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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.
7                                              Psoralen 4 (Pso4) is an evolutionarily conserved protein
8  immunosuppressant PAP-1 (5-(4-phenoxybutoxy)psoralen), a high-affinity blocker of Kv1.3 channels in
9         The assay is based on mutagenesis by psoralen, a photoactive DNA cross-linker.
10 t, largely accounting for the differences in psoralen accessibility between active and inactive genes
11 l are transcribed and maintained in an open, psoralen-accessible conformation.
12  enhanced effectiveness of the clamp ODNs to psoralen activation.
13 inked to psoralen, have been shown to direct psoralen adduct formation in cells, leading to mutagenes
14 , neither XPA nor XPC is cross-linked to the psoralen adduct.
15 nd are required for XPD cross-linking to the psoralen-adducted base, neither XPA nor XPC is cross-lin
16 excision nuclease assembled at the site of a psoralen-adducted thymine.
17              We previously demonstrated that psoralen adducts targeted by triple-helix-forming oligon
18                                   Removal of psoralen adducts was blocked in XPC-deficient cells but
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
21 t mutations induced by third-strand-directed psoralen adducts.
22         XPC protein was rapidly recruited to psoralen adducts.
23            In addition to the ICL formation, psoralens also readily form various monoadducts (MAs) wi
24 or pathogen inactivation using the synthetic psoralen amotosalen HCl.
25 re densely biotinylated using a biotinylated psoralen analog plus UVA light and hybridized on microar
26 NEIL3 is the primary unhooking mechanism for psoralen and abasic site ICLs.
27 further characterized the inhibition of four psoralen and coumarin derivatives toward ALDH2 and compa
28                      The TFOs were linked to psoralen and designed to target and mutagenize a site in
29                                              Psoralen and its derivatives are widely applied for the
30 sensitive to photochemical inactivation with psoralen and long-wavelength ultraviolet light.
31 he collagenase gene upon treatment with free psoralen and subsequent photoactivation.
32      In this study, APS165 was modified with psoralen and the extent of triplex formation with alpha1
33 tation equilibrium of 3'-linked intercalated psoralen and to develop conditions that lead to preferen
34                                 Sunlight and psoralen and ultraviolet A (PUVA) are risk factors for t
35                                              Psoralen and ultraviolet A light (PUVA) are used to kill
36 es that themselves had never been exposed to psoralen and ultraviolet A radiation.
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.
39 tive to photochemical inactivation with S-59 psoralen and UV light.
40 om 30 minute reactions were crosslinked with psoralen and UV, linearized with restriction enzymes and
41  with photochemical therapy (PCT) using S-59 psoralen and UVA light to prevent proliferation.
42 s are widely consumed foods that are rich in psoralens and furocoumarins, a group of naturally occurr
43                             A combination of psoralens and ultraviolet A radiation is widely used to
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
47 DNA damage, thus ICL-inducing agents such as psoralen, are clinically useful chemotherapeutics.
48  Upon near-ultraviolet irradiation (360 nm), psoralen-Asp41-Tat(37-72) cross-linked to a single site
49                                          The psoralen-bis-PNA conjugate was found to direct photoaddu
50 ks was dependent on precise placement of the psoralen by the triple helix-forming oligonucleotide at
51                                Photoreactive psoralens can form interstrand crosslinks (ICLs) in doub
52                  Upon exposure to UVA light, psoralens can induce DNA interstrand cross-links (ICLs),
53 s (TFOs) linked to DNA damaging agents (e.g. psoralen) can stimulate HR, providing the potential to i
54      Triplex formation by an oligonucleotide-psoralen conjugate was used to form a covalent photoaddu
55                                 We show that psoralen-conjugated pcPNAs can deliver site-specific pho
56 imethylaminopropylamine, in a 10-nucleotide, psoralen-conjugated TFO confers substantial increases in
57                                      Using a psoralen-conjugated TFO designed to bind to a site overl
58 was induced efficiently by injection of both psoralen-conjugated TFOs (followed by long-wave UVA ligh
59                                              Psoralen-conjugated triplex-forming oligonucleotides (ps
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
62       These results indicate that TFO-linker-psoralen conjugates allow simultaneous, efficient target
63 ree, two, or no strands covalently linked by psoralen conjugation and photoaddition.
