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1 and Bloom's complexes at the site of the DNA interstrand crosslink.
2 -distorting DNA damage and the repair of DNA interstrand crosslinks.
3 be informative about the metabolism of other interstrand crosslinks.
4 modification and repair of bulky adducts and interstrand crosslinks.
5 the stimulation of DNA synthesis by psoralen interstrand crosslinks.
6 fficient in vitro DNA resynthesis induced by interstrand crosslinks.
7 NA polymerase-helicase involved in repair of interstrand crosslinks.
8 s, including monoadducts and intrastrand and interstrand crosslinks.
9 links were preferred targets for the ER over interstrand crosslinks.
10 ms, Pol theta also promotes tolerance of DNA interstrand crosslinks.
11 f different types of DNA damage, such as DNA interstrand crosslinks.
12 y covalently modifying the template DNA with interstrand crosslinks.
13 activity of enzymes acting on DNA and causes interstrand crosslinks.
14 f damage, such as double-stranded breaks and interstrand crosslinks.
15 and facilitates replication traverse of DNA interstrand crosslinks.
16 tion, an essential step in the repair of DNA interstrand crosslinks.
17 ncreased activity of DNA2 and WRN at the DNA interstrand crosslinks.
18 core complex that mediates the repair of DNA interstrand crosslinks.
19 that senses and repairs damage caused by DNA interstrand crosslinks.
20 interfere with normal cellular processing of interstrand crosslinks.
21 A core complex to chromatin in repairing DNA interstrand crosslinks.
22 hor complex that recognizes damage caused by interstrand crosslinks, a multisubunit ubiquitin ligase
23 nts cause defective cellular response to DNA interstrand crosslinking agent and telomere maintenance,
24 diazepine (PBD) dimer, is a highly efficient interstrand crosslinking agent that reacts with guanine
25 n, knockdown of NONO sensitizes cells to the interstrand crosslinking agent, cisplatin, whereas knock
26 Upon exposure to ionizing radiation or an interstrand crosslinking agent, the number of cells exhi
27 characterized by cellular sensitivity to DNA interstrand crosslinking agents and a high risk of cance
28 en shown to be specifically sensitive to DNA interstrand crosslinking agents but not sensitive to mon
29 y can result in a marked hypersensitivity to interstrand crosslinking agents, such as mitomycin C.
35 Here we generate acetaldehyde-induced DNA interstrand crosslinks and determine their repair mechan
36 and repair of DNA double-strand breaks, DNA interstrand crosslinks and DNA damage during DNA replica
37 erphase, TRAIP helps replisomes overcome DNA interstrand crosslinks and DNA-protein crosslinks, where
38 fective in promoting replication traverse of interstrand crosslinks and is also inefficient in promot
39 involved in the recognition or repair of DNA interstrand crosslinks and perhaps other forms of DNA da
40 re rapidly recruited to forks stalled by DNA interstrand crosslinks, and both are required for cellul
43 stards selectively formed two base-staggered interstrand crosslinks between the 5'G and the G opposit
45 as well as trioxsalen (psoralen)-induced DNA interstrand crosslinks, but not to angelicin monoadducts
46 ke MUS81-EME1, is required for repair of DNA interstrand crosslinks, but this role appears to be inde
48 se results define the repair pathways of DNA interstrand crosslinks caused by an endogenous and alcoh
49 nalogous to the mechanism used to repair the interstrand crosslinks caused by the chemotherapeutic ag
51 ified NEIL1 protein bound stably to psoralen interstrand crosslink-containing synthetic oligonucleoti
53 e FA repair pathway being overwhelmed by DNA interstrand crosslink damage caused by alcohol and tobac
54 onoaziridinyl-1,4-benzoquinones were able to interstrand crosslink DNA after reduction and were cytot
56 otoxic agents that generate alkylated bases, interstrand crosslinks, DNA-protein crosslinks, and doub
57 acted doses of 14 alkylating and similar DNA interstrand crosslinking drugs from medical records.
58 this groove for efficient digestion past DNA interstrand crosslinks, facilitating the key DNA repair
59 ifference in the extent of N-alkyl purine or interstrand crosslink formation in the N-ras, c-myc or C
62 resolution of non-B DNA structures including interstrand crosslinks, G quadruplexes and DNA triplexes
63 e phosphodiester backbone that surrounds the interstrand crosslink, generating a double-strand-break
64 roduces a number of DNA adducts with the DNA interstrand crosslink (ICL) considered to be the critica
65 pression, abrogation of BRIP1 foci after DNA interstrand crosslink (ICL) damage and hypersensitivity
67 HES1, to form complexes that participate in interstrand crosslink (ICL) DNA repair and MEC different
69 other key cellular processes, including DNA interstrand crosslink (ICL) repair and DNA double-strand
71 s roles in nucleotide excision repair (NER), interstrand crosslink (ICL) repair, homologous recombina
77 ynthesis (TLS) past a nitrogen mustard-based interstrand crosslink (ICL) with an 8-atom linker betwee
78 date factors affecting TFO-directed psoralen interstrand crosslink (ICL)-induced recombination, we co
80 oligonucleotides (TFOs) conjugated to a DNA interstrand crosslinking (ICL) agent, psoralen (pTFO-ICL
81 (FA) patients are extremely sensitive to DNA interstrand crosslinking (ICL) agents, but the molecular
82 nd FANCD2, is required for the repair of DNA interstrand crosslinks (ICL) and related lesions(1).
