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1 ed to methylated and other modified forms of cytidine.
2 igns four nucleotides upstream of the edited cytidine.
3 synthesized from suitably protected 5'-O-DMT cytidines.
4 ride, and the binding of ribonuclease A with cytidine 2'-monophosphate within reaction volumes of app
5 ficiency include phophoglucomutase 3 (PGM3), cytidine 5' triphosphate synthase 1 (CTPS1), nuclear fac
6 or cytosine, 1-methylcytosine, cytidine, and cytidine 5'-phosphate, and also for cytosine residues in
7 f two polar metabolites (acetylcarnitine and cytidine-5-diphosphocholine) during epiboly.
8 atives of 5-fluorouridine (4l), N(4)-benzoyl-cytidine (7f), N(4)-[ O-(4-benzyloxy)]-cytidine (9h), an
9 (9h), and N(4)-[ O-(4-naphth-2-ylmethyloxy)]-cytidine (9e) ( K(i) values 5-10 nM at human CD73).
10 nzoyl-cytidine (7f), N(4)-[ O-(4-benzyloxy)]-cytidine (9h), and N(4)-[ O-(4-naphth-2-ylmethyloxy)]-cy
11 oreover, acetylation of the N(4) position of cytidine (ac4C) was recently reported to increase the tr
12  the distribution, dynamics and functions of cytidine acetylation have yet to be fully elucidated.
13  and poly(U)-adding enzymes, we identified a cytidine-adding enzyme that is likely to be part of a tw
14         Here, we show that the nonmethylable cytidine analog zebularine induces a DNA damage response
15 ty over related enzymes and synergize with a cytidine analogue against leukemic cells.
16 able activity is observed with cytarabine, a cytidine analogue without DNA-hypomethylating properties
17  the design and synthesis of a new tricyclic cytidine analogue, 8-diethylamino-tC (8-DEA-tC), that re
18                                          The cytidine analogues azacytidine and 5-aza-2'-deoxycytidin
19 ibitors that enhance the cytotoxic effect of cytidine analogues in leukemia cells.
20  cytarabine and various structurally related cytidine analogues, such as 2'deoxycytidine and gemcitab
21 on and are resistant to treatment with other cytidine analogues.
22 s can be achieved by fusing SauriCas9 to the cytidine and adenine deaminase.
23                          Monomethylations of cytidine and adenosine are common post-transcriptional m
24 e distribution, with a strong preference for cytidine and guanosine, and identified hotspots of ribon
25 n criteria are outlined and the syntheses of cytidine and uridine azo dye analogues derived from 6-am
26 of the canonical pyrimidine ribonucleosides (cytidine and uridine), and we show that, once generated,
27 o a mixture of deoxyadenosine, deoxyinosine, cytidine and uridine.
28 sition, where the interactions between deoxy-cytidines and CTD loop-1 and loop-7 residues were differ
29 ytic C-terminal domain (CTD) that deaminates cytidine, and a N-terminal domain (NTD) that binds to ss
30 imilar rates for cytosine, 1-methylcytosine, cytidine, and cytidine 5'-phosphate, and also for cytosi
31 cynomolgus monkey embryos using CRISPR-based cytidine- and adenine-base editors.
32 but not with doxorubicin or arabinofuranosyl cytidine (Ara-C).
33 ery of the antimitotic drug arabinofuranosyl cytidine (AraC) blunted food intake, body weight gain, a
34                    In angiosperm organelles, cytidines are converted to uridines by a deamination rea
35                                   The edited cytidines are often flanked by inverted repeats, but are
36 al specific nucleoside kinase is involved in cytidine as well as uridine salvage.
37 in antisense elements that target the wobble cytidine at position 34 of human elongator tRNA(Met)(CAT
38      A dinucleoside containing guanosine and cytidine at the end groups has been prepared using a mod
39 in mice with Cre-conditional expression of a cytidine base editor and tested their utility for precis
40 Cas9-Ung supplements the current adenine and cytidine BEs (ABE and CBE, respectively) and could be us
41 unction mutants accumulating high amounts of cytidine but also CMP, cytosine, and some uridine in see
42                  Plant RNA editosomes modify cytidines (C) to uridines (U) at specific sites in plast
43 e units for healthy volunteers (P = .02) and cytidine concentrations were 1.44 (0.95-1.73) relative u
44 ng a link between EBV and activation-induced cytidine deaminase (AICDA) activity.
