after aminoflavon