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1 hat ends with reversion of 5mC to unmodified cytosine.
2 mC) state and do not resolve to unmethylated cytosine.
3 lating position, as compared with unmodified cytosine.
4  the hydroxymethylation and glucosylation of cytosine.
5 at cleaves foreign DNA-containing methylated cytosines.
6 nd specificity, without affecting unmodified cytosines.
7    Sixty-five percent of the pause sites are cytosines.
8 urement of methylation frequencies at single cytosines.
9 rallel profiling of activity on all modified cytosines.
10  the T4(C) mutant, which contains unmodified cytosines.
11  editors can only convert either adenines or cytosines.
12 1-(2'-deoxy-2'-(18)F-fluoroarabinofuranosyl) cytosine ((18)F-FAC) is a PET radiotracer that measures
13                    TET3 in turn mediates DNA cytosine 5'-hydroxymethylation (5hmC) and upregulates ge
14                          We propose that RNA cytosine 5-hydroxymethylation by Tets is a mark of trans
15                                              Cytosine-5 methylation (m5C) has been detected in mitoch
16  have been studied, the impact of the global cytosine-5 methylome on development, homeostasis and str
17                      Here, we identified the cytosine-5 RNA methyltransferase NSUN2 as a sensor for e
18 , we report that a clonal population of DNA (cytosine-5)-methyltransferase 1 (DNMT1)-only cells produ
19 ion enzymes produces three oxidized forms of cytosine: 5-hydroxmethylcytosine, 5-formylcytosine, and
20 yl-labeled DNA at the C5 and N6 positions of cytosine (5mC) and adenine (6mA) nucleobases, respective
21         DNA methylation at the 5-position of cytosine (5mC) plays vital roles in mammalian developmen
22 tides can be methylated at the 5-position of cytosine (5mC), and then may undergo successive oxidatio
23 NA is the product of oxidation of methylated cytosines (5mC) by Ten-Eleven-Translocation (TET) enzyme
24                               Methylation of cytosine 69 in VTRNA1.1 occurs frequently in human cells
25 mutations in a homopolymeric tract (HT) of 7 cytosines (7C) in the glpK gene.
26 hado-Joseph disease (SCA3/MJD), the expanded cytosine adenine guanine (CAG) repeat in ATXN3 is the ca
27                        We assessed 9 SNP and cytosine-adenine (CA) repeats in IFNG by nucleotide sequ
28 evaluated using the disease burden score and cytosine-adenine-guanine age product score.
29 linical onset after age 18 years, 36 or more cytosine-adenine-guanine repeats in the huntingtin gene,
30 s an anti conformation opposite a templating cytosine and a syn conformation opposite adenine.
31            The DNA methylations occurring at cytosine and adenine are carried out by SAM-dependent me
32 base editors improves the targeting scope of cytosine and adenine base editing.
33                                              Cytosine and adenine base editors (CBEs and ABEs) are pr
34 erized sequence-activity relationships of 11 cytosine and adenine base editors (CBEs and ABEs) on 38,
35                            CRISPR-guided DNA cytosine and adenine base editors are widely used for ma
36                        However, the existing cytosine and adenine base editors can only install trans
37 ation of dual AAVs for the delivery of split cytosine and adenine base editors that are then reconsti
38 -N bonds to endo- and exocyclic nitrogens of cytosine and adenine.
39                   The comparison of modified cytosine and enzyme levels in Tet KO cells revealed dist
40 larly permuted Cas9 variants to produce four cytosine and four adenine base editors with an editing w
41 treating donors with phosphorothioate-linked cytosine and guanine rich oligodeoxynucleotides (CpG ODN
42 tabilizes the pai-pai stacking of the target cytosine and H257, resulting in dislocation of the targe
43 provides further insight into tautomerism of cytosine and suggests a new method to study the tautomer
44 tricate hydrogen bond network with the first cytosine and the two opposing guanine nucleotides to con