45 nal pattern suggestive of activation-induced cytidine deaminase (AID) activity.
46 ed to the Igh locus in an activation-induced cytidine deaminase (AID) and H2AX-dependent fashion.
47 n of DSBs is initiated by activation-induced cytidine deaminase (AID) and requires base excision repa
48 tudies have reported that activation-induced cytidine deaminase (AID) and ten-eleven-translocation (T
49 nt with the activities of activation-induced-cytidine deaminase (AID) and the A-T mutator, DNA polyme
50   Conditional deletion of activation-induced cytidine deaminase (AID) between heterologous challenges
51                           Activation-induced cytidine deaminase (AID) converts cytosine into uracil t
52                           Activation-induced cytidine deaminase (AID) generates U:G mismatches in Ig
53                Endogenous activation-induced cytidine deaminase (AID) in engineered cells allowed for
54                           Activation-induced cytidine deaminase (AID) initiates both class switch rec
55                           Activation-induced cytidine deaminase (AID) initiates CSR by promoting deam
56                           Activation-induced cytidine deaminase (AID) initiates immunoglobulin (Ig) c
57                           Activation-induced cytidine deaminase (AID) initiates somatic hypermutation
58                           Activation-induced cytidine deaminase (AID) is a B-cell-specific enzyme tha
59                           Activation-induced cytidine deaminase (AID) is a genome-mutating enzyme tha
60                           Activation-induced cytidine deaminase (AID) is a key regulator of class swi
61                           Activation-induced cytidine deaminase (AID) is a mutator enzyme that target
62                           Activation-induced cytidine deaminase (AID) mediates cytosine deamination a
63     Because CTNNBL1 binds activation-induced cytidine deaminase (AID) that catalyzes SHM, we tested A
64       In E. coli, we used activation-induced cytidine deaminase (AID) to construct AID-nCas9-Ung and
65 ul R loops, we used human activation-induced cytidine deaminase (AID) to identify genes preventing R
66 on-coupled recruitment of activation-induced cytidine deaminase (AID) to Ig switch regions (S regions
67      Precise targeting of activation-induced cytidine deaminase (AID) to immunoglobulin (Ig) loci pro
68  Likewise, recruitment of activation-induced cytidine deaminase (AID) to S regions is critical for CS
69 ed with less targeting of activation-induced cytidine deaminase (AID) to the Igh locus.
70 ically inactive dCas9 to recruit variants of cytidine deaminase (AID) with MS2-modified sgRNAs, we ca
71 e we report the fusion of activation-induced cytidine deaminase (AID) with nuclease-inactive clustere
72 nes and activators induce activation-induced cytidine deaminase (AID)(2) and I-promoter transcription
73 nal expansion and express activation-induced cytidine deaminase (AID), a DNA mutator.
74  the expression levels of activation-induced cytidine deaminase (AID), a key player in B-cell respons
75 s in AICDA, which encodes activation-induced cytidine deaminase (AID), display an impaired peripheral
76 ion (CSR) is initiated by activation-induced cytidine deaminase (AID), the activity of which leads to
77      These biomarkers are activation-induced cytidine deaminase (AID), the enzyme of class switch rec
78                           Activation-induced cytidine deaminase (AID), the enzyme responsible for ind
79                           Activation-induced cytidine deaminase (AID), the enzyme-mediating class-swi
80 ng the DNA-editing enzyme activation-induced cytidine deaminase (AID), which is required in affinity
81 eliberate introduction of activation-induced cytidine deaminase (AID)-instigated DNA double-strand br
82  B cells having undergone activation-induced cytidine deaminase (AID)-mediated somatic hypermutation
83 ntial activity of the DNA activation-induced cytidine deaminase (AID).
84 nsiently-expressed enzyme Activation-induced cytidine Deaminase (AID).
85 tations introduced by the activation-induced cytidine deaminase (AID).
86  of cytidine to uracil by activation-induced cytidine deaminase (AID).
87 he B-cell mutator protein activation-induced cytidine deaminase (AID).
