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1 ific photoadduct formation by the conjugated psoralen.
2 on, we tested dimeric bis-PNAs conjugated to psoralen.
3 henylphosphine oxide-1, or 5-(4-phenylbutoxy)psoralen.
4 ICLs) induced by drugs such as cisplatin and psoralen.
5 t to angelicin but eliminated recruitment 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
34 tation equilibrium of 3'-linked intercalated psoralen and to develop conditions that lead to preferen
38 king the ciclosporin who had been exposed to psoralen and ultraviolet-A light (PUVA) and other treatm
39 elix-forming oligonucleotides were linked to psoralen and used to form triplexes on the plasmids.
41 om 30 minute reactions were crosslinked with psoralen and UV, linearized with restriction enzymes and
43 s are widely consumed foods that are rich in psoralens and furocoumarins, a group of naturally occurr
45 patients with severe psoriasis treated with psoralens and ultraviolet-A therapy (PUVA) who enrolled
46 from Xenopus laevis has been shown to cleave psoralen- and abasic site-induced ICLs in Xenopus egg ex
47 ary using this system identified the angular psoralen angelicin and the insect growth regulator fenox
50 Upon near-ultraviolet irradiation (360 nm), psoralen-Asp41-Tat(37-72) cross-linked to a single site
52 ks was dependent on precise placement of the psoralen by the triple helix-forming oligonucleotide at
55 s (TFOs) linked to DNA damaging agents (e.g. psoralen) can stimulate HR, providing the potential to i
57 imethylaminopropylamine, in a 10-nucleotide, psoralen-conjugated TFO confers substantial increases in
59 was induced efficiently by injection of both psoralen-conjugated TFOs (followed by long-wave UVA ligh
61 Interactions between nuclease-resistant, 5'-psoralen-conjugated, chimeric methylphosphonate oligodeo
62 of pyrimidine deoxyribo- or 2'-O-methylribo-psoralen-conjugated, triplex-forming oligonucleotides, p
68 ation of TBP from DNA was not prevented by a psoralen cross-link positioned immediately preceding the
72 porter gene, we showed that a single defined psoralen cross-link was removed in repair-proficient cel
73 l incisions 5' to the cross-linked base of a psoralen cross-link, generating a gap of 22 to 28 nucleo
75 epair of plasmid molecules carrying a single psoralen cross-link, psoralen monoadduct, or double-stra
78 understand the relationship between triplex psoralen cross-linking products and the fate of RNA Pol
80 These studies have low sensitivity, because psoralen cross-linking suggested few (estimated <10%) of
86 comparison, the ability of triplex-directed psoralen cross-links to induce recombination was only pa
88 repair of laser-localized lesions formed by psoralen (cross-links/monoadducts) and angelicin (only m
92 develop PARIS, a method based on reversible psoralen crosslinking for global mapping of RNA duplexes
94 ve fraction from yeast nuclei, and selective psoralen crosslinking was used to distinguish between ac
96 demonstrate that TFOs can be used to direct psoralen crosslinks adjacent to a gene as a way of activ
97 protection assay to detect triplex-directed psoralen crosslinks in genomic DNA prepared from TFO-tra
99 blocked by infrequent, randomly distributed psoralen crosslinks, but the bacterial population was ab
100 se that RPA70 makes the initial contact with psoralen-damaged DNA but that within preincision complex
106 A glycosylases Nei and NEIL1 excise unhooked psoralen-derived ICLs in three-stranded DNA via hydrolys
107 lusion, the Nei-like DNA glycosylases unhook psoralen-derived ICLs in various DNA structures via a ge
108 ikingly, crosslinking of the siRNA duplex by psoralen did not completely block RNA interference, indi
109 WRN facilitates ATM activation in cells with psoralen DNA cross-link-induced collapsed replication fo
112 PA has also been suggested to play a role in psoralen DNA interstrand cross-link (ICL) repair, but a
113 ucts low-efficiency nonmutagenic bypass of a psoralen DNA interstrand cross-link (ICL), whose structu
115 -forming oligonucleotides (TFOs) to direct a psoralen-DNA interstrand cross-link (ICL) to a specific
116 TPE can initiate photochemistry resulting in psoralen-DNA photoadducts, target DNA sequences were inc
118 tion, 8-p-anisyl-5-p-cyanophenyl-substituted psoralen exhibits aggregation-induced emission propertie
119 cs on platelet membrane extracts showed that psoralen forms adducts with unsaturated carbon bonds of
120 h purine and pyrimidine TFOs, when linked to psoralen, have been shown to direct psoralen adduct form
122 designed a model substrate DNA with a single psoralen ICL at a three-way junction (Y-shaped DNA), whi
127 generated a defined substrate with a single psoralen ICL that mimics a postincision structure genera
128 triplex technology to direct a site-specific psoralen ICL to a target DNA substrate to determine whet