45  HIV-1 replication by deaminating viral cDNA cytosines and interfering with reverse transcription.
46                                 The adenine, cytosine, and guanine bases of DNA are susceptible to al
47 at distal sites from the original deaminated cytosine, and these repair intermediates could generate
48  deaminate at higher rates than unmethylated cytosines, and the lesions they produce are repaired les
49 erization of three tautomers of deprotonated cytosine anions, [trans-keto-amino-N3H-H8b] (tKAN3H8b(-)
50 specific DNA stretches where guanines and/or cytosines are 30 base pairs apart and the intervening se
51                      As a result, methylated cytosines are mutational hotspots.
52 -guanine (CpG) DNA as well as DNA containing cytosine at the second position from 5'-end (5'-xCx DNA)
53   Systematic variation in the methylation of cytosines at CpG sites plays a critical role in early de
54 tructural data for DNA containing methylated cytosine, automated analysis of structural information i
55 y molecular self-assembly of a fused guanine-cytosine base (G C base).
56  Methylation of the first but not the second cytosine base abolishes AceCas9 activity, consistent wit
57 d target sites with varied levels of guanine-cytosine base content.
58                                 By contrast, cytosine base editing induced SNVs at more than 20-fold
59              We developed a dual adenine and cytosine base editor (A&C-BEmax) by fusing both deaminas
60               These results demonstrate that cytosine base editor-mediated editing may result in unin
61                                              Cytosine base editors (CBEs) enable efficient, programma
62                                              Cytosine base editors (CBEs) enable targeted C*G-to-T*A
63                                              Cytosine base editors (CBEs) generate C-to-T nucleotide
64                         The most widely used cytosine base editors (CBEs) induce deamination of DNA c
65                    We used BE-PACE to evolve cytosine base editors (CBEs) that overcome target sequen
66  inhibitor resulted in RNA-free DddA-derived cytosine base editors (DdCBEs) that catalyse C*G-to-T*A
67                                              Cytosine base editors and adenine base editors (ABEs) ca
68                         Existing adenine and cytosine base editors induce only a single type of modif
69                                    Recently, cytosine base editors with rAPOBEC1 were reported to ind
70               We observed frequent on-target cytosine base edits at the BCL11A erythroid enhancer at
71 H257, resulting in dislocation of the target cytosine base from the catalytic position.
72                   Adding a methyl group to a cytosine base locally modifies the structural features o
73              The strong increase of oxidized cytosine bases (5hmC, 5fC, and 5caC) was accompanied by
74  that the APOBEC3B protein can deaminate the cytosine bases at two sites whose mutant states are subj
75      Moreover, the conversion of adenine and cytosine bases can be achieved by fusing SauriCas9 to th
76 model shows that both mono- or di-methylated cytosine bases could specify the C:T pair and induce the
77  also proficient as direct N-demethylases of cytosine bases.
78 ects mutation dynamics not only at the focal cytosine but also at neighboring nucleotides.
79 tify multiple causes underlying selection of cytosines by APOBEC3A for deamination, and demonstrate t
80                      Directed methylation of cytosines by the de novo methyltransferases DNMT3A and D
81 g a "flipped-out" conformation of the target cytosine bypass the SNF2 domain's requirement for hemime
82 base pairs of adenine (A) and thymine (T) or cytosine (C) and guanine (G), but G-rich DNA can form fo
83  attenuating mutations such as uracil (U) to cytosine (C) at nucleotide 472 in the 5' noncoding regio
84                                          The cytosine (C)-rich sequences that can fold into tetraplex
85 t is dependent on the actions of an intronic cytosine (C)-rich splice regulatory determinant and its
86                          Given that all DNA-(cytosine C5)-methyltransferases have a common catalytic
87 , it has been discovered that different DNA-(cytosine C5)-methyltransferases including DNMT3A generat
88        Incomplete conversion of unmethylated cytosines can introduce false positive methylation call.
89 cited-state dynamics for the i-motif form of cytosine chains (dC)(10), using the ultrafast fluorescen
90 epared by co-assembly between pemetrexed and cytosine-containing diselenide through hydrogen bonds.