88 on efficient induction of activation-induced cytidine deaminase (AID).
89 re, we have proposed that activation-induced cytidine deaminase (AID, encoded by AICDA) links chronic
90 ed CRISPR-Cas9 to disrupt activation-induced cytidine deaminase (AID; Aicda) directly in BXSB zygotes
91 ment through induction of activation-induced cytidine deaminase (AID; also known as AICDA) in precurs
92      APOBEC3G, a member of the double-domain cytidine deaminase (CD) APOBEC, binds RNA to package int
93 s and identified that L306 in the C-terminal cytidine deaminase (CD) domain contributed to its core l
94                                              CYTIDINE DEAMINASE (CDA) catalyzes the deamination of cy
95  new possibilities for anti-cancer treatment.Cytidine deaminase (CDA) deficiency leads to genome inst
96 y bioavailable because of rapid clearance by cytidine deaminase (CDA) in the gut and liver.
97 DNMT1 and tetrahydrouridine (THU) to inhibit cytidine deaminase (CDA), the enzyme that otherwise rapi
98 ions in the pyrimidine metabolic pathway and cytidine deaminase (CDA).
99  that the susceptible cell lines overexpress cytidine deaminase (CDA).
100 on of a long isoform of the bacterial enzyme cytidine deaminase (CDDL), seen primarily in Gammaproteo
101  because a single enzyme, activation-induced cytidine deaminase (encoded by Aicda), initiates both re
102 f Cpf1 (Cas12a) and nCas9-activation-induced cytidine deaminase (nCas9-Target-AID) systems to mutagen
103 ctors contains residues conserved with known cytidine deaminase active sites; however, some PPR editi
104                 We also queried the data for cytidine deaminase activity on the viral genome, which c
105 uplex and, despite the bound RNA, has potent cytidine deaminase activity.
106 ription factors and Aicda (which encodes the cytidine deaminase AID) and thus silenced B cell-specifi
107  editors (GBEs) consist of a Cas9 nickase, a cytidine deaminase and a uracil-DNA glycosylase (Ung).
108 in B mRNA-editing enzyme complex 1 (APOBEC1) cytidine deaminase and Deadend-1, which are involved in
109 found a synthetic lethal interaction between cytidine deaminase and microtubule-associated protein Ta
110 autoreactivity, expresses activation-induced cytidine deaminase and T-bet, and exhibits evidence of s
111 ivate NF-kappaB to induce activation-induced cytidine deaminase and, therefore, Ig class switch DNA r
112 edominant mutation signature associated with cytidine deaminase APOBEC, which correlates with the upr
113                             In DART-seq, the cytidine deaminase APOBEC1 is fused to the m(6)A-binding
114              The catalytic activity of human cytidine deaminase APOBEC3B (A3B) has been correlated wi
115              The single-stranded DNA (ssDNA) cytidine deaminase APOBEC3F (A3F) deaminates cytosine (C
116           Functional analyses identified the cytidine deaminase APOBEC3G as a barrier for chimpanzee-
117                    The enzymatic reaction of cytidine deaminase appears to be a distinct example.
118 ls, lesions introduced by activation-induced cytidine deaminase are processed by multiple error-prone
119 es, uracils introduced by activation-induced cytidine deaminase are processed by uracil-DNA glycosyla
120                         Signatures of APOBEC cytidine deaminase DNA-editing exhibited substantial flu
121 nd that conserved catalytic residues in both cytidine deaminase domains are required for RNA editing.
122 e engineered base editors containing mutated cytidine deaminase domains that narrow the width of the
123                                APOBEC3A is a cytidine deaminase driving mutagenesis, DNA replication
124                           CURE comprises the cytidine deaminase enzyme APOBEC3A fused to dCas13 and a
125   We engineered fusions of CRISPR/Cas9 and a cytidine deaminase enzyme that retain the ability to be
126                         Several adenosine or cytidine deaminase enzymes deaminate transcript sequence
127 associated with increased activation-induced cytidine deaminase expression, and correlate with increa
128 ation ex vivo by altering activation-induced cytidine deaminase expression.
129 eaminase is unique within the zinc-dependent cytidine deaminase family as being allosterically regula
130 f these findings to the wider zinc-dependent cytidine deaminase family is also discussed.
