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1 ICLs) induced by drugs such as cisplatin and psoralen.
2 t to angelicin but eliminated recruitment to psoralen.
3 henylphosphine oxide-1, or 5-(4-phenylbutoxy)psoralen.
4 ific photoadduct formation by the conjugated psoralen.
5 on, we tested dimeric bis-PNAs conjugated to psoralen.
6 account for some of the mutations induced by psoralens.
8 immunosuppressant PAP-1 (5-(4-phenoxybutoxy)psoralen), a high-affinity blocker of Kv1.3 channels in
10 t, largely accounting for the differences in psoralen accessibility between active and inactive genes
13 inked to psoralen, have been shown to direct psoralen adduct formation in cells, leading to mutagenes
15 nd are required for XPD cross-linking to the psoralen-adducted base, neither XPA nor XPC is cross-lin
19 , a more rapid removal of digoxigenin-tagged psoralen adducts, and decreased cellular sensitivity to
20 e helices, even in the absence of associated psoralen adducts, are able to provoke DNA repair and cau
25 re densely biotinylated using a biotinylated psoralen analog plus UVA light and hybridized on microar
27 further characterized the inhibition of four psoralen and coumarin derivatives toward ALDH2 and compa
33 tation equilibrium of 3'-linked intercalated psoralen and to develop conditions that lead to preferen
37 king the ciclosporin who had been exposed to psoralen and ultraviolet-A light (PUVA) and other treatm
38 elix-forming oligonucleotides were linked to psoralen and used to form triplexes on the plasmids.
40 om 30 minute reactions were crosslinked with psoralen and UV, linearized with restriction enzymes and
42 s are widely consumed foods that are rich in psoralens and furocoumarins, a group of naturally occurr
44 patients with severe psoriasis treated with psoralens and ultraviolet-A therapy (PUVA) who enrolled
45 from Xenopus laevis has been shown to cleave psoralen- and abasic site-induced ICLs in Xenopus egg ex
46 ary using this system identified the angular psoralen angelicin and the insect growth regulator fenox
48 Upon near-ultraviolet irradiation (360 nm), psoralen-Asp41-Tat(37-72) cross-linked to a single site
50 ks was dependent on precise placement of the psoralen by the triple helix-forming oligonucleotide at
53 s (TFOs) linked to DNA damaging agents (e.g. psoralen) can stimulate HR, providing the potential to i
56 imethylaminopropylamine, in a 10-nucleotide, psoralen-conjugated TFO confers substantial increases in
58 was induced efficiently by injection of both psoralen-conjugated TFOs (followed by long-wave UVA ligh
60 Interactions between nuclease-resistant, 5'-psoralen-conjugated, chimeric methylphosphonate oligodeo
61 of pyrimidine deoxyribo- or 2'-O-methylribo-psoralen-conjugated, triplex-forming oligonucleotides, p
67 ation of TBP from DNA was not prevented by a psoralen cross-link positioned immediately preceding the
71 porter gene, we showed that a single defined psoralen cross-link was removed in repair-proficient cel
72 l incisions 5' to the cross-linked base of a psoralen cross-link, generating a gap of 22 to 28 nucleo
74 epair of plasmid molecules carrying a single psoralen cross-link, psoralen monoadduct, or double-stra
77 understand the relationship between triplex psoralen cross-linking products and the fate of RNA Pol
79 These studies have low sensitivity, because psoralen cross-linking suggested few (estimated <10%) of
85 comparison, the ability of triplex-directed psoralen cross-links to induce recombination was only pa
87 repair of laser-localized lesions formed by psoralen (cross-links/monoadducts) and angelicin (only m
91 develop PARIS, a method based on reversible psoralen crosslinking for global mapping of RNA duplexes
93 ve fraction from yeast nuclei, and selective psoralen crosslinking was used to distinguish between ac
95 demonstrate that TFOs can be used to direct psoralen crosslinks adjacent to a gene as a way of activ
96 protection assay to detect triplex-directed psoralen crosslinks in genomic DNA prepared from TFO-tra
98 blocked by infrequent, randomly distributed psoralen crosslinks, but the bacterial population was ab
99 se that RPA70 makes the initial contact with psoralen-damaged DNA but that within preincision complex
105 A glycosylases Nei and NEIL1 excise unhooked psoralen-derived ICLs in three-stranded DNA via hydrolys