64         A defined template DNA with a single psoralen cross-link and the SV40 origin of replication w
65                                          The psoralen cross-link defines the intramolecular interacti
66                                          The psoralen cross-link inhibited DNA replication by termina
67 ation of TBP from DNA was not prevented by a psoralen cross-link positioned immediately preceding the
68                         The major pathway of psoralen cross-link repair in yeast is error-free and in
69 ontaining four adjacent cytosines, next to a psoralen cross-link site.
70                              A site-specific psoralen cross-link was placed between the promoter and
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
73                                  We compared psoralen cross-link, psoralen monoadduct, and DSB repair
74 epair of plasmid molecules carrying a single psoralen cross-link, psoralen monoadduct, or double-stra
75                                   UV-induced psoralen cross-linking is used to probe the secondary st
76                       Nuclease digestion and psoralen cross-linking mapped the PIC between positions
77  understand the relationship between triplex psoralen cross-linking products and the fate of RNA Pol
78 ed after UV irradiation, which initiates the psoralen cross-linking reaction.
79  These studies have low sensitivity, because psoralen cross-linking suggested few (estimated <10%) of
80 embedded sequences for triplex formation and psoralen cross-linking.
81 e characterized by elevated accessibility to psoralen cross-linking.
82       In the yeast Saccharomyces cerevisiae, psoralen cross-links are processed by nucleotide excisio
83                Our observations suggest that psoralen cross-links can be repaired by three pathways:
84                                              Psoralen cross-links induced both recombination and muta
85  comparison, the ability of triplex-directed psoralen cross-links to induce recombination was only pa
86                 Site-specific mutagenesis by psoralen cross-links was dependent on precise placement
87  repair of laser-localized lesions formed by psoralen (cross-links/monoadducts) and angelicin (only m
88               Inhibition of transcription by psoralen-cross-linked triplexes results in both arrest a
89 x DNA containing a site-directed interstrand psoralen crosslink.
90                       Chloroquine titration, psoralen crosslinking and supercoiling-sensitive reporte
91  develop PARIS, a method based on reversible psoralen crosslinking for global mapping of RNA duplexes
92                              A light-induced psoralen crosslinking reaction was used to attach a puro
93 ve fraction from yeast nuclei, and selective psoralen crosslinking was used to distinguish between ac
94 ld be detected only after analysis following psoralen crosslinking.
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
97                         NEIL1 recruitment to psoralen crosslinks was independent of the nucleotide ex
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
100 omplex is formed, containing HMGB1, RPA, and psoralen-damaged DNA.
101                                      Using a psoralen delivery system mediated by a DNA third strand
102                                     Some new psoralen derivatives were synthesized and evaluated as i
103                                    Among the psoralen derivatives, 8-methoxypsoralen (8-MOP) is conve
104 chemical cross-linking of DNA to immobilized psoralen derivatives.
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
109 n control cells 6 and 16 h after exposure to psoralen DNA cross-links.
110 ay of NER is critical for the recognition of psoralen DNA ICLs in the mammalian genome.
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
113 age recognition proteins to triplex-directed psoralen DNA interstrand cross-links (ICLs).
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
116       DNA from irradiated cells treated with psoralen exhibited a 4- to 7-fold increase in tritium ac
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
119 L with a greater efficiency than that of the psoralen ICL alone.
120 designed a model substrate DNA with a single psoralen ICL at a three-way junction (Y-shaped DNA), whi
121 f a DNA substrate containing a site-specific psoralen ICL can be monitored in vitro.
122                          Using laser-induced psoralen ICL formation in cells, we find that FANCA inte
123 A and PCNA are involved in an early stage of psoralen ICL processing.
124 d MUS81-EME1 incises DNA at the 5' side of a psoralen ICL residing in fork structures.
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
128                    However, how TFO-directed psoralen ICLs (Tdp-ICLs) are recognized and processed in
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
134             Here, we show that processing of psoralen ICLs in mammalian cell extracts is dependent up
135                            The processing of psoralen ICLs is also dependent upon the nucleotide exci
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
140 air (MMR) complex MutSbeta were sensitive to psoralen ICLs.