131                                        Using cytidine deaminase fused to Cas9 nickase, up to 28% of s
132  targeted mutagenesis in human cells using a cytidine deaminase fused to T7 RNA polymerase.
133 -mediated ablation of the activation-induced cytidine deaminase gene required for class switch recomb
134 pts and to upregulate the activation-induced cytidine deaminase gene through in vitro T-dependent and
135  NF-kappaB activation and activation-induced cytidine deaminase induction, and boosts IgG Ab and auto
136 ve DNA strand breakage at activation-induced cytidine deaminase off-target genes, its role at the hyp
137                       The activation-induced cytidine deaminase protein induces genome-wide DNA break
138 report extensive computer simulations of the cytidine deaminase reaction and its temperature dependen
139 reates a potent substrate for APOBEC3A (A3A) cytidine deaminase that can promote formation of mutatio
140                    Human APOBEC3H (A3H) is a cytidine deaminase that inhibits HIV-1 replication.
141  downstream effector APOBEC3, an IFN-induced cytidine deaminase that introduces lethal mutations duri
142                 APOBEC3G (A3G) is a cellular cytidine deaminase that restricts HIV-1 replication by i
143               We used a Cas9 nickase (nCas9)-cytidine deaminase to conduct C to T editing of the Ethy
144 t essential for targeting activation-induced cytidine deaminase to S regions, as was suggested.
145 gs for cancer tissues presenting concomitant cytidine deaminase underexpression and Tau upregulation
146 int to TC motifs as activity hotspots of the cytidine deaminase used.
147 l DNA N-glycosylase (eUNG) and a rat APOBEC1 cytidine deaminase variant (R33A) previously shown to ha
148                      APOBEC3B, an anti-viral cytidine deaminase which induces DNA mutations, has been
149 sent the crystal structure of a complex of a cytidine deaminase with ssDNA bound in the active site a
150                                APOBEC3G is a cytidine deaminase with two homologous domains and restr
151 or stromal remodeling and down-regulation of cytidine deaminase without depletion of tumor stromal co
152            Single-strand DNA-specific APOBEC cytidine deaminase(s) are major source(s) of mutation in
153 the miR-155 target Aicda (activation-induced cytidine deaminase) in this process and, in combination
154                                Expression of cytidine deaminase, a dC-catabolizing enzyme, in leukemi
155                         Unlike for bacterial cytidine deaminase, addition of two putative transition-
156 lly defective Streptococcus pyogenes Cas9, a cytidine deaminase, and an inhibitor of base excision re
157 or model based on a mitochondrially-targeted cytidine deaminase, APOBEC1.
158               Here, we show that the related cytidine deaminase, APOBEC3G, induces site-specific C-to
159 ons arise from the preference of APOBEC3A, a cytidine deaminase, for DNA stem-loops.
160 oduction was dependent on activation-induced cytidine deaminase, hematopoietic MyD88 expression, and
161                           Activation-induced cytidine deaminase, one of the APOBEC members, was repor
162 uences rarely targeted by activation-induced cytidine deaminase, the enzyme responsible for antibody
163 ed genomic loci that are more susceptible to cytidine deaminase, we set up a high-throughput assay fo
164 ation (CSR) is induced by activation-induced cytidine deaminase, which initiates a cascade of events
165 ase-based CBE(7), and the Petromyzon marinus cytidine deaminase-based CBE Target-AID(4) induce less e
166 BEC3A-based CBE(6), human activation-induced cytidine deaminase-based CBE(7), and the Petromyzon mari
167 identify genes enabling BLM-deficient and/or cytidine deaminase-deficient cells to tolerate constitut
168                      Tau is overexpressed in cytidine deaminase-deficient cells, and its depletion wo
169 ere Tau functions in maintaining survival of cytidine deaminase-deficient cells, and ribosomal DNA tr
170 ction factors that inhibit HIV-1 through DNA cytidine deaminase-dependent and -independent mechanisms
171 lated high frequencies of activation-induced cytidine deaminase-dependent IgH locus chromosomal break
172                       The activation-induced cytidine deaminase-induced DNA lesions and error-prone r
173 3B activity, providing new insights into how cytidine deaminase-induced mutagenesis might be activate
174 (PPR) protein SLO2, which lacks a C-terminal cytidine deaminase-like DYW domain, interacts in vivo wi
175          Here we investigate the fidelity of cytidine deaminase-mediated base editing in human induce
176  SAMHD1 deficiency during activation-induced cytidine deaminase-mediated genomic instability.
177 to a defective BLM and the downregulation of cytidine deaminase.