106 lusion, the Nei-like DNA glycosylases unhook psoralen-derived ICLs in various DNA structures via a ge
107 ikingly, crosslinking of the siRNA duplex by psoralen did not completely block RNA interference, indi
108 WRN facilitates ATM activation in cells with psoralen DNA cross-link-induced collapsed replication fo
111 PA has also been suggested to play a role in psoralen DNA interstrand cross-link (ICL) repair, but a
112 ucts low-efficiency nonmutagenic bypass of a psoralen DNA interstrand cross-link (ICL), whose structu
114 -forming oligonucleotides (TFOs) to direct a psoralen-DNA interstrand cross-link (ICL) to a specific
115 TPE can initiate photochemistry resulting in psoralen-DNA photoadducts, target DNA sequences were inc
117 cs on platelet membrane extracts showed that psoralen forms adducts with unsaturated carbon bonds of
118 h purine and pyrimidine TFOs, when linked to psoralen, have been shown to direct psoralen adduct form
120 designed a model substrate DNA with a single psoralen ICL at a three-way junction (Y-shaped DNA), whi
125 generated a defined substrate with a single psoralen ICL that mimics a postincision structure genera
126 triplex technology to direct a site-specific psoralen ICL to a target DNA substrate to determine whet
127 the UvrABC nuclease cleaved the TFO-directed psoralen ICL with a greater efficiency than that of the
129 1 (HMGB1) protein bound to triplex-directed psoralen ICLs (TFO-ICLs) in vitro, cooperatively with NE
130 ors believed to be involved in the repair of psoralen ICLs [xeroderma pigmentosum (XP)-A, XP-C, XP-F,
131 simultaneously, demonstrating not only that psoralen ICLs are recognized by XPC-hHR23B alone, but al
132 The induction of p53 phosphorylation by psoralen ICLs did not require factors believed to be inv
133 kade of transcription and DNA replication by psoralen ICLs during S-phase elicits a strong apoptotic
136 protein complexes were also observed to bind psoralen ICLs simultaneously, demonstrating not only tha
137 binds with high affinity and specificity to psoralen ICLs, and interacts with the essential NER prot
138 eta complex is shown to specifically bind to psoralen ICLs, and this binding is stimulated by the add
139 sults demonstrate that XPC-hHR23B recognizes psoralen ICLs, which have a structure fundamentally diff
142 f a Holliday junction, suggesting a role for psoralen in the mechanism to initiate repair of psoralen
143 sing the docked poses of 29 (the most active psoralen in the series) as templates for alignment of th
144 nocytogenes as a model platform, recombinant psoralen-inactivated Lm DeltauvrAB vaccines induced pote
146 oxidative DNA damage, as well as trioxsalen (psoralen)-induced DNA interstrand crosslinks, but not to
147 Here we report that human NEIL3 cleaves psoralen-induced DNA-DNA cross-links in three-stranded a
148 rthermore, while Nei and NEIL1 also cleave a psoralen-induced four-stranded DNA substrate to generate
149 The HMT-adduct of d(CCGCTAGCGG) forms a psoralen-induced Holliday junction, showing for the firs
151 produce monoadducts and ICLs and found that psoralen-induced ICLs induced phosphorylation of the Ser
152 CJ recruitment to laser-induced DSBs but not psoralen-induced ICLs is dependent on nuclease-active MR
154 136R, and E181K, to oxidative DNA damage and psoralen-induced interstrand crosslinks was differential
156 photoadducts directed by PNAs conjugated to psoralen-induced mutations at frequencies in the range o
158 in production of incisions at the site of a psoralen interstrand cross-link and that in Fanconi anem
159 oduction of the 5' incision at the site of a psoralen interstrand cross-link as well as the 3' incisi
163 nuclei, specifically binds to DNA containing psoralen interstrand cross-links and that the FANCA, FAN
165 To elucidate factors affecting TFO-directed psoralen interstrand crosslink (ICL)-induced recombinati
166 vity, purified NEIL1 protein bound stably to psoralen interstrand crosslink-containing synthetic olig
169 mage, are in close physical proximity to the psoralen lesion and thus are cross-linked to the damaged
170 XPF-ERCC1 complex makes an incision 5' to a psoralen lesion on Y-shaped DNA in a damage-dependent ma
172 r a 72 h period, suggesting that TFO-induced psoralen lesions are not repaired on this time scale.