85 ssor BRCA1, is crucial for the repair of DNA interstrand crosslinks (ICL), a highly toxic lesion that
90 s time points, suggested an unexpected, late interstrand-crosslinking (ICL) repair pathway response t
92 tients and mouse models are sensitive to DNA interstrand crosslinks (ICLs) and FA mice are moderately
93 ay plays a central role in the repair of DNA interstrand crosslinks (ICLs) and regulates cellular res
94 CA pathway is critical for the repair of DNA interstrand crosslinks (ICLs) and the maintenance of chr
108 esolving double-strand DNA breaks (DSBs) and interstrand crosslinks (ICLs) by homologous recombinatio
109 ins thought to function in the repair of DNA interstrand crosslinks (ICLs) comprise what is known as
113 ed that fludarabine enhanced accumulation of interstrand crosslinks (ICLs) in specific regions of the
117 not essential for cells to survive toxic DNA interstrand crosslinks (ICLs), although MMR proteins bin
119 otein network is necessary for repair of DNA interstrand crosslinks (ICLs), but its control mechanism
120 Several important anti-tumor agents form DNA interstrand crosslinks (ICLs), but their clinical effici
123 le-deficient cells are hypersensitive to DNA interstrand crosslinks (ICLs), indicating that BRCA1 has
125 r hypersensitivity to agents that induce DNA interstrand crosslinks (ICLs), such as mitomycin C (MMC)
127 agents used in cancer chemotherapy cause DNA interstrand crosslinks (ICLs), which covalently link bot
129 itin are required for localizing SLX4 to DNA interstrand crosslinks (ICLs), yet how SLX4 is targeted
140 NEIL1 recognizes specifically and distinctly interstrand crosslinks in DNA, and can obstruct the effi
141 es or a novel tetrafunctional mustard caused interstrand crosslinks in the target DNA and were more m
143 that EcoR124I can translocate past covalent interstrand crosslinks, inconsistent with an obligatory
144 veloped a mammalian cell free assay in which interstrand crosslinks induce DNA synthesis in both dama
146 ovarian cancer often include the use of DNA interstrand crosslink-inducing agents (e.g., platinum dr
147 cts, the collision of replication forks with interstrand crosslinks initiates two distinct repair pat
148 th biomolecules, including DNA base adducts, interstrand crosslinks, intrastrand crosslinks, and DNA-
150 the cellular level, hypersensitivity to DNA interstrand crosslinks is the defining feature in Fancon
151 es profound cellular hypersensitivity to DNA interstrand crosslink lesions in vivo, highlighting the
152 itutional genomic disorders, suggesting that interstrand crosslinks may play a pathogenic role in suc
154 to aid replication machines to traverse DNA interstrand crosslinks prior to post-replication repair.
155 emonstrated that neither mismatch repair nor interstrand crosslink repair affects the production of t
156 la MUS308, which is essential for normal DNA interstrand crosslink repair and is unique in that it co
157 ing replication and its participation in DNA interstrand crosslink repair and/or heteroduplex rejecti
158 CM participates in recombination-independent interstrand crosslink repair by facilitating recruitment
159 esults suggest that FAN1 has a minor role in interstrand crosslink repair compared with true FA genes
161 roper RAD51 function is important during DNA interstrand crosslink repair outside of homologous recom
162 the deficiency in replication-dependent DNA interstrand crosslink repair pathway commonly referred t
163 protein families, namely the PSO2 (SNM1) DNA interstrand crosslink repair proteins and the 73-kD subu
164 nstability, is caused by a deficiency in DNA interstrand crosslink repair resulting in chromosome bre
165 ce that BRCA1 plays an important role in DNA interstrand crosslink repair that is distinct from its e
166 be important for nucleotide excision repair, interstrand crosslink repair, and DNA double-strand repa
167 including nucleotide excision repair (NER), interstrand crosslink repair, and meiotic recombination.
168 connected to a pathway that is deficient in interstrand crosslink repair, and that at least one othe
169 genetic complementation groups implicated in interstrand crosslink repair, FANCJ encodes a DNA helica
170 found the depletion of reduced both HDR and interstrand crosslink repair, phenocopying the loss of t
171 ty-DNA double-strand break (DSB) repair, DNA interstrand crosslink repair, repair of stalled replicat
172 monoubiquitinated FANCD2 and is required for interstrand crosslink repair, suggesting that mutation o
173 lication-dependent and transcription-coupled interstrand crosslink repair, while SNM1B/Apollo is requ
184 were exposed to chemicals that generate DNA interstrand crosslinks (repaired by FA proteins), but no
187 by ATR activates Fanconi anemia signaling at interstrand crosslink-stalled replication forks by recru
188 n in vitro assay in which the presence of an interstrand crosslink stimulates the incorporation of ra
189 alter the accumulation of NEIL1 at sites of interstrand crosslinks, suggesting distinct recognition
190 leotides (TFOs) that target a psoralen (pso) interstrand crosslink to a specific chromosomal site in
191 n C, which is consistent with the ability of interstrand crosslinks to induce homologous recombinatio
194 ntral and crucial step for the repair of DNA interstrand crosslinks via the Fanconi anaemia pathway.
195 to oxidative DNA damage and psoralen-induced interstrand crosslinks was differentially affected by th
196 repair (BER) proteins in the response to DNA interstrand crosslinks, which block replication and tran
197 Their main role is in the repair of DNA interstrand crosslinks, which, by covalently binding the