129 the UvrABC nuclease cleaved the TFO-directed psoralen ICL with a greater efficiency than that of the
131 epistatic with both NEIL3 and FA pathways in psoralen-ICL repair, suggesting that TRAIP may function
134 NEIL3 pathway is the major pathway to repair psoralen-ICL through a unique DSB-free mechanism in huma
135 3 pathway is the major pathway for repairing psoralen-ICL, and the FA/BRCA pathway is only activated
137 1 (HMGB1) protein bound to triplex-directed psoralen ICLs (TFO-ICLs) in vitro, cooperatively with NE
138 ors believed to be involved in the repair of psoralen ICLs [xeroderma pigmentosum (XP)-A, XP-C, XP-F,
139 simultaneously, demonstrating not only that psoralen ICLs are recognized by XPC-hHR23B alone, but al
140 The induction of p53 phosphorylation by psoralen ICLs did not require factors believed to be inv
141 kade of transcription and DNA replication by psoralen ICLs during S-phase elicits a strong apoptotic
144 protein complexes were also observed to bind psoralen ICLs simultaneously, demonstrating not only tha
145 binds with high affinity and specificity to psoralen ICLs, and interacts with the essential NER prot
146 eta complex is shown to specifically bind to psoralen ICLs, and this binding is stimulated by the add
147 sults demonstrate that XPC-hHR23B recognizes psoralen ICLs, which have a structure fundamentally diff
151 f a Holliday junction, suggesting a role for psoralen in the mechanism to initiate repair of psoralen
152 sing the docked poses of 29 (the most active psoralen in the series) as templates for alignment of th
153 nocytogenes as a model platform, recombinant psoralen-inactivated Lm DeltauvrAB vaccines induced pote
155 oxidative DNA damage, as well as trioxsalen (psoralen)-induced DNA interstrand crosslinks, but not to
156 Here we report that human NEIL3 cleaves psoralen-induced DNA-DNA cross-links in three-stranded a
157 rthermore, while Nei and NEIL1 also cleave a psoralen-induced four-stranded DNA substrate to generate
158 The HMT-adduct of d(CCGCTAGCGG) forms a psoralen-induced Holliday junction, showing for the firs
160 produce monoadducts and ICLs and found that psoralen-induced ICLs induced phosphorylation of the Ser
161 CJ recruitment to laser-induced DSBs but not psoralen-induced ICLs is dependent on nuclease-active MR
163 136R, and E181K, to oxidative DNA damage and psoralen-induced interstrand crosslinks was differential
165 photoadducts directed by PNAs conjugated to psoralen-induced mutations at frequencies in the range o
167 in production of incisions at the site of a psoralen interstrand cross-link and that in Fanconi anem
168 oduction of the 5' incision at the site of a psoralen interstrand cross-link as well as the 3' incisi
172 nuclei, specifically binds to DNA containing psoralen interstrand cross-links and that the FANCA, FAN
174 To elucidate factors affecting TFO-directed psoralen interstrand crosslink (ICL)-induced recombinati
175 vity, purified NEIL1 protein bound stably to psoralen interstrand crosslink-containing synthetic olig
178 mage, are in close physical proximity to the psoralen lesion and thus are cross-linked to the damaged
179 XPF-ERCC1 complex makes an incision 5' to a psoralen lesion on Y-shaped DNA in a damage-dependent ma
181 r a 72 h period, suggesting that TFO-induced psoralen lesions are not repaired on this time scale.
184 We have constructed chemically modified, psoralen-linked TFOs that mediate site-specific mutagene
189 o-severe disease if they had been prescribed psoralen, methotrexate, cyclosporine, acitretin, adalimu
190 at(42-72) and Tat(37-72), and incorporated a psoralen-modified amino acid at position 41 during solid
195 onucleotide third strands with a 3'-terminal psoralen moiety attached by linkers that differ in lengt
197 igonucleotides attached with a photoreactive psoralen molecule (psoTFO) can be used to induce site-sp
199 cules carrying a single psoralen cross-link, psoralen monoadduct, or double-strand break in yeast cel
200 ence, the kinetics of formation and yield of psoralen monoadducts and crosslinks with pyrimidine resi
202 nnel blockers Margatoxin, 5-(4-Phenoxybutoxy)psoralen, or broad-spectrum K(+) channel blocker 4-Amino
203 compound of this series, 5-(4-phenoxybutoxy)psoralen (PAP-1), blocks Kv1.3 in a use-dependent manner
206 derived from photoaffinity cross-linking by psoralen, phenphi (cis-Rh(1,10-phenanthroline)(9,10-phen
207 GM847, GM847-Tert, and WI-38 VA13 ALT cells, psoralen photo-cross-linked in situ, and the telomere re
208 te the mechanism of photoadduct-formation by psoralen photo-cross-linking, triplex structures were ge
212 eriments that monitored the formation of the psoralen photoadducts also suggested that the length of
213 Northern blots indicated that TFO-directed psoralen photoadducts blocked progression of RNA polymer
215 he only pathway that can metabolize targeted psoralen photoadducts into recombinagenic intermediates.