141 clease UvrABC plays a key role in processing psoralen ICLs.
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
145 followed by G1 (G3/G1) VLPs, or with live or psoralen-inactivated SA11.
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
150                                              Psoralen-induced ICLs blocked transcription and replicat
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
153 l cycle arrest and genomic instability after psoralen-induced ICLs.
154 136R, and E181K, to oxidative DNA damage and psoralen-induced interstrand crosslinks was differential
155 p53 and apoptosis much more effectively than psoralen-induced monoadducts.
156  photoadducts directed by PNAs conjugated to psoralen-induced mutations at frequencies in the range o
157         In particular, using the N-4 linker, psoralen interaction with the residues of the non-coding
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
160                  Here, we show that a single psoralen interstrand cross-link induces DNA synthesis in
161 ps of psoralen photoadducts: monoadducts and psoralen interstrand cross-link products.
162 ' and 3' incisions that occur at a site of a psoralen interstrand cross-link.
163 nuclei, specifically binds to DNA containing psoralen interstrand cross-links and that the FANCA, FAN
164                                The repair of psoralen interstrand cross-links in the yeast Saccharomy
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
167 cient in the stimulation of DNA synthesis by psoralen interstrand crosslinks.
168                     Although the presence of psoralen is not required for targeting nor is it alone a
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
171 the position of its subunits relative to the psoralen lesion.
172 r a 72 h period, suggesting that TFO-induced psoralen lesions are not repaired on this time scale.
173 ralen in the mechanism to initiate repair of psoralen-lesions in mammalian DNA.
174                                              Psoralens linked to triplex-forming oligonucleotides (ps
175     We have constructed chemically modified, psoralen-linked TFOs that mediate site-specific mutagene
176                            We have described psoralen-linked TFOs with 2'-O-methyl and 2'-O-(2-aminoe
177                             We have prepared psoralen-linked TFOs with varying amounts of the AE-modi
178  site was greatly improved by shortening the psoralen linker.
179                          We combined in vivo psoralen-mediated RNA-RNA crosslinking and high-throughp
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
182                                              Psoralen-modified TFOs and UVA irradiation were used to
183                                 We have used psoralen-modified triplex-forming oligonucleotides (TFOs
184                                              Psoralen-modified triplex-forming oligonucleotides (TFOs
185                                              Psoralen-modified triplex-forming oligonucleotides (TFOs
186 onucleotide third strands with a 3'-terminal psoralen moiety attached by linkers that differ in lengt
187  for G-quadruplex binders characterized by a psoralen moiety.
188 igonucleotides attached with a photoreactive psoralen molecule (psoTFO) can be used to induce site-sp
189             We compared psoralen cross-link, psoralen monoadduct, and DSB repair using plasmid substr
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
192          Target DNA acquired strand-specific psoralen monoadducts in a light dose-dependent fashion.
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
195                          Most of the induced psoralen-pcPNA mutations were single-base substitutions
196                                         Such psoralen-peptide conjugates provide a new class of probe
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
200             Gene activation was dependent on psoralen photo-crosslinking.
201                  These results indicate that psoralen photo-crosslinks play a prominent role in activ
202                                              Psoralen photoadduct formation was shown to be essential
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
205 ate the mechanism for creating site-specific psoralen photoadducts in a target duplex DNA.
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
209                       The formation of these psoralen photoadducts was also photoreversible through e
210                                          The psoralen photoadducts were then analyzed after UV irradi
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
213 was investigated by micrococcal nuclease and psoralen photocrosslinking.
214 d for their ability to form triplex-directed psoralen photoproducts with both the mutant T residue of
215                                              Psoralen photoreacts with DNA to form interstrand cross-
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
219 aviolet-A-emitting fluorescent tubes used in psoralen plus ultraviolet A therapy.
220                                     Although psoralen plus ultraviolet A treatment is highly effectiv
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
223 the standard dose used in photochemotherapy (psoralen plus ultraviolet A).
224 Derm, a reconstituted human skin equivalent, psoralen plus ultraviolet A-induced 8-methoxypsoralen-DN
225 resulted in an almost complete abrogation of psoralen plus ultraviolet A-induced erythema.
