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1 ed DNA by Chlorella virus DNA ligase (PBCV-1 DNA ligase).
2 s six proteins: UvrA-D, DNA polymerase I and DNA ligase.
3 gth can be modulated by the concentration of DNA ligase.
4 nd the resulting termini are ligated with T4 DNA ligase.
5 n of linear DNA molecules in the presence of DNA ligase.
6 ulation of end-joining in the presence of T4 DNA ligase.
7 uclease 1 to DNA polymerase beta and then to DNA ligase.
8 of a 5' exonuclease, a DNA polymerase and a DNA ligase.
9 incubation times than required when using T4 DNA ligase.
10 ith ligation of these strands mediated by T4 DNA ligase.
11 PO4) and 5'-OH ends that cannot be sealed by DNA ligases.
12 g the mechanism and specificity of mammalian DNA ligases.
13 nd illustrates examples using the Taq and T4 DNA ligases.
14 Therefore, MHEJ and NHEJ require different DNA ligases.
15 l mRNA-capping enzymes and all ATP-dependent DNA ligases.
16 unds was also active against the other human DNA ligases.
17 s, there are three families of ATP-dependent DNA ligases.
18 sis by DNA polymerases or sealing by classic DNA ligases.
19 by DNA exonucleases or ligated by T3 and T4 DNA ligases.
20 DNA ligation reactions used by ATP-dependent DNA ligases.
21 A splint are notoriously poor substrates for DNA ligases.
22 AP) endonuclease 1, DNA polymerase beta, and DNA ligases.
24 omosomal DSBs and raise the possibility that DNA ligase 1 (Lig1) may contribute more to A-EJ than pre
27 ow that the tomato (Solanum lycopersicum L.) DNA ligase 1 specifically and efficiently catalyzes circ
29 is study we propose that PSTVd subverts host DNA ligase 1, converting it to an RNA ligase, for the fi
36 s is associated with increased expression of DNA ligase 3alpha, poly(ADP-ribose) polymerase 1 (PARP1)
39 ne or more requisite C-NHEJ factors, such as DNA ligase 4 (Lig4) or XRCC4, end-joining during CSR occ
45 r-chromosomal fusion events in cells lacking DNA ligase 4, in contrast to a remarkably consistent pro
49 4 (LIG4) form a tight complex that provides DNA ligase activity for classical non-homologous end joi
50 duction in the rate of pol beta synthesis or DNA ligase activity on any of the fragments bound to GR-
51 e I whereas LigIII is the only mitochondrial DNA ligase and is essential for the survival of cells de
52 es expressing BCR-ABL1 to the combination of DNA ligase and PARP inhibitors correlates with the stead
53 on of these cell lines with a combination of DNA ligase and PARP inhibitors inhibited ALT NHEJ and se
56 n strategy which expliots the specificity of DNA ligase and the speed of isothermal amplification to
57 plications for the biological specificity of DNA ligases and functions of PARP-like zinc fingers.
