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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
8 atives of 5-fluorouridine (4l), N(4)-benzoyl-cytidine (7f), N(4)-[ O-(4-benzyloxy)]-cytidine (9h), an
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
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
20 cytarabine and various structurally related cytidine analogues, such as 2'deoxycytidine and gemcitab
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,
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
33 ery of the antimitotic drug arabinofuranosyl cytidine (AraC) blunted food intake, body weight gain, a
37 in antisense elements that target the wobble cytidine at position 34 of human elongator tRNA(Met)(CAT
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
43 e units for healthy volunteers (P = .02) and cytidine concentrations were 1.44 (0.95-1.73) relative u
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
63 Because CTNNBL1 binds activation-induced cytidine deaminase (AID) that catalyzes SHM, we tested A
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
68 Likewise, recruitment of activation-induced cytidine deaminase (AID) to S regions is critical for CS
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
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
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
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
93 s and identified that L306 in the C-terminal cytidine deaminase (CD) domain contributed to its core l
95 new possibilities for anti-cancer treatment.Cytidine deaminase (CDA) deficiency leads to genome inst
97 DNMT1 and tetrahydrouridine (THU) to inhibit cytidine deaminase (CDA), the enzyme that otherwise rapi
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
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
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
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
125 We engineered fusions of CRISPR/Cas9 and a cytidine deaminase enzyme that retain the ability to be
127 associated with increased activation-induced cytidine deaminase expression, and correlate with increa
129 eaminase is unique within the zinc-dependent cytidine deaminase family as being allosterically regula
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
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
141 downstream effector APOBEC3, an IFN-induced cytidine deaminase that introduces lethal mutations duri
145 gs for cancer tissues presenting concomitant cytidine deaminase underexpression and Tau upregulation
147 l DNA N-glycosylase (eUNG) and a rat APOBEC1 cytidine deaminase variant (R33A) previously shown to ha
149 sent the crystal structure of a complex of a cytidine deaminase with ssDNA bound in the active site a
151 or stromal remodeling and down-regulation of cytidine deaminase without depletion of tumor stromal co
153 the miR-155 target Aicda (activation-induced cytidine deaminase) in this process and, in combination
156 lly defective Streptococcus pyogenes Cas9, a cytidine deaminase, and an inhibitor of base excision re
160 oduction was dependent on activation-induced cytidine deaminase, hematopoietic MyD88 expression, and
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
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
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
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.
189 indirect activation of DNA editing by APOBEC cytidine deaminases and of an endogenous clocklike mutat
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
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
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
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
219 n silico evidence have revealed that APOBEC3 cytidine-deaminases, including human APOBEC3G (hA3G), ca
221 normalities but demonstrated elevated global cytidine deamination at deaminase intrinsic binding site
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
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
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
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
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
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
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
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
266 250 muM MPA) and upregulation of uridine and cytidine nucleotides (p < 0.001 at 24 h; 5 muM MPA) occu
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
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
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
285 DEAMINASE (CDA) catalyzes the deamination of cytidine to uridine and ammonia in the catabolic route o
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
291 ects of inhibiting viral cDNA production and cytidine-to-uridine-driven hypermutation of this cDNA.
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
300 ls can tolerate high doses of these modified cytidines without any deleterious effects on physiology.