178  receptors are damaged by activation-induced cytidine deaminase.
179 targeting activity of the activation-induced cytidine deaminase.
180 ature B cells mediated by activation-induced cytidine deaminase.
181  of the tumor stroma, and down-regulation of cytidine deaminase.
182 d deoxyguanosine resistant to degradation by cytidine deaminase.
183 ically required in the reaction catalyzed by cytidine deaminase.
184 re shown to interact with activation-induced cytidine deaminase.
185  (RESCUE), by directly evolving ADAR2 into a cytidine deaminase.
186 c mice (quasimonoclonal, activation-induced [cytidine] deaminase-Cre-tamoxifen-dependent estrogen rec
187  belongs to the AID/APOBEC protein family of cytidine deaminases (CDA) that bind to nucleic acids.
188                             Although APOBEC3 cytidine deaminases A3G, A3F, A3D and A3H are packaged i
189 indirect activation of DNA editing by APOBEC cytidine deaminases and of an endogenous clocklike mutat
190              Here we engineered programmable cytidine deaminases and test if we could introduce site-
191                                      APOBEC3 cytidine deaminases are largely known for their innate i
192                        The APOBEC3 family of cytidine deaminases cause lethal hypermutation of retrov
193 show a frequent deletion polymorphism in the cytidine deaminases gene cluster APOBEC3 resulting in in
194 ptide-like (APOBEC) proteins are a family of cytidine deaminases involved in various important biolog
195                                       APOBEC cytidine deaminases mutate cancer genomes by converting
196                        The APOBEC3 family of cytidine deaminases mutate the cancer genome in a range
197                            Several antiviral cytidine deaminases of the human APOBEC3 (hA3) family ha
198                 Because previously described cytidine deaminases operate on single-stranded nucleic a
199                     We also tested CBEs with cytidine deaminases other than APOBEC1 and found that th
200 polypeptide-like 3 (APOBEC3 or A3) family of cytidine deaminases restrict viral infections by mutatin
201 e catalytic subunit 3 (APOBEC-3) enzymes are cytidine deaminases that are broadly and constitutively
202 e earliest-diverged AID orthologs are active cytidine deaminases that exhibit unique substrate specif
203       The AID / APOBEC genes are a family of cytidine deaminases that have evolved in vertebrates, an
204 c polypeptide 3 (APOBEC3) family members are cytidine deaminases that play important roles in intrins
205 otein B editing complex 3 family members are cytidine deaminases that play important roles in intrins
206        Base editing relies on recruitment of cytidine deaminases to introduce changes (rather than do
207             Members of the APOBEC3 family of cytidine deaminases vary in their proportions of a virio
208 in both the nematode Caenorhabditis elegans (cytidine deaminases) and its food (Escherichia coli); wh
209 zyme-catalytic, polypeptide-like 3 (APOBEC3) cytidine deaminases, and SAMHD1 (a cell cycle-regulated
210 ily of restriction factors, the APOBEC3 (A3) cytidine deaminases, has undergone positive selection an
211  enzyme, catalytic polypeptide-like (APOBEC) cytidine deaminases, raising questions about molecular m
212 o T base editing by both rAPOBEC1 and PmCDA1 cytidine deaminases.
213 ociation with lineage-specific expression of cytidine deaminases.
214 tivating host antiviral factors, the APOBEC3 cytidine deaminases.
215  (A3B), a member of the AID/APOBEC family of cytidine deaminases.
216 d major source of mutation in cancer, APOBEC cytidine deaminases.
217 lieved, and that this is largely due to host cytidine deaminases.
218  enzyme, catalytic polypeptide-like (APOBEC) cytidine deaminases.