91 -U and G-to-A transitions in the already low cytosine content SARS-CoV-2 genome.
92 e-molecule real-time sequencing uncovers the cytosine conversion patch as a D-loop footprint.
93  detecting whole-genome DNA methylation with cytosine coverage as high as 96% and unbiased coverage o
94 mediated base pairing in duplexes containing cytosine-cytosine mismatches.
95 the ER stress-associated apoptosis regulator cytosine-cytosine-adenosine-adenosine-thymidine (CCAAT)/
96                           Flura-seq utilizes cytosine deaminase (CD) to convert fluorocytosine to flu
97 uced A3B expression and concomitant cellular cytosine deaminase activity.
98 RF2 stoichiometrically inhibits APOBEC3B DNA cytosine deaminase activity.
99 HPV-positive OSCCs, the signatures of APOBEC cytosine deaminase editing, associated with anti-viral i
100                 The mutagenic APOBEC3B (A3B) cytosine deaminase is frequently over-expressed in cance
101 if are likely to bind this single-domain DNA cytosine deaminase on physically distinct surfaces.
102 BEC3G (A3G) is a single-stranded DNA (ssDNA) cytosine deaminase that can restrict HIV-1 infection by
103                                      APOBEC1 cytosine deaminase was initially characterized as pairin
104 POBEC3 members, is a single-stranded (ss)DNA cytosine deaminase with antiviral activity.
105 as five members of the APOBEC3 family of DNA cytosine deaminases are capable of inhibiting HIV-1 repl
106 enzymes.IMPORTANCE The APOBEC3 family of DNA cytosine deaminases constitutes a vital innate immune de
107          The APOBEC3 family of antiviral DNA cytosine deaminases is implicated as the second largest
108 POBEC) family of single-stranded DNA (ssDNA) cytosine deaminases provides innate immunity against vir
109       Human cells express up to 9 active DNA cytosine deaminases with functions in adaptive and innat
110 is the APOBEC3 family of single-stranded DNA cytosine deaminases, which inhibits virus replication th
111                                   Methylated cytosines deaminate at higher rates than unmethylated cy
112  the nucleus, and nuclear extracts displayed cytosine deamination activity.
113 mothriptic breakpoints is the consequence of cytosine deamination by APOBEC3B.
114                 APOBEC3B (A3B)-catalyzed DNA cytosine deamination contributes to the overall mutation
115 ignature found in melanomas, suggesting that cytosine deamination encountered by the replicative poly
116 many of these mutations are a consequence of cytosine deamination events occurring on the non-target
117                                      We find cytosine deamination follows a conventional thermal age
118 th rAPOBEC1 were reported to induce unguided cytosine deamination in genomic DNA and cellular RNA.
119                                              Cytosine deamination is often needed for TEs to take on
120                      While the CTD catalyzes cytosine deamination, the NTD is believed to provide add
121 tated and nonfunctional virus in addition to cytosine deamination.
122 promote extensive APOBEC3A/APOBEC3B-mediated cytosine deaminations in human keratinocytes.
123                           The elucidation of cytosine demethylation has drawn added attention the thr
124                          N(4)-(Aryl)alkyloxy-cytosine derivatives, especially with bulky benzyloxy su
125                                              Cytosine DNA bases can be methylated by DNA methyltransf
126 hylation (examined using H3K4/K27me3 marks), cytosine DNA methylation and differential gene expressio
127 cing (WGBS) has been widely used to quantify cytosine DNA methylation frequency in an expanding array
128                                              Cytosine DNA methylation is essential for mammalian deve
129 thway in plants controls gene expression via cytosine DNA methylation.
