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1 ass switch recombination (activation-induced cytidine deaminase).
2 d deoxyguanosine resistant to degradation by cytidine deaminase.
3 ically required in the reaction catalyzed by cytidine deaminase.
4 re shown to interact with activation-induced cytidine deaminase.
5 or of transcription 3 and activation-induced cytidine deaminase.
6 ulating the expression of activation-induced cytidine deaminase.
7 on of dG:dU mismatches by activation-induced cytidine deaminase.
8 he B cell-specific factor activation-induced cytidine deaminase.
9 nsity that are targets of activation-induced cytidine deaminase.
10 of Dnd1 is related to Apobec1 activity as a cytidine deaminase.
11 similar to the action of activation-induced cytidine deaminase.
12 , and Blimp-1, and of the activation-induced cytidine deaminase.
13 f DNA breaks initiated by activation-induced cytidine deaminase.
14 inhibits the activity of activation-induced cytidine deaminase.
15 to a defective BLM and the downregulation of cytidine deaminase.
16 receptors are damaged by activation-induced cytidine deaminase.
17 targeting activity of the activation-induced cytidine deaminase.
18 of the tumor stroma, and down-regulation of cytidine deaminase.
19 nding motif that shares characteristics with cytidine deaminases.
20 ein B mRNA-editing enzyme complex) family of cytidine deaminases.
21 l immunity afforded by the APOBEC3 family of cytidine deaminases.
22 ociation with lineage-specific expression of cytidine deaminases.
23 tivating host antiviral factors, the APOBEC3 cytidine deaminases.
24 (A3B), a member of the AID/APOBEC family of cytidine deaminases.
25 d major source of mutation in cancer, APOBEC cytidine deaminases.
26 lieved, and that this is largely due to host 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
31 self-regulating aspect of activation-induced cytidine deaminase action that is conserved in evolution
33 ctors contains residues conserved with known cytidine deaminase active sites; however, some PPR editi
34 A3FDelta2 and A3FDelta2-4 displayed reduced cytidine deaminase activity and moderate antiviral activ
40 d functions in antibody diversification, the cytidine deaminase AID can catalyze off-target DNA damag
42 obulin class-switch recombination (CSR), the cytidine deaminase AID induces double-strand breaks into
43 ription factors and Aicda (which encodes the cytidine deaminase AID) and thus silenced B cell-specifi
44 riven expression of AICDA (which encodes the cytidine deaminase AID), the immunoglobulin receptor CD2
48 on of the genomic mutator activation-induced cytidine deaminase (AID) and AID-dependent DNA double-st
49 ed to the Igh locus in an activation-induced cytidine deaminase (AID) and H2AX-dependent fashion.
50 Fs ectopically expressing activation-induced cytidine deaminase (AID) and observed an excess of AID s
51 ed the expression of both activation-induced cytidine deaminase (AID) and of germline transcripts of
52 osine deaminases, such as activation-induced cytidine deaminase (AID) and other members of the APOBEC
53 n of DSBs is initiated by activation-induced cytidine deaminase (AID) and requires base excision repa
54 tudies have reported that activation-induced cytidine deaminase (AID) and ten-eleven-translocation (T
56 y, it has been shown that activation-induced cytidine deaminase (AID) contributes to the demethylatio
58 genome rearrangements via activation-induced cytidine deaminase (AID) followed by base excision repai
59 s studies have implicated activation-induced cytidine deaminase (AID) in B-cell translocations but ha
60 Finally, we find that activation-induced cytidine deaminase (AID) induces the rearrangement of ma
69 mmunization or infection, activation-induced cytidine deaminase (AID) initiates diversification of im
88 tected GC B cells against activation-induced cytidine deaminase (AID) mutagenesis, facilitated cell c
90 The antibody gene mutator activation-induced cytidine deaminase (AID) promiscuously damages oncogenes
93 t targeting of the enzyme activation-induced cytidine deaminase (AID) results in the accumulation of
94 ion (CSR) is initiated by activation-induced cytidine deaminase (AID) that catalyzes numerous DNA cyt
95 diversification relies on activation-induced cytidine deaminase (AID) to create U:G mismatches that a
97 ul R loops, we used human activation-induced cytidine deaminase (AID) to identify genes preventing R
98 on-coupled recruitment of activation-induced cytidine deaminase (AID) to Ig switch regions (S regions
99 Likewise, recruitment of activation-induced cytidine deaminase (AID) to S regions is critical for CS
100 on-coupled recruitment of activation-induced cytidine deaminase (AID) to switch regions and by the su
102 ically inactive dCas9 to recruit variants of cytidine deaminase (AID) with MS2-modified sgRNAs, we ca
103 e we report the fusion of activation-induced cytidine deaminase (AID) with nuclease-inactive clustere
104 the C-terminal region of activation-induced cytidine deaminase (AID), 14-3-3gamma targets this enzym
106 the expression levels of activation-induced cytidine deaminase (AID), a key player in B-cell respons
107 , we apply this screen to activation-induced cytidine deaminase (AID), a poorly soluble protein that
108 RNA and protein levels of activation-induced cytidine deaminase (AID), a protein essential for SHM an
109 The Aicda gene encodes Activation-Induced cytidine Deaminase (AID), an enzyme essential for remode
110 e B cell specific enzyme, activation-induced cytidine deaminase (AID), and can be replicated in non-B
111 tion (SHM), which require activation-induced cytidine deaminase (AID), and plasma cell differentiatio
112 genes is initiated by the activation-induced cytidine deaminase (AID), and requires target gene trans
113 itch recombination (CSR), activation-induced cytidine deaminase (AID), and stability of E47 mRNA.