219 n silico evidence have revealed that APOBEC3 cytidine-deaminases, including human APOBEC3G (hA3G), ca
220 lation and enzymatic basis of RNA editing by cytidine deamination are incompletely understood.
221 normalities but demonstrated elevated global cytidine deamination at deaminase intrinsic binding site
222                No viruses showed evidence of cytidine deamination by mouse or human APOBEC3s.
223                             Programmable RNA cytidine deamination has recently been achieved using a
224 egration intermediates from APOBEC3-mediated cytidine deamination in vitro.
225 troviruses during replication as a result of cytidine deamination of minus-strand DNA transcripts.
226 of reverse transcriptase inhibition, and DNA cytidine deamination.IMPORTANCE APOBEC3 proteins are hos
227 long with tetrahydrouridine, an inhibitor of cytidine/deoxycytidine deaminase, in patients with a var
228 ion of a new radical species and a "trapped" cytidine derivative that can break down to cytosine.
229  Furthermore, sA3G was shown to bind a deoxy-cytidine dinucleotide near the catalytic Zn(2+), yet not
230 hosphatidylcholine (PC) biosynthesis via the cytidine diphosphate (CDP)-choline pathway at the expens
231 ta mutant, which cannot synthesize PE by the cytidine diphosphate diacylglycerol (CDP-DAG) pathway, i
232            This reaction is catalyzed by the cytidine diphosphate-alcohol phosphotransferase phosphat
233 r bacterial species, is the reaction between cytidine diphosphate-diacylglycerol and inositol-phospha
234  ppGpp, to PRPP, to NAD(+), to adenosine and cytidine diphosphates, and to precursors of thiamine bio
235                            Activities of the cytidine diphosphocholine (CDP-choline) and phosphatidyl
236  mice with the DNA-demethylating agent 5-aza-cytidine distinctly enhanced the antitumor response, int
237 21 nt and with the adenosine adjacent to the cytidine-guanosine (CG) dinucleotide motif led to a sign
238                                              Cytidine hydrolysis in cda mutants is likely caused by N
239 cleotides and found the lowest affinity to 5'cytidine in correlation with the translational stress-re
240 binary DNA product complex revealed that the cytidine in the first templating site was in an extrahel
241 hloroplasts and plant mitochondria, specific cytidines in mRNAs are posttranscriptionally converted t
242 et, A3G displays no deamination activity for cytidines in viral RNA.
243 aminases mutate cancer genomes by converting cytidines into uridines within ssDNA during replication.
244 s indicate the methylation at N4-position of cytidine is a molecular mechanism to fine tune base pair
245 ine ribonucleosides, which rely upon uridine-cytidine kinase 2 (UCK2) for activation, 2'-AzCyd is pho
246 o alter the substrate specificity of uridine-cytidine kinase 2 (UCK2), a key enzyme in the pyrimidine
247 l molecule-enzyme pair consisting of uridine/cytidine kinase 2 and 2'-azidouridine.
248 nly incorporated in cells expressing uridine/cytidine kinase 2 and characterize selectivity mechanism
249 o Arabidopsis (Arabidopsis thaliana) uridine/cytidine kinases, UCK1 and UCK2, which are located in th
250  motif, a cap analog (m(7)GTP), and a capped cytidine (m(7)GpppC), resolved to 2.6, 1.8 and 1.7 A, re
251                        The N4-methylation of cytidine (m4C and m42C) in RNA plays important roles in
252 more efficiently metabolized to their active cytidine monophosphate analogues, reaching higher effect
253 ate diphosphohydrolase 5/ adenylate kinase 1/cytidine monophosphate kinase 1 axis and the mitochondri
254 n unprecedented ability to attach a terminal cytidine monophosphate to cognate precursor peptide in c
255                                          The cytidine monophosphate-binding site in the C-terminal al
256 e structure and function of the prototypical cytidine monophosphate-Kdo-dependent alpha-Kdo glycosylt
257 ic acid (Neu5Gc), due to pseudogenization of cytidine monophosphate-N-acetylneuraminic acid (Neu5Ac)
258 , 3-galactosyltransferase (GGTA1) KO, GGTA1/ cytidine monophosphate-N-acetylneuraminic acid hydroxyla
259  induce anti-Neu5Gc antibody when grafted in cytidine monophosphate-N-acetylneuraminic acid hydroxyla
260               Here we demonstrate that Cmah (cytidine monophosphate-sialic acid hydroxylase)-deficien
261                 Unlike most animals in which cytidine-monophosphate-N-acetylneuraminic acid hydroxyla
262             Levels of the precursor molecule cytidine monophospho-N-acetylneuraminic acid (CMP-Neu5Ac
263 of AML patients receiving treatment with the cytidine nucleoside analogue cytarabine.
