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1 ass switch recombination (activation-induced cytidine deaminase).
2 receptors are damaged by activation-induced cytidine deaminase.
3 targeting activity of the activation-induced cytidine deaminase.
4 of the tumor stroma, and down-regulation of cytidine deaminase.
5 d deoxyguanosine resistant to degradation by cytidine deaminase.
6 ically required in the reaction catalyzed by cytidine deaminase.
7 re shown to interact with activation-induced cytidine deaminase.
8 or of transcription 3 and activation-induced cytidine deaminase.
9 ulating the expression of activation-induced cytidine deaminase.
10 on of dG:dU mismatches by activation-induced cytidine deaminase.
11 he B cell-specific factor activation-induced cytidine deaminase.
12 nsity that are targets of activation-induced cytidine deaminase.
13 of Dnd1 is related to Apobec1 activity as a cytidine deaminase.
14 similar to the action of activation-induced cytidine deaminase.
15 , and Blimp-1, and of the activation-induced cytidine deaminase.
16 (RESCUE), by directly evolving ADAR2 into a cytidine deaminase.
17 ature B cells mediated by activation-induced cytidine deaminase.
18 to a defective BLM and the downregulation of cytidine deaminase.
19 ociation with lineage-specific expression of cytidine deaminases.
20 tivating host antiviral factors, the APOBEC3 cytidine deaminases.
21 (A3B), a member of the AID/APOBEC family of cytidine deaminases.
22 d major source of mutation in cancer, APOBEC cytidine deaminases.
23 lieved, and that this is largely due to host cytidine deaminases.
24 nding motif that shares characteristics with cytidine deaminases.
25 enzyme, catalytic polypeptide-like (APOBEC) cytidine deaminases.
26 o T base editing by both rAPOBEC1 and PmCDA1 cytidine deaminases.
28 The human APOBEC3 family consists of seven cytidine deaminases (A3A to A3H), some of which display
30 se findings indicate that activation-induced cytidine deaminase acting on V-region sequences is suffi
32 ctors contains residues conserved with known cytidine deaminase active sites; however, some PPR editi
40 d functions in antibody diversification, the cytidine deaminase AID can catalyze off-target DNA damag
41 ription factors and Aicda (which encodes the cytidine deaminase AID) and thus silenced B cell-specifi
42 riven expression of AICDA (which encodes the cytidine deaminase AID), the immunoglobulin receptor CD2
45 on of the genomic mutator activation-induced cytidine deaminase (AID) and AID-dependent DNA double-st
46 ed to the Igh locus in an activation-induced cytidine deaminase (AID) and H2AX-dependent fashion.
47 Fs ectopically expressing activation-induced cytidine deaminase (AID) and observed an excess of AID s
48 n of DSBs is initiated by activation-induced cytidine deaminase (AID) and requires base excision repa
49 tudies have reported that activation-induced cytidine deaminase (AID) and ten-eleven-translocation (T
50 nt with the activities of activation-induced-cytidine deaminase (AID) and the A-T mutator, DNA polyme
52 Conditional deletion of activation-induced cytidine deaminase (AID) between heterologous challenges
54 genome rearrangements via activation-induced cytidine deaminase (AID) followed by base excision repai
56 s studies have implicated activation-induced cytidine deaminase (AID) in B-cell translocations but ha
77 tected GC B cells against activation-induced cytidine deaminase (AID) mutagenesis, facilitated cell c
79 The antibody gene mutator activation-induced cytidine deaminase (AID) promiscuously damages oncogenes
82 t targeting of the enzyme activation-induced cytidine deaminase (AID) results in the accumulation of