175 We have constructed chemically modified, psoralen-linked TFOs that mediate site-specific mutagene
180 o-severe disease if they had been prescribed psoralen, methotrexate, cyclosporine, acitretin, adalimu
181 at(42-72) and Tat(37-72), and incorporated a psoralen-modified amino acid at position 41 during solid
186 onucleotide third strands with a 3'-terminal psoralen moiety attached by linkers that differ in lengt
188 igonucleotides attached with a photoreactive psoralen molecule (psoTFO) can be used to induce site-sp
190 cules carrying a single psoralen cross-link, psoralen monoadduct, or double-strand break in yeast cel
191 ence, the kinetics of formation and yield of psoralen monoadducts and crosslinks with pyrimidine resi
193 nnel blockers Margatoxin, 5-(4-Phenoxybutoxy)psoralen, or broad-spectrum K(+) channel blocker 4-Amino
194 compound of this series, 5-(4-phenoxybutoxy)psoralen (PAP-1), blocks Kv1.3 in a use-dependent manner
197 derived from photoaffinity cross-linking by psoralen, phenphi (cis-Rh(1,10-phenanthroline)(9,10-phen
198 GM847, GM847-Tert, and WI-38 VA13 ALT cells, psoralen photo-cross-linked in situ, and the telomere re
199 te the mechanism of photoadduct-formation by psoralen photo-cross-linking, triplex structures were ge
203 eriments that monitored the formation of the psoralen photoadducts also suggested that the length of
204 Northern blots indicated that TFO-directed psoralen photoadducts blocked progression of RNA polymer
206 he only pathway that can metabolize targeted psoralen photoadducts into recombinagenic intermediates.
207 e mechanism associated with the formation of psoralen photoadducts that are directed by psoTFO during
208 soTFOs) were designed to deliver UVA-induced psoralen photoadducts to two distinct sequences within t
211 DNA duplex generated two distinct groups of psoralen photoadducts: monoadducts and psoralen interstr
212 site-specific cross-linking method based on psoralen photochemistry to determine the effect of core
214 d for their ability to form triplex-directed psoralen photoproducts with both the mutant T residue of
216 ultimately offering the potential to define psoralen plus ultraviolet A dosage regimes in terms of m
217 nificantly altered the threshold response to psoralen plus ultraviolet A erythema but not the rate of
218 etectable effect on the maximum slope of the psoralen plus ultraviolet A erythema dose-response curve
221 tment with standardized green tea extract in psoralen plus ultraviolet A treatment populations abroga
222 ed green tea extract per cm2 30 min prior to psoralen plus ultraviolet A treatment resulted in an alm
224 Derm, a reconstituted human skin equivalent, psoralen plus ultraviolet A-induced 8-methoxypsoralen-DN
226 violet A treatment populations abrogates the psoralen plus ultraviolet A-induced photochemical damage
227 to reduce the risk of cancer development in psoralen plus ultraviolet A-treated populations are high
228 traviolet A. c-fos and p53 positive cells in psoralen plus ultraviolet A-treated skin were found to b
230 ein induction following a single exposure to psoralen plus ultraviolet A. c-fos and p53 positive cell
233 are hypersensitive to DNA damage induced by psoralen plus UVA irradiation (PUVA) or UVC radiation, s
235 argeting in the episomal shuttle vector, the psoralen-PNA-induced mutation frequency was 0.13%, 3.5-f
237 orming oligonucleotides (TFOs) that target a psoralen (pso) interstrand crosslink to a specific chrom