264               Thus, AML cells have increased cytidine nucleoside kinase activity that regulates mtDNA
265 armacokinetics of a series of 4'-substituted cytidine nucleosides.
266 250 muM MPA) and upregulation of uridine and cytidine nucleotides (p < 0.001 at 24 h; 5 muM MPA) occu
267        APOBEC3A, which is known to deaminate cytidines of single-stranded DNA and to inhibit viruses
268 als, and humans modifies genomically encoded cytidine or adenosine nucleotides to uridine or inosine,
269 NAs, dCas9-AID-P182X (AIDx) directly changed cytidines or guanines to the other three bases independe
270 y DNA hypermethylation of its canonical CpG (cytidine-phosphate-guanidine) island (CGI) promoter in g
271  and the Toll-like receptor 9 (TLR9) agonist cytidine-phosphate-guanosine oligodeoxynucleotide (CpG)
272 genomes, methylation occurs on adenosine and cytidine residues to include N6-methyladenine (m6A), 5-m
273 ations, including methylation of adenine and cytidine residues, are now recognized as key regulators
274 ccount for discrimination against methylated cytidine residues.
275  report the development of "CURE", the first cytidine-specific C-to-U RNA Editor.
276 ase inhibitor, dCas9-AIDx converted targeted cytidines specifically to thymines, creating specific po
277     If the first templating nucleotide was a cytidine, there was a significantly higher probability t
278 sis and polymerase activity of a fluorescent cytidine TNA triphosphate analogue (1,3-diaza-2-oxo-phen
279             tRNA(Arg1) is also modified from cytidine to 2-thiocytidine at position 32 (s(2)C(32)).
280 and test if we could introduce site-specific cytidine to thymidine transitions in the absence of targ
281 lls and are initiated through deamination of cytidine to uracil by activation-induced cytidine deamin
282 tion-induced deaminase (AID), which converts cytidine to uracil within the Ig variable (IgV) regions.
283 te Open Reading Frames (ORFs) resulting from Cytidine to Uridine (c->u) editing substitutions which o
284 majority of land plants are modified through cytidine to uridine (C-to-U) RNA editing.
285 DEAMINASE (CDA) catalyzes the deamination of cytidine to uridine and ammonia in the catabolic route o
286  found to be the main specificity factors of cytidine to uridine RNA editing.
287 breaks, and mediate the direct conversion of cytidine to uridine, thereby effecting a C-->T (or G-->A
288 able deaminases effectively convert specific cytidines to thymidines with 13% efficiency in Escherich
289 ion with the DNA methylation inhibitor 5-aza-cytidine, to activate an early skeletal muscle transcrip
290                            Here, we report a cytidine-to-uridine (C-to-U) RNA editor, referred to as
291 ects of inhibiting viral cDNA production and cytidine-to-uridine-driven hypermutation of this cDNA.
292 A by detecting crosslink-specific uridine to cytidine transitions in NGS data.
293 s demonstrated to catalyze the conversion of cytidine triphosphate (CTP) to 3'-deoxy-3',4'-didehydro-
294 n shown to be highly active against modified cytidine triphosphates, such as 5-methyl-dCTP, which, if
295          Four nucleoside substitutes, namely cytidine, uridine, adenosine, and guanosine, were identi
296 sugars, and, most notably, four nucleosides: cytidine, uridine, adenosine, and thymidine.
297       Using 2'-deoxy-2'-fluorine substituted cytidines, we show that a 2'-endo sugar conformation of
298         The resulting 'base editors' convert cytidines within a window of approximately five nucleoti
299 name DddA, that catalyses the deamination of cytidines within dsDNA.
300 ls can tolerate high doses of these modified cytidines without any deleterious effects on physiology.

 
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