216 e mechanism associated with the formation of psoralen photoadducts that are directed by psoTFO during
217 soTFOs) were designed to deliver UVA-induced psoralen photoadducts to two distinct sequences within t
220 DNA duplex generated two distinct groups of psoralen photoadducts: monoadducts and psoralen interstr
221 site-specific cross-linking method based on psoralen photochemistry to determine the effect of core
223 d for their ability to form triplex-directed psoralen photoproducts with both the mutant T residue of
225 ultimately offering the potential to define psoralen plus ultraviolet A dosage regimes in terms of m
226 nificantly altered the threshold response to psoralen plus ultraviolet A erythema but not the rate of
227 etectable effect on the maximum slope of the psoralen plus ultraviolet A erythema dose-response curve
230 ed green tea extract per cm2 30 min prior to psoralen plus ultraviolet A treatment resulted in an alm
236 are hypersensitive to DNA damage induced by psoralen plus UVA irradiation (PUVA) or UVC radiation, s
238 argeting in the episomal shuttle vector, the psoralen-PNA-induced mutation frequency was 0.13%, 3.5-f
240 orming oligonucleotides (TFOs) that target a psoralen (pso) interstrand crosslink to a specific chrom
241 ple helix-forming oligonucleotides linked to psoralen (pso-TFO) to introduce a DNA interstrand cross-
242 helix-forming DNA oligonucleotides linked to psoralen (psoTFOs) were designed to deliver UVA-induced
243 a DNA interstrand crosslinking (ICL) agent, psoralen (pTFO-ICLs), to improve the gene targeting effi
244 and the KV1.3/1.5 blocker 5-(4-phenylbutoxy)psoralen reduced H2O2-elicited dilation to a similar ext
249 We conclude that directing DNA damage with psoralen-TFOs is an efficient and specific means for blo
250 of cells after transfection with plasmid and psoralen-TFOs produced photoadducts inside the cells and
252 rate the ability of bis-PNAs conjugated with psoralen to mediate site-specific gene modification, and
253 UV-A and UV-B, when used in combination with psoralens, topical corticosteroids, vitamin D analogues,
255 e time of maximal erythema, the slope of the psoralen ultraviolet A dose-response curve was approxima
256 we determined that only 67% of mean maximum psoralen ultraviolet A erythemal intensity had developed
258 gs, it seems appropriate to consider whether psoralen ultraviolet A minimal phototoxic dose measureme
259 r to determine the separate contributions of psoralen + ultraviolet A and other ultraviolet exposures
260 here was some evidence that high exposure to psoralen + ultraviolet A before a first basal cell carci
262 s with low pre-first squamous cell carcinoma psoralen + ultraviolet A exposure, 95% confidence interv
264 lop a squamous cell carcinoma after starting psoralen + ultraviolet A therapy should be closely monit
266 rates of post-first squamous cell carcinoma psoralen + ultraviolet A treatment also were associated
269 he development of nonmelanoma skin cancer in psoralen + ultraviolet A-treated patients, but these mut
272 carcinomas were studied in a cohort of 1380 psoralen + ultraviolet A-treated psoriasis patients pros
273 ultraviolet B for skin cancer development in psoralen + ultraviolet A-treated psoriasis patients.
274 let-type mutations, two (5%) tumors had only psoralen + ultraviolet A-type mutations, and 18 (49%) tu
277 er risk among patients who have discontinued psoralen+ultraviolet A and the risk of a first tumor wit
280 onmelanoma skin cancer and prior exposure to psoralen+ultraviolet A remains an important issue in the
281 5 years, about 7% of patients with < or =200 psoralen+ultraviolet A treatments and more than half of
286 gulation of CYP2S1 by ultraviolet radiation, psoralen-ultraviolet A (PUVA), and topical drugs used to
293 ous times after introduction into cells, the psoralen was activated by exposure to long wave ultravio
294 was shown to establish the position at which psoralen was added to the target DNA duplex and determin
296 Gene activation by pso-TFOs in which the psoralen was linked to the TFO via a disulfide bond was
299 clude topical corticosteroids, phototherapy (psoralen with UVA or UVB), topical chemotherapy, topical
300 o attract TnsC, we show that the location of psoralen within the pyrimidine motif triplex does alter
301 roblasts were incubated with tritium-labeled psoralen without TFO to maximize detectable damage and i