238 ple helix-forming oligonucleotides linked to psoralen (pso-TFO) to introduce a DNA interstrand cross-
239 helix-forming DNA oligonucleotides linked to psoralen (psoTFOs) were designed to deliver UVA-induced
240 a DNA interstrand crosslinking (ICL) agent, psoralen (pTFO-ICLs), to improve the gene targeting effi
241 and the KV1.3/1.5 blocker 5-(4-phenylbutoxy)psoralen reduced H2O2-elicited dilation to a similar ext
245 We conclude that directing DNA damage with psoralen-TFOs is an efficient and specific means for blo
246 of cells after transfection with plasmid and psoralen-TFOs produced photoadducts inside the cells and
248 rate the ability of bis-PNAs conjugated with psoralen to mediate site-specific gene modification, and
249 UV-A and UV-B, when used in combination with psoralens, topical corticosteroids, vitamin D analogues,
251 A tetrafluorphenyl (TFP) ester of trimethyl psoralen (trioxalen) was synthesized, and the procedure
252 e time of maximal erythema, the slope of the psoralen ultraviolet A dose-response curve was approxima
254 we determined that only 67% of mean maximum psoralen ultraviolet A erythemal intensity had developed
256 gs, it seems appropriate to consider whether psoralen ultraviolet A minimal phototoxic dose measureme
257 esponses to ultraviolet B, ultraviolet A and psoralen ultraviolet A were assessed visually and using
258 r to determine the separate contributions of psoralen + ultraviolet A and other ultraviolet exposures
259 here was some evidence that high exposure to psoralen + ultraviolet A before a first basal cell carci
261 s with low pre-first squamous cell carcinoma psoralen + ultraviolet A exposure, 95% confidence interv
263 lop a squamous cell carcinoma after starting psoralen + ultraviolet A therapy should be closely monit
265 rates of post-first squamous cell carcinoma psoralen + ultraviolet A treatment also were associated
268 he development of nonmelanoma skin cancer in psoralen + ultraviolet A-treated patients, but these mut
271 carcinomas were studied in a cohort of 1380 psoralen + ultraviolet A-treated psoriasis patients pros
272 ultraviolet B for skin cancer development in psoralen + ultraviolet A-treated psoriasis patients.
273 let-type mutations, two (5%) tumors had only psoralen + ultraviolet A-type mutations, and 18 (49%) tu
276 er risk among patients who have discontinued psoralen+ultraviolet A and the risk of a first tumor wit
279 onmelanoma skin cancer and prior exposure to psoralen+ultraviolet A remains an important issue in the
280 5 years, about 7% of patients with < or =200 psoralen+ultraviolet A treatments and more than half of
285 gulation of CYP2S1 by ultraviolet radiation, psoralen-ultraviolet A (PUVA), and topical drugs used to
292 ous times after introduction into cells, the psoralen was activated by exposure to long wave ultravio
293 was shown to establish the position at which psoralen was added to the target DNA duplex and determin
295 Gene activation by pso-TFOs in which the psoralen was linked to the TFO via a disulfide bond was
298 clude topical corticosteroids, phototherapy (psoralen with UVA or UVB), topical chemotherapy, topical
299 o attract TnsC, we show that the location of psoralen within the pyrimidine motif triplex does alter
300 roblasts were incubated with tritium-labeled psoralen without TFO to maximize detectable damage and i
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