83 ion (CSR) is initiated by activation-induced cytidine deaminase (AID) that catalyzes numerous DNA cyt
84 Because CTNNBL1 binds activation-induced cytidine deaminase (AID) that catalyzes SHM, we tested A
87 ul R loops, we used human activation-induced cytidine deaminase (AID) to identify genes preventing R
88 on-coupled recruitment of activation-induced cytidine deaminase (AID) to Ig switch regions (S regions
90 Likewise, recruitment of activation-induced cytidine deaminase (AID) to S regions is critical for CS
91 on-coupled recruitment of activation-induced cytidine deaminase (AID) to switch regions and by the su
93 ically inactive dCas9 to recruit variants of cytidine deaminase (AID) with MS2-modified sgRNAs, we ca
94 e we report the fusion of activation-induced cytidine deaminase (AID) with nuclease-inactive clustere
95 nes and activators induce activation-induced cytidine deaminase (AID)(2) and I-promoter transcription
96 the C-terminal region of activation-induced cytidine deaminase (AID), 14-3-3gamma targets this enzym
98 the expression levels of activation-induced cytidine deaminase (AID), a key player in B-cell respons
99 , we apply this screen to activation-induced cytidine deaminase (AID), a poorly soluble protein that
100 RNA and protein levels of activation-induced cytidine deaminase (AID), a protein essential for SHM an
101 The Aicda gene encodes Activation-Induced cytidine Deaminase (AID), an enzyme essential for remode
102 e B cell specific enzyme, activation-induced cytidine deaminase (AID), and can be replicated in non-B
103 tion (SHM), which require activation-induced cytidine deaminase (AID), and plasma cell differentiatio
104 genes is initiated by the activation-induced cytidine deaminase (AID), and requires target gene trans
105 itch recombination (CSR), activation-induced cytidine deaminase (AID), and stability of E47 mRNA.
106 f that machinery, such as activation-induced cytidine deaminase (AID), as well as factors central to
107 s in AICDA, which encodes activation-induced cytidine deaminase (AID), display an impaired peripheral
108 eration and expression of activation-induced cytidine deaminase (AID), DNA repair enzymes, and post-c
109 DNA lesions initiated by activation-induced cytidine deaminase (AID), in the absence of mammalian-ty
110 ion (CSR) is initiated by activation-induced cytidine deaminase (AID), the activity of which leads to
111 These biomarkers are activation-induced cytidine deaminase (AID), the enzyme of class switch rec
115 pathway, thereby inducing activation-induced cytidine deaminase (AID), which is critical for class sw
116 omes who are deficient in activation-induced cytidine deaminase (AID), which is required for class-sw
117 ng the DNA-editing enzyme activation-induced cytidine deaminase (AID), which is required in affinity
118 instability in B cells as activation-induced cytidine deaminase (AID), which mediates this process, i
119 +) B cells stimulated for activation-induced cytidine deaminase (AID)-dependent IgH class switch reco
120 eliberate introduction of activation-induced cytidine deaminase (AID)-instigated DNA double-strand br
121 B cells having undergone activation-induced cytidine deaminase (AID)-mediated somatic hypermutation
133 re, we have proposed that activation-induced cytidine deaminase (AID, encoded by AICDA) links chronic
134 ed CRISPR-Cas9 to disrupt activation-induced cytidine deaminase (AID; Aicda) directly in BXSB zygotes
136 ment through induction of activation-induced cytidine deaminase (AID; also known as AICDA) in precurs
137 ous and accessible DNMT1-targeted therapy is cytidine deaminase, an enzyme highly expressed in the in
138 editors (GBEs) consist of a Cas9 nickase, a cytidine deaminase and a uracil-DNA glycosylase (Ung).