59 profiling of the substrate specificities of DNA ligases and illustrates examples using the Taq and T
60 fferent nucleotide content parallels that of DNA ligase, and optimal ligation efficiency is attained
61 omotes DNA end-joining in the presence of T4 DNA ligase, and this property is mediated by the C-termi
63 ajor DNA polymerases (Pol I and Pol III) and DNA ligase are directly involved with oligo recombinatio
64 rase B (PolB), flap endonuclease (Fen1), and DNA ligase are required to complete ribonucleotide proce
67 jacent to the catalytic region of eukaryotic DNA ligases are involved in specific protein-protein int
69 f base excision repair can be mediated by T4 DNA ligase as well as human DNA ligase I or ligase IIIal
70 nd an OB domain (these two are common to all DNA ligases) as well as a distinctive beta-hairpin latch
71 he ligation fidelity of Thermus thermophilus DNA ligase at a range of temperatures, buffer pH and mon
72 ction instead of the existing chemical or T4 DNA ligase-based methods allows quantitative conversion
77 ed DNA structures with abnormal DNA termini, DNA ligase catalytic activity can generate and/or exacer
80 The development and in-depth analysis of T4 DNA ligase-catalyzed DNA templated oligonucleotide polym
87 nformational dynamics of the Chlorella virus DNA ligase (ChVLig), a minimized eukaryal ATP-dependent
89 e homodimeric DNA end-binding protein Ku and DNA ligase D (LigD), a modular enzyme composed of a C-te
99 RNA ligase 1; Rnl1) and the NAD(+)-dependent DNA ligase family (Escherichia coli LigA), captured as t
102 trand phosphates at the outer margins of the DNA ligase footprint; (ii) essential contacts of Ser-41,
103 stereochemical preferences of AP endo and T4 DNA ligase for phosphorothioate substrates, we show that
104 notion that DNA ligase III (LIG3), the only DNA ligase found in mitochondria, is essential for viabi
115 Based on the crystal structure of human DNA ligase I complexed with nicked DNA, computer-aided d
119 nockdown of DCAF7 reduced the degradation of DNA ligase I in response to inhibition of proliferation
120 lication factor C, DNA polymerase delta, and DNA ligase I in the absence of DNA via its non-conserved
121 biquitylated lysine residues and showed that DNA ligase I interacts with and is targeted for ubiquity
123 14 nuclear extracts with an antibody against DNA ligase I or III also significantly reduced MHEJ.
124 found that siRNA mediated down-regulation of DNA ligase I or ligase III in human HTD114 cells led to
126 the enzymes flap endonuclease 1 (FEN-1) and DNA ligase I that complete the processing and joining of
130 cleus, LigIII has functional redundancy with DNA ligase I whereas LigIII is the only mitochondrial DN
133 ropriate relative stoichiometry of FEN-1 and DNA ligase I, which compete for binding to proliferating
140 L82 inhibited DNA ligase I, L67 inhibited DNA ligases I and III, and L189 inhibited DNA ligases I,
142 ed DNA ligases I and III, and L189 inhibited DNA ligases I, III, and IV in DNA joining assays with pu
144 le lines of evidence support the notion that DNA ligase III (LIG3), the only DNA ligase found in mito
146 ymerase-1, X-ray cross-complementing factor1-DNA ligase III and enzymes involved in processing 3'-blo
149 amilies are found in all eukaryotes, whereas DNA ligase III family members are restricted to vertebra
151 separate, independent DNA-binding modules in DNA ligase III that each bind specifically to nicked DNA
153 on with other experiments, demonstrated that DNA ligase III, but not ligase IV or ligase I, is primar
155 demonstrated high levels of PARylated Chd1L, DNA ligase III, SSrp1, Xrcc-6/Ku70, and Parp2 in pluripo
159 with a FLT3 inhibitor demonstrate decreased DNA ligase IIIalpha and a reduction in DNA deletions, su
160 is significant functional redundancy between DNA ligase IIIalpha and DNA ligase I in excision repair.
162 ame is true for a protein complex comprising DNA ligase IIIalpha and the scaffolding protein X-ray re
165 rmed that the expression levels of PARP1 and DNA ligase IIIalpha correlated with the sensitivity to t
166 ike its other nuclear functions, the role of DNA ligase IIIalpha in alternative NHEJ is independent o
170 therapy to inhibit FLT3/ITD signaling and/or DNA ligase IIIalpha may lead to repair that reduces repa
173 Thus, the expression levels of PARP1 and DNA ligase IIIalpha serve as biomarkers to identify a su
176 d DNA ligase IV, are down-regulated, whereas DNA ligase IIIalpha, and the protein deleted in Werner s
177 , poly-(ADP-ribose) polymerase 1 (PARP1) and DNA ligase IIIalpha, were increased in the BCR-ABL1-posi
178 ermore, the interaction between PNKP and the DNA ligase IIIalpha-XRCC1 complex significantly increase
179 ular apurinic/apyrimidinic endonuclease, and DNA ligase IIIalpha-XRCC1, performs uracil-initiated bas
181 IIIalpha and the association between MRN and DNA ligase IIIalpha/XRCC1 are altered in cell lines defe
183 en two factors, hMre11/hRad50/Nbs1 (MRN) and DNA ligase IIIalpha/XRCC1, that have been linked with al
184 ge T4 RNA ligase 2, as well as against human DNA ligase IIIbeta, indicated a considerable degree of s
186 system to show increased sensitivity over T4 DNA ligase in the specific detection of a target mRNA.