130 y, in Cryptococcus neoformans, the loss of a cytosine DNA methyltransferase at least 50 million years
131 ighlights the existence of a new predominant cytosine DNA modification pathway in P. falciparum and o
132                                              Cytosine (DNA) methylation in plants regulates the expre
133 ation of nucleolytic processing by TREX1 and cytosine editing by APOBEC3B.
134 9-based synchronous programmable adenine and cytosine editor (SPACE) that can concurrently introduce
135 uppressed in the nucleotide combination of a cytosine followed by a guanosine (CpG), indicating that
136  of the TYR gene, with the substitution of a cytosine for a thymine nucleotide (C64T) at codon 22, le
137                    We observe that guanine + cytosine (G + C) content and CpG density surrounding tRN
138 ific codon bias is determined by the guanine-cytosine (GC) content of differentially expressed genes.
139 etween open reading frame length and guanine-cytosine (GC) content presents universally substantial d
140 ed very high evolutionary rates, low Guanine-Cytosine (GC) content, small genome sizes, and lower gen
141 tion rates correlates with increased guanine-cytosine (GC) content, suggesting a key role for GC-bias
142 ats, or too high or too low windowed guanine-cytosine (GC) content.
143 s of Z-linked inversions, repeat and guanine-cytosine (GC) contents, as well as W-linked gene loss ra
144               By surveying more than 400 000 cytosine guanine dinucleotide (CpG) sites measured from
145 ibly due to impaired H3K27me3 spreading from cytosine guanine dinucleotide islands, which is reminisc
146  quantification of targeted panels of single cytosine guanine dinucleotides from multiple independent
147 s (EWAS) further identified 155, 46, and 168 cytosine-guanine dinucleotide regions associated (FDR-P
148       We identified significantly associated cytosine-guanine dinucleotide regions for 82 transcripts
149 and DNA methylation was assessed at >400,000 cytosine-guanine dinucleotides (CpGs) in whole blood or
150 n models to quantify associations at 720,077 cytosine-guanine dinucleotides (CpGs), with adjustment f
151 erived DNA methylation at over 400 000 CpGs (cytosine-guanine dinucleotides) in 5 population-based co
152 n pathway within a cellular setting, whereby cytosine-guanosine binding appeared to disrupt this cell
153 r (GM-CSF), the Toll-like-receptor-9 agonist cytosine-guanosine oligodeoxynucleotide and one or multi
154 lls, whose ligands include phosphorothioated cytosine-guanosine oligonucleotides, a motif often seen
155                         Tautomers of neutral cytosine have been studied in the gas phase, but much le
156                                              Cytosine hydroxymethylation (5hmC) in mammalian DNA is t
157 ve to the unmodified cognate sequence, while cytosine hydroxymethylation (particularly at the CpA sit
158 e found that the phage T4 genome modified by cytosine hydroxymethylation and glucosylation (ghmC) exh
159 rted microRNA profiles, and a global loss of cytosine hydroxymethylation marks.
160 ytosine methylation and formylation, reduced cytosine hydroxymethylation, decreased histone acetylati
161 ors (such as Eed and Jarid2), show decreased cytosine hydroxymethylation.
162 e that act on the amino groups of adenine or cytosine in DNA, have conserved motifs in a particular o
163 , is up to 26-fold more efficient at editing cytosine in the GC context, a disfavored context for wil
164 able for analyzing the methylation status of cytosines in any sequence context.
165 on and methylation estimates for all genomic cytosines in different contexts (CpG and non-CpG) and a
166  Tet-enzyme-mediated 5-hydroxymethylation of cytosines in DNA plays a crucial role in mouse embryonic
167 ensive transcriptome-wide deamination of RNA cytosines in human cells, inducing tens of thousands of
168 pe composition and differentially methylated cytosines in individual cell-types (DMCTs) for a range o
169                                      1.4% of cytosines in Saccharina japonica were methylated mainly
170 C3, A3) family member proteins can deaminate cytosines in single-strand (ss) DNA, which restricts hum
171             The AID/APOBEC enzymes deaminate cytosines in single-stranded DNA (ssDNA) and play key ro
172 nthesis of APOBEC3A, an enzyme that converts cytosines in single-stranded DNA to uracil, and mutation
173 calculation confirmed that APOBEC3A modifies cytosines in the lagging-strand template during replicat
174 mily, APOBEC3A (A3A) and APOBEC3B, deaminate cytosines in the lagging-strand template during replicat
175 quitous chromatin feature, present in 25% of cytosines in the maize genome, but variation and evoluti
176 silio-ME3) to streamline removal of oxidized cytosine intermediates to enhance activation of targeted
177 teps in the assay is converting unmethylated cytosines into thymines (BS conversion).