139 in B mRNA-editing enzyme complex 1 (APOBEC1) cytidine deaminase and Deadend-1, which are involved in
140 found a synthetic lethal interaction between cytidine deaminase and microtubule-associated protein Ta
141 eamination of cytidine by activation-induced cytidine deaminase and subsequent DNA repair generates m
142 autoreactivity, expresses activation-induced cytidine deaminase and T-bet, and exhibits evidence of s
143 ivate NF-kappaB to induce activation-induced cytidine deaminase and, therefore, Ig class switch DNA r
144 indirect activation of DNA editing by APOBEC cytidine deaminases and of an endogenous clocklike mutat
146 dinated DNA demethylation pathway, utilizing cytidine deaminases and thymidine glycosylases, has been
147 in both the nematode Caenorhabditis elegans (cytidine deaminases) and its food (Escherichia coli); wh
149 lly defective Streptococcus pyogenes Cas9, a cytidine deaminase, and an inhibitor of base excision re
150 llicular dendritic cells, activation-induced cytidine deaminase, and IL-21(+)PD1(+) follicular helper
151 in binds a zinc metal ion, as expected for a cytidine deaminase, and is potentially the catalytic com
152 oliferation, induction of activation-induced cytidine deaminase, and the production of circle and ger
153 zyme-catalytic, polypeptide-like 3 (APOBEC3) cytidine deaminases, and SAMHD1 (a cell cycle-regulated
154 edominant mutation signature associated with cytidine deaminase APOBEC, which correlates with the upr
155 more controversially, the activation-induced cytidine deaminase/APOBEC deaminases have the capacity t
167 nfectivity factor (Vif) targets the cellular cytidine deaminases APOBEC3G (A3G) and APOBEC3F (A3F) fo
170 ls, lesions introduced by activation-induced cytidine deaminase are processed by multiple error-prone
171 es, uracils introduced by activation-induced cytidine deaminase are processed by uracil-DNA glycosyla
174 vation with expression of activation-induced cytidine deaminase, as well as local differentiation of
175 ase-based CBE(7), and the Petromyzon marinus cytidine deaminase-based CBE Target-AID(4) induce less e
176 BEC3A-based CBE(6), human activation-induced cytidine deaminase-based CBE(7), and the Petromyzon mari
177 tion of U:G mismatches by activation-induced cytidine deaminase but differ in their subsequent mutage
180 APOBEC3G, a member of the double-domain cytidine deaminase (CD) APOBEC, binds RNA to package int
181 s and identified that L306 in the C-terminal cytidine deaminase (CD) domain contributed to its core l
184 new possibilities for anti-cancer treatment.Cytidine deaminase (CDA) deficiency leads to genome inst
186 (18)F-FAC tumor uptake is also influenced by cytidine deaminase (CDA), a determinant of resistance to
187 m revealed that TAMs induced upregulation of cytidine deaminase (CDA), the enzyme that metabolizes th
188 DNMT1 and tetrahydrouridine (THU) to inhibit cytidine deaminase (CDA), the enzyme that otherwise rapi
192 belongs to the AID/APOBEC protein family of cytidine deaminases (CDA) that bind to nucleic acids.
193 on of a long isoform of the bacterial enzyme cytidine deaminase (CDDL), seen primarily in Gammaproteo
194 V regions, expression of activation-induced cytidine deaminase, clonal H chain switch, and an invert
195 man APOBEC3 protein family of polynucleotide cytidine deaminases contributes to intracellular defense
196 c mice (quasimonoclonal, activation-induced [cytidine] deaminase-Cre-tamoxifen-dependent estrogen rec
197 identify genes enabling BLM-deficient and/or cytidine deaminase-deficient cells to tolerate constitut
199 ere Tau functions in maintaining survival of cytidine deaminase-deficient cells, and ribosomal DNA tr
200 germline IgM produced in activation-induced cytidine deaminase-deficient mice (aicda(-/-)) provided
202 Igs and hypermutated IgM (activation-induced cytidine deaminase-deficient), or fully agammaglobulemic
203 ction factors that inhibit HIV-1 through DNA cytidine deaminase-dependent and -independent mechanisms
204 to mount dominant IgM and activation-induced cytidine deaminase-dependent IgG anti-FtL responses that
205 lated high frequencies of activation-induced cytidine deaminase-dependent IgH locus chromosomal break
207 nd that conserved catalytic residues in both cytidine deaminase domains are required for RNA editing.