187 DNA was dependent on expression of the viral DNA ligase, in accord with previous proteomic studies.
193 r (Yku70-Yku80), MRX (Mre11-Rad50-Xrs2), and DNA ligase IV (Dnl4-Lif1), as well as the ligase-associa
197 logous end-joining (NHEJ) DNA repair protein DNA ligase IV (LIG4) lead to immunodeficiency with varyi
198 nduced apoptosis after ionizing radiation or DNA ligase IV (Lig4) loss in the Mre11(ATLD1/ATLD1) nerv
200 ical NHEJ (c-NHEJ) components, which include DNA ligase IV (LIG4), and instead arise from alternative
201 reviously, we showed that mice deficient for DNA ligase IV (Lig4), another key NHEJ factor, succumbed
202 ns, including KU70, KU80, ARTEMIS, DNA-PKcs, DNA ligase IV (LIG4), Ataxia telangiectasia mutated (ATM
203 double-strand break repair (DSBR) proteins, DNA Ligase IV (Lig4), Xrcc2, and Brca2, or combined Lig4
206 seven genes Ku70, Ku86, DNA-PK(cs), Artemis, DNA Ligase IV (LIGIV), X-ray cross-complementing group 4
207 of nucleases, DNA polymerases, and the XRCC4-DNA ligase IV (X4-LIV) complex in an order influenced by
208 a model in which XLF, by in situ recharging DNA ligase IV after the first ligation event, promotes d
209 nce of some end joining on only Ku and XRCC4.DNA ligase IV allows us to formulate a physical model th
211 have evolved mechanisms based on the loss of DNA ligase IV and perhaps other unknown molecules to dis
214 te that APLF promotes the retention of XRCC4/DNA ligase IV complex in chromatin, suggesting that PARP
215 se mu and lambda to add nucleotides; and the DNA ligase IV complex to ligate the ends with the additi
217 protein kinase catalytic subunit, and XRCC4-DNA ligase IV do not modulate PALF nuclease activity on
218 the precise visualization of XRCC4, XLF, and DNA ligase IV filaments adjacent to DSBs, which bridge t
220 as well as the association of XLF with XRCC4.DNA ligase IV in vivo suggested a role in the final liga
222 e-molecule FRET analysis of the Ku/XRCC4/XLF/DNA ligase IV NHEJ ligation complex, that end-to-end syn
224 3' overhanging nucleotides and permit XRCC4-DNA ligase IV to complete the joining process in a manne
226 t disruption of DSB repair factors (Rad51 or DNA ligase IV) or DSB sensing factors (ATRIP or MDC1) re
229 mote HDR at the expense of NHEJ, we targeted DNA ligase IV, a key enzyme in the NHEJ pathway, using t
230 espectively) cause the degradation of Mre11, DNA ligase IV, and p53, infection with Ad3, Ad7, Ad9, an
232 ed end joining assay that includes Ku, XRCC4-DNA ligase IV, and PALF, PALF is able to resect 3' overh
233 athway that operates in the absence of XRCC4/DNA ligase IV, and that the requirement for PARP-3 and A
234 teins in the major NHEJ pathway, Artemis and DNA ligase IV, are down-regulated, whereas DNA ligase II
235 by RNA interference diminished expression of DNA ligase IV, Artemis, and Ku80 components in DNA-depen
236 largely resemble those from patients lacking DNA ligase IV, Artemis, or ATM, suggesting that these fa
238 s been known that Ku-dependent NHEJ requires DNA ligase IV, it is unclear which DNA ligase(s) is requ
240 recipients deficient in the NHEJ component, DNA ligase IV, the majority of products arise by HR with
244 XLF-Cernunnos (XLF) is a component of the DNA ligase IV-XRCC4 (LX) complex, which functions during
249 Thr181 to trigger its dissociation from the DNA ligase IV/XRCC4 complex, and promotes its interactio
251 entral to the molecular mechanism of NHEJ is DNA ligase IV/XRCC4/XLF complex, which rejoins the DNA.