178                                   Methylated cytosine is an effector of epigenetic gene regulation.
179                                     5-methyl cytosine is widespread in plant genomes in both CG and n
180 nes is slightly reduced, whereas activity on cytosines is higher and RNA off-target activity is subst
181 ion of a methyl group to the fifth carbon of cytosine, is the most prevalent DNA modification in huma
182                     The methylation level of cytosines located at CG sites was higher than those at C
183                   Methylation of carbon-5 of cytosines (m(5) C) is a post-transcriptional nucleotide
184  high sensitivity of AceCas9 to the modified cytosine makes it a potential device for detecting epige
185 are significantly higher than the methylated cytosine (mC) levels of 0.01-0.05%.
186  overlaying the methylation frequency of two cytosines measured independently.
187                                     Three 3' cytosine metallo-base pairs stabilize a parallel A-form-
188                                              Cytosine methylation (5-methylcytosine [5mC]) of DNA is
189 bout the predominant cytosine modifications, cytosine methylation (5mC) and hydroxymethylation (5hmC)
190 indings suggest that loss of balance between cytosine methylation and demethylation during the circad
191               Integrated network analysis of cytosine methylation and expression datasets has the pot
192 ombination led to increased levels of global cytosine methylation and formylation, reduced cytosine h
193                                  Genome-wide cytosine methylation and gene expression profiling showe
194 smoke significantly affected the patterns of cytosine methylation and hydroxymethylation in the lungs
195  the demethylase TET enzyme led to decreased cytosine methylation and increased hydroxymethylation du
196                              However, beyond cytosine methylation and its oxidated derivatives, very
197  been shown to result in widespread aberrant cytosine methylation and loss of 5-hydroxymethylcytosine
198 s 1258 SUMMARY: Heritable gains or losses of cytosine methylation can arise stochastically in plant g
199                                  We identify cytosine methylation changes associated with kidney stru
200 replicating nuclei and determine genome-wide cytosine methylation dynamics during the plant cell cycl
201                   Our findings indicate that cytosine methylation has a broader mutational footprint
202  is a nuclear protein that binds to sites of cytosine methylation in the genome.
203                                              Cytosine methylation is a ubiquitous modification in mam
204                                RNA-dependent cytosine methylation is also reduced, but only ~20%, sug
205                                              Cytosine methylation is an epigenetic mark that dictates
206                 An inevitable consequence of cytosine methylation is an increase in C-to-T transition
207 es and transposable elements, DNMT1-mediated cytosine methylation is essential for kidney development
208 y removes thymine from DNA contexts in which cytosine methylation is prevalent, including CG and one
209                                              Cytosine methylation of DNA is a widespread modification
210                             Here we examined cytosine methylation of human kidney tubules using Illum
211                                              Cytosine methylation of regulatory regions, such as prom
212           Nonetheless, regional variation of cytosine methylation states was widespread in the tetrap
213 nerated CAFs demonstrated widespread loss of cytosine methylation that was associated with overexpres
214                                              Cytosine methylation was measured in blood using pyroseq
215        The data herein provide evidence that cytosine methylation, although occurring at a low level,
216 ex interplay among nuclear receptor ligands, cytosine methylation, and the metabolome in both the ind
217 ts have found that epigenetics, particularly cytosine methylation, could play a role in the etiologic
218 sures post-replication temporal evolution of cytosine methylation, thus enabling genome-wide monitori
219  is mainly independent of age divergence and cytosine methylation.