114 f that machinery, such as activation-induced cytidine deaminase (AID), as well as factors central to
115 s in AICDA, which encodes activation-induced cytidine deaminase (AID), display an impaired peripheral
116 eration and expression of activation-induced cytidine deaminase (AID), DNA repair enzymes, and post-c
117 DNA lesions initiated by activation-induced cytidine deaminase (AID), in the absence of mammalian-ty
118 The Aicda gene product, activation-induced cytidine deaminase (AID), initiates somatic hypermutatio
120 ion (CSR) is initiated by activation-induced cytidine deaminase (AID), the activity of which leads to
121 These biomarkers are activation-induced cytidine deaminase (AID), the enzyme of class switch rec
125 pathway, thereby inducing activation-induced cytidine deaminase (AID), which is critical for class sw
126 omes who are deficient in activation-induced cytidine deaminase (AID), which is required for class-sw
127 instability in B cells as activation-induced cytidine deaminase (AID), which mediates this process, i
128 mutation are initiated by activation-induced cytidine deaminase (AID), which preferentially recognize
129 +) B cells stimulated for activation-induced cytidine deaminase (AID)-dependent IgH class switch reco
130 B lymphocytes induced for activation-induced cytidine deaminase (AID)-dependent IgH class switching.
131 o rapid proliferation and activation-induced cytidine deaminase (AID)-dependent remodeling of immunog
132 eliberate introduction of activation-induced cytidine deaminase (AID)-instigated DNA double-strand br
145 re, we have proposed that activation-induced cytidine deaminase (AID, encoded by AICDA) links chronic
147 ous and accessible DNMT1-targeted therapy is cytidine deaminase, an enzyme highly expressed in the in
149 in B mRNA-editing enzyme complex 1 (APOBEC1) cytidine deaminase and Deadend-1, which are involved in
150 found a synthetic lethal interaction between cytidine deaminase and microtubule-associated protein Ta
152 eamination of cytidine by activation-induced cytidine deaminase and subsequent DNA repair generates m
153 autoreactivity, expresses activation-induced cytidine deaminase and T-bet, and exhibits evidence of s
154 indirect activation of DNA editing by APOBEC cytidine deaminases and of an endogenous clocklike mutat
156 dinated DNA demethylation pathway, utilizing cytidine deaminases and thymidine glycosylases, has been
157 in both the nematode Caenorhabditis elegans (cytidine deaminases) and its food (Escherichia coli); wh
159 lly defective Streptococcus pyogenes Cas9, a cytidine deaminase, and an inhibitor of base excision re
160 llicular dendritic cells, activation-induced cytidine deaminase, and IL-21(+)PD1(+) follicular helper
161 in binds a zinc metal ion, as expected for a cytidine deaminase, and is potentially the catalytic com
162 oliferation, induction of activation-induced cytidine deaminase, and the production of circle and ger
163 zyme-catalytic, polypeptide-like 3 (APOBEC3) cytidine deaminases, and SAMHD1 (a cell cycle-regulated
164 edominant mutation signature associated with cytidine deaminase APOBEC, which correlates with the upr
165 more controversially, the activation-induced cytidine deaminase/APOBEC deaminases have the capacity t
176 It functions as an adaptor that binds to the cytidine deaminases APOBEC3G (A3G) and APOBEC3F (A3F) an
177 nfectivity factor (Vif) targets the cellular cytidine deaminases APOBEC3G (A3G) and APOBEC3F (A3F) fo
180 es, uracils introduced by activation-induced cytidine deaminase are processed by uracil-DNA glycosyla
182 vation with expression of activation-induced cytidine deaminase, as well as local differentiation of
183 tion of U:G mismatches by activation-induced cytidine deaminase but differ in their subsequent mutage
185 veral members of the human APOBEC3 family of cytidine deaminases can potently restrict retroviruses s
188 s and identified that L306 in the C-terminal cytidine deaminase (CD) domain contributed to its core l
192 new possibilities for anti-cancer treatment.Cytidine deaminase (CDA) deficiency leads to genome inst
193 (18)F-FAC tumor uptake is also influenced by cytidine deaminase (CDA), a determinant of resistance to
194 m revealed that TAMs induced upregulation of cytidine deaminase (CDA), the enzyme that metabolizes th
195 DNMT1 and tetrahydrouridine (THU) to inhibit cytidine deaminase (CDA), the enzyme that otherwise rapi
198 belongs to the AID/APOBEC protein family of cytidine deaminases (CDA) that bind to nucleic acids.