208 e engineered base editors containing mutated cytidine deaminase domains that narrow the width of the
210 because a single enzyme, activation-induced cytidine deaminase (encoded by Aicda), initiates both re
212 We engineered fusions of CRISPR/Cas9 and a cytidine deaminase enzyme that retain the ability to be
214 associated with increased activation-induced cytidine deaminase expression, and correlate with increa
216 eaminase is unique within the zinc-dependent cytidine deaminase family as being allosterically regula
218 polypeptide-like-3 (APOBEC3) innate cellular cytidine deaminase family, particularly APOBEC3F and APO
223 -mediated ablation of the activation-induced cytidine deaminase gene required for class switch recomb
224 pts and to upregulate the activation-induced cytidine deaminase gene through in vitro T-dependent and
225 show a frequent deletion polymorphism in the cytidine deaminases gene cluster APOBEC3 resulting in in
227 ily of restriction factors, the APOBEC3 (A3) cytidine deaminases, has undergone positive selection an
228 oduction was dependent on activation-induced cytidine deaminase, hematopoietic MyD88 expression, and
229 s recently proposed for the APOBEC family of cytidine deaminases in generating particular genome-wide
231 the miR-155 target Aicda (activation-induced cytidine deaminase) in this process and, in combination
232 n silico evidence have revealed that APOBEC3 cytidine-deaminases, including human APOBEC3G (hA3G), ca
234 3B activity, providing new insights into how cytidine deaminase-induced mutagenesis might be activate
235 NF-kappaB activation and activation-induced cytidine deaminase induction, and boosts IgG Ab and auto
237 ptide-like (APOBEC) proteins are a family of cytidine deaminases involved in various important biolog
240 (PPR) protein SLO2, which lacks a C-terminal cytidine deaminase-like DYW domain, interacts in vivo wi
245 ous, and likely caused by activation-induced cytidine deaminase-mediated somatic hypermutation, as sh
247 c antibody showed loss of activation-induced cytidine deaminase mRNA induction in all mutation-bearin
251 f Cpf1 (Cas12a) and nCas9-activation-induced cytidine deaminase (nCas9-Target-AID) systems to mutagen
253 ve DNA strand breakage at activation-induced cytidine deaminase off-target genes, its role at the hyp
254 drouridine (THU), a competitive inhibitor of cytidine deaminase, on the pharmacokinetics and pharmaco
261 enzyme, catalytic polypeptide-like (APOBEC) cytidine deaminases, raising questions about molecular m
262 report extensive computer simulations of the cytidine deaminase reaction and its temperature dependen
263 polypeptide-like 3 (APOBEC3 or A3) family of cytidine deaminases restrict viral infections by mutatin
265 strate of some single strand-specific APOBEC cytidine deaminases, similar to the mutations that can t
266 reates a potent substrate for APOBEC3A (A3A) cytidine deaminase that can promote formation of mutatio
271 downstream effector APOBEC3, an IFN-induced cytidine deaminase that introduces lethal mutations duri
274 Human APOBEC3A is a single-stranded DNA cytidine deaminase that restricts viral pathogens and en
275 e catalytic subunit 3 (APOBEC-3) enzymes are cytidine deaminases that are broadly and constitutively
276 e earliest-diverged AID orthologs are active cytidine deaminases that exhibit unique substrate specif
278 otein B editing complex 3 family members are cytidine deaminases that play important roles in intrins
279 c polypeptide 3 (APOBEC3) family members are cytidine deaminases that play important roles in intrins
280 uences rarely targeted by activation-induced cytidine deaminase, the enzyme responsible for antibody
281 ed with overexpression of activation-induced cytidine deaminase, the hotspot length increases even fu
284 ssibilities, we used a chemical inhibitor of cytidine deaminase to stabilize and thereby artificially
286 gs for cancer tissues presenting concomitant cytidine deaminase underexpression and Tau upregulation
288 l DNA N-glycosylase (eUNG) and a rat APOBEC1 cytidine deaminase variant (R33A) previously shown to ha
290 regulate transcription of activation-induced cytidine deaminase via Akt, repression of epsilonGLT and
291 ed genomic loci that are more susceptible to cytidine deaminase, we set up a high-throughput assay fo
292 signature attributed to the APOBEC family of cytidine deaminases, whereas others are confined to a si
294 on (CSR) is instigated by activation-induced cytidine deaminase, which converts cytosines in switch r
295 ation (CSR) is induced by activation-induced cytidine deaminase, which initiates a cascade of events
296 t studies indicate that a subclass of APOBEC cytidine deaminases, which convert cytosine to uracil du
297 EC3 activity of Vif variants against several cytidine deaminases will help reveal the requirement for
298 sent the crystal structure of a complex of a cytidine deaminase with ssDNA bound in the active site a
300 or stromal remodeling and down-regulation of cytidine deaminase without depletion of tumor stromal co