220  efficient only in contexts known to feature cytosine methylation.
221 3D genome organization, gene expression, and cytosine methylation.
222 ugh flipping in the presence or absence of a cytosine modification and that specific interactions of
223 epletion in a neuronal cell model results in cytosine modification changes that are reciprocal to tho
224 stematic measurement of global levels of DNA cytosine modification in wild-type and Apc(Min/+) mouse
225  upregulation of TET2, a master-regulator of cytosine modification status.
226 Extending our recent findings of oscillating cytosine modifications (osc-modCs) in mice, in this stud
227                                          DNA cytosine modifications are key epigenetic regulators of
228             We find a widespread increase in cytosine modifications at enhancers in PD neurons, which
229 ites by HR-MAS (1)H NMR spectroscopy and DNA cytosine modifications by LC/MS, in normal small intesti
230           The ensuing cyclic biochemistry of cytosine modifications gives rise to a continuous, out-o
231 hogen, little is known about the predominant cytosine modifications, cytosine methylation (5mC) and h
232 ults reveal a hierarchical interplay between cytosine modifications, nucleosome positions, and DNA se
233        To dissect the contributions of these cytosine modifying enzymes, we generated combinations of
234 el hybrid bioinspired amphiphile featuring a cytosine moiety, which self-assembles into liposomes can
235                                          The cytosines most sensitive to modification were next to th
236 n the close vicinity (+/-3 bp) of methylated cytosines mutate less frequently.
237                                              Cytosine N (4)-methylation (m(4)C) at position 839 (m(4)
238 igated the catalytic mechanism of DNMT3A for cytosine N3 methylation.
239 NA substrates containing either a templating cytosine (nonmutagenic) or adenine (mutagenic).
240 e (pAcF) that universally bind all mammalian cytosine nucleobases, but selectively form diaminooxy-li
241  other hand, reactions of 5-ethynyluracil or cytosine nucleosides with TMSN(3) led to the chemoselect
242 contain different proportions of guanine and cytosine nucleotides.
243 -denaturing bisulfite treatment modifies the cytosines on the displaced strand of the D-loop to uraci
244 f them the edited adenosines mis-paired with cytosines on the pre-miRNA structure.
245  (GO) reporter system that indicates precise cytosine or adenine base editing in situ with high sensi
246                                              Cytosine or adenine base editors (CBEs or ABEs) can intr
247 further demonstrated that different forms of cytosine or adenine base editors containing SpCas9-NG wo
248 DNA tightropes that contain 8-oxoG:A, 8-oxoG:cytosine, or apurinic product analog sites.
249       While its binding preference for multi-cytosine-patch (C-patch) containing RNA is well document
250  dimerization is facilitated by unmethylated cytosine-phosphate-guanine (CpG) DNA as well as DNA cont
251                 TLR9 recognizes unmethylated cytosine-phosphate-guanine (CpG) motifs present in viral
252  used two approaches, one focusing on single cytosine-phosphate-guanine (CpG) sites and another on di
253 vel random intercept to identify significant Cytosine-phosphate-Guanine (CpG) sites and differentiall
254  placental DNA methylation (DNAm) at 720,077 cytosine-phosphate-guanine (CpG) sites and prenatal mate
255 DNAm during this period at asthma-associated cytosine-phosphate-guanine (CpG) sites and such an assoc
256  nucleotide resolution of DNA methylation in cytosine-phosphate-guanine (CpG) sites and surrounding r
257         DNA methylation patterns at specific cytosine-phosphate-guanine (CpG) sites predictably chang
258  independent marginal analysis at individual cytosine-phosphate-guanine (CpG) sites, thus ignoring co
259 05 genes with altered DNA methylation at 605 cytosine-phosphate-guanine (CpG) sites, which were assoc
260 drinks per week and DNA methylation at 5,458 cytosine-phosphate-guanine (CpG) sites.