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
229 sfully in combination with ultraviolet B and psoralen plus ultraviolet A.
230 ein induction following a single exposure to psoralen plus ultraviolet A. c-fos and p53 positive cell
231                Psoriatic patients undergoing psoralen plus ultraviolet radiation (PUVA) therapy are s
232                                          The Psoralen plus Ultraviolet-A (PUVA) cohort study has been
233  are hypersensitive to DNA damage induced by psoralen plus UVA irradiation (PUVA) or UVC radiation, s
234                                              Psoralen plus UVA light (PUVA) is commonly used to treat
235 argeting in the episomal shuttle vector, the psoralen-PNA-induced mutation frequency was 0.13%, 3.5-f
236                                     Using UV/psoralen (Ps)-inactivated virus to block viral transcrip
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
242       Photochemical treatment (PCT) with the psoralen S-59 and long wavelength ultraviolet light (UVA
243                                We used these psoralen-Tat conjugates to form specific complexes with
244                                              Psoralen-TFO conjugates formed DNA cross-links with high
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
247 gments containing either an abasic site or a psoralen-thymine monoadduct.
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,
250 unctional survival assays indicated that the psoralen-TPE treatment was not toxic to cells.
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
253                                         Peak psoralen ultraviolet A erythema, assessed by minimal pho
254  we determined that only 67% of mean maximum psoralen ultraviolet A erythemal intensity had developed
255                             If assessment of psoralen ultraviolet A erythemal sensitivity had been ma
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
260                     Risk increased with high psoralen + ultraviolet A exposure prior to the first squ
261 s with low pre-first squamous cell carcinoma psoralen + ultraviolet A exposure, 95% confidence interv
262             Long-term, high-dose exposure to psoralen + ultraviolet A is associated with an increased
263 lop a squamous cell carcinoma after starting psoralen + ultraviolet A therapy should be closely monit
264 d 258 a basal cell carcinoma after beginning psoralen + ultraviolet A therapy.
265  rates of post-first squamous cell carcinoma psoralen + ultraviolet A treatment also were associated
266                      Higher post-first tumor psoralen + ultraviolet A treatment rates also increased
267               This study's data suggest that psoralen + ultraviolet A-induced p53 mutations may play
268 he development of nonmelanoma skin cancer in psoralen + ultraviolet A-treated patients, but these mut
269                                              Psoralen + ultraviolet A-treated psoriasis patients appe
270                                              Psoralen + ultraviolet A-treated psoriasis patients are
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
274                               Interestingly, psoralen + ultraviolet A-type p53 mutations were more fr
275 ising in patients with high-dose exposure to psoralen + ultraviolet A.
276 er risk among patients who have discontinued psoralen+ultraviolet A and the risk of a first tumor wit
277       In conclusion, substantial exposure to psoralen+ultraviolet A dramatically increases the risk o
278 ents because the cancer risk associated with psoralen+ultraviolet A is persistent.
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
281 sk was noted during the first 15 years after psoralen+ultraviolet A was discontinued.
282                                              Psoralen+ultraviolet A-treated psoriasis patients are at
283 ort of 1,380 psoriasis patients treated with psoralen+ultraviolet A.
284 of which 59.4% were considered years without psoralen+ultraviolet.
285 gulation of CYP2S1 by ultraviolet radiation, psoralen-ultraviolet A (PUVA), and topical drugs used to
286 nventional one-photon excitation, as used in psoralen + UV A radiation (320-400 nm) therapy.
287                       In this study, using a psoralen-UV cross-linking method and an in vitro RdRP as
288 ral replication by attenuating the VVVs with psoralen-UV light treatment.
289                       Electron microscopy of psoralen/UV cross-linked DNA revealed t-loops in enriche
290                                              Psoralen/UV photocrosslinking studies revealed that meta
291             Similar data were obtained using psoralen/UVA, signifying that MLH1 influences the cellul
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
294                                              Psoralen was conjugated to the 5'-end of these clamp-for
295     Gene activation by pso-TFOs in which the psoralen was linked to the TFO via a disulfide bond was
296          The activity of this TFO, linked to psoralen, was measured in a mammalian cell line that was
297 f the 5-propynyl-U change the orientation of psoralen with respect to the upper-strand C.
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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