252 plex of NHEJ factors that includes a ligase (DNA Ligase IV; L4) that relies on juxtaposition of 3 hyd
253 autonomous enzymatic modules: ATP-dependent DNA ligase (LIG), DNA/RNA polymerase (POL), and 3' phosp
254 cribe a complete NHEJ complex, consisting of DNA ligase (Lig), polymerase (Pol), phosphoesterase (PE)
256 d by deletion of either of the two remaining DNA ligases (Lig1 and nuclear Lig3) in Lig4(-/-) cells.
259 r in mammalian cells involves three distinct DNA ligases: ligase I (Lig1), ligase III (Lig3) and liga
264 ning (NHEJ) system that includes a dedicated DNA ligase (LigD) and the DNA end-binding protein Ku.
267 ssential step in most repair pathways is the DNA ligase-mediated rejoining of single- and double-stra
268 out a synthetic lethal screen with cdc9-p, a DNA ligase mutation with two substitutions (F43A/F44A) i
269 es the Vsr endonuclease, DNA polymerase I, a DNA ligase, MutS, and MutL to function at peak efficienc
271 ndicating that the rate-limiting step for T4 DNA ligase nick sealing is not a chemical step but rathe
272 SplintR Ligase is 100X faster than either T4 DNA Ligase or T4 RNA Ligase 2 for RNA splinted DNA ligat
275 3 gene is unique in that it encodes multiple DNA ligase polypeptides with different cellular function
276 y classic ATP-dependent and NAD(+)-dependent DNA ligases, prevents template-independent nucleotide ad
277 nM at 25 degrees C under conditions where T4 DNA ligase produced only 5'-adenylylated DNA with a 20-f
278 n of Ku80 and a molecular mechanism by which DNA ligase proficient complexes are assembled during NHE
279 protein that recruits the DNA polymerase and DNA ligase required for filling and sealing the damaged
284 findings led to a series of experiments with DNA ligase that reveal, contrary to expectation based up
285 e mitochondria or expressing Chlorella virus DNA ligase, the minimal eukaryal nick-sealing enzyme, or
287 city of a DNA-dependent RNA polymerase and a DNA ligase to act as RNA-dependent RNA polymerase and RN
289 ely functionalized nucleic acids by using T4 DNA ligase to mediate the DNA-templated polymerization o
290 bearing deletions or mutations in Ku or the DNA ligases to interrogate the contributions of LigD's t
291 ng a DNA polymerase, an RNA polymerase and a DNA ligase, to use Fe2+ in place of Mg2+ as a cofactor d
292 utants of KU70, KU80, and the plant-specific DNA Ligase VI (LIG6) showed increased stable transformat
295 with the DNA-binding domain of Ligase IV, a DNA Ligase which plays essential roles in DNA repair and
296 igation strategy based on USER Enzyme and T4 DNA ligase, which allows the simultaneous and seamless a
297 Mammalian cells have three ATP-dependent DNA ligases, which are required for DNA replication and
299 he cyclase pathway resemble those of RNA and DNA ligases, with the key distinction being that ligases
300 t the modification site that is sealed by T4-DNA ligase, yielding a product strand missing the modifi
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