261 42, 1, 592, and 17 differentially methylated cytosine-phosphate-guanine (dmCpG) sites (false discover
262 trol, 134 participants and 414,818 autosomal cytosine-phosphate-guanine sites were used for epigenome
263 rs11740584 and rs2299007 risk alleles create cytosine-phosphate-guanine sites, which are highly methy
264 on uniquely mapped cytosines within the CpG (cytosine-phosphate-guanine) dinucleotide context across
265                Methylation levels at 52 CpG (cytosine-phosphate-guanine) sites were associated with i
266 tivation, only demethylation of histones and cytosine-phosphate-guanines (CpGs) in gene promoters and
267                        We identified 1189 5'-cytosine-phosphate-guanosine-3' (CpG) sites that were di
268  process involves spontaneous deamination of cytosine, producing uracil in pyrimidine dimers, followe
269 that rotationally position highly methylated cytosines relative to phased nucleosomes.
270                               Methylation of cytosine residues in DNA, the best studied epigenetic mo
271 enrich for DNA fragments carrying deaminated cytosine residues, we were able to sequence 70 and 0.4 m
272                                              Cytosine-rich DNA can fold into secondary structures kno
273                                   Preventing cytosine-rich exon inclusion in mutant KRAS/p53 PDACs de
274 ing regulator hnRNPK to promote inclusion of cytosine-rich exons within GTPase-activating proteins (G
275 e, which consists of 16,569 bp of DNA with a cytosine-rich light (L) strand and a heavy (H) strand, e
276                                 Guanine- and cytosine-rich nucleic acid sequences have the potential
277 re constructed from double-stranded DNA with cytosine-rich stick ends (C-monomer) and are internalize
278                  Adenine base editor-induced cytosine substitutions occur independently of adenosine
279 ed with SLAMseq, which introduces thymine to cytosine (T>C) conversions at the sites of the incorpora
280 caused by an inverted binding of the flipped cytosine target base into the active-site pocket of the
281          As these structures are composed of cytosine, they are potential sites for epigenetic modifi
282                               Methylation of cytosine to 5-methylcytosine (5mC) is a prevalent DNA mo
283                               Methylation of cytosine to 5-methylcytosine (mC) is a prevalent reversi
284 o guanine, adenine base editors also convert cytosine to guanine or thymine in a narrow editing windo
285                                            A cytosine to thymine mutation at nucleotide 654 of human
286 es of DNA damage include a high frequency of cytosine to thymine substitutions (C-to-T) at the ends o
287 on-induced deaminase (AID), which deaminates cytosine to uracil in DNA.
288 neration of mutations through deamination of cytosine to uracil in single-stranded HIV-1 (-) DNA is t
289  microsatellites and methylation-informative cytosines to characterize both lineage and cell type, re
290 (SHM), and gene conversion by converting DNA cytosines to uracils at specific genomic regions.
291 eatment catalyzes the conversion of unpaired cytosines to uracils, creating permanent genetic tags fo
292 e catalytic subunit (APOBEC) enzymes convert cytosines to uracils, creating signature mutations that
293 s (hydroxyurea and 1-beta-d-arabinofuranosyl cytosine) to trap single strand breaks that are formed d
294 xpand the base editing toolbox by developing cytosine transversion base editors.
295 ine-5'-monophosphate (IMP) dehydrogenase and cytosine triphosphate (CTP) synthase.
296 ase editors (CBEs) induce deamination of DNA cytosines using the rat APOBEC1 enzyme, which is targete
297                               In particular, cytosine was novel and associated with the lowest risk.
298  methyl marks on >10 million uniquely mapped cytosines within the CpG (cytosine-phosphate-guanine) di
299 an also support base editing if they contain cytosines within the deaminase activity window.
300 uch as methylation and hydroxymethylation on cytosine would greatly impact the binding of transcripti

 
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