199 ent the crystal structure of a tRNA-specific cytidine deaminase, CDAT8, which has the cytidine deamin
200 on of a long isoform of the bacterial enzyme cytidine deaminase (CDDL), seen primarily in Gammaproteo
201 V regions, expression of activation-induced cytidine deaminase, clonal H chain switch, and an invert
202 man APOBEC3 protein family of polynucleotide cytidine deaminases contributes to intracellular defense
203 c mice (quasimonoclonal, activation-induced [cytidine] deaminase-Cre-tamoxifen-dependent estrogen rec
204 identify genes enabling BLM-deficient and/or cytidine deaminase-deficient cells to tolerate constitut
206 ere Tau functions in maintaining survival of cytidine deaminase-deficient cells, and ribosomal DNA tr
207 germline IgM produced in activation-induced cytidine deaminase-deficient mice (aicda(-/-)) provided
209 Igs and hypermutated IgM (activation-induced cytidine deaminase-deficient), or fully agammaglobulemic
210 to mount dominant IgM and activation-induced cytidine deaminase-dependent IgG anti-FtL responses that
211 lated high frequencies of activation-induced cytidine deaminase-dependent IgH locus chromosomal break
212 neous loss of MSH6 and of activation-induced cytidine deaminase did not appreciably affect the surviv
214 fic cytidine deaminase, CDAT8, which has the cytidine deaminase domain linked to a tRNA-binding THUMP
215 nd that conserved catalytic residues in both cytidine deaminase domains are required for RNA editing.
216 e engineered base editors containing mutated cytidine deaminase domains that narrow the width of the
217 because a single enzyme, activation-induced cytidine deaminase (encoded by Aicda), initiates both re
218 We engineered fusions of CRISPR/Cas9 and a cytidine deaminase enzyme that retain the ability to be
221 associated with increased activation-induced cytidine deaminase expression, and correlate with increa
223 eaminase is unique within the zinc-dependent cytidine deaminase family as being allosterically regula
226 polypeptide-like-3 (APOBEC3) innate cellular cytidine deaminase family, particularly APOBEC3F and APO
229 -mediated ablation of the activation-induced cytidine deaminase gene required for class switch recomb
230 pts and to upregulate the activation-induced cytidine deaminase gene through in vitro T-dependent and
231 show a frequent deletion polymorphism in the cytidine deaminases gene cluster APOBEC3 resulting in in
233 itical to both processes, activation-induced cytidine deaminase, has been identified, it remains uncl
234 oduction was dependent on activation-induced cytidine deaminase, hematopoietic MyD88 expression, and
235 s recently proposed for the APOBEC family of cytidine deaminases in generating particular genome-wide
237 the miR-155 target Aicda (activation-induced cytidine deaminase) in this process and, in combination
239 3B activity, providing new insights into how cytidine deaminase-induced mutagenesis might be activate
242 ptide-like (APOBEC) proteins are a family of cytidine deaminases involved in various important biolog
246 (PPR) protein SLO2, which lacks a C-terminal cytidine deaminase-like DYW domain, interacts in vivo wi
249 ous, and likely caused by activation-induced cytidine deaminase-mediated somatic hypermutation, as sh
251 c antibody showed loss of activation-induced cytidine deaminase mRNA induction in all mutation-bearin
257 drouridine (THU), a competitive inhibitor of cytidine deaminase, on the pharmacokinetics and pharmaco
259 2- to 6-fold increase for activation-induced cytidine deaminase, PAX5, and the nonexcised rearranged
263 report extensive computer simulations of the cytidine deaminase reaction and its temperature dependen
264 he structural gene encoding the RNA-specific cytidine deaminase responsible for production of apolipo
266 strate of some single strand-specific APOBEC cytidine deaminases, similar to the mutations that can t
267 nized individual to study activation-induced cytidine deaminase targeting and found that hypermutatio
273 downstream effector APOBEC3, an IFN-induced cytidine deaminase that introduces lethal mutations duri
276 Human APOBEC3A is a single-stranded DNA cytidine deaminase that restricts viral pathogens and en
278 e catalytic subunit 3 (APOBEC-3) enzymes are cytidine deaminases that are broadly and constitutively
279 e earliest-diverged AID orthologs are active cytidine deaminases that exhibit unique substrate specif
282 APOBEC3F (A3F) is a member of the family of cytidine deaminases that is often coexpressed with APOBE
283 otein B editing complex 3 family members are cytidine deaminases that play important roles in intrins
284 ed with overexpression of activation-induced cytidine deaminase, the hotspot length increases even fu
286 ssibilities, we used a chemical inhibitor of cytidine deaminase to stabilize and thereby artificially
288 gs for cancer tissues presenting concomitant cytidine deaminase underexpression and Tau upregulation
290 regulate transcription of activation-induced cytidine deaminase via Akt, repression of epsilonGLT and
291 signature attributed to the APOBEC family of cytidine deaminases, whereas others are confined to a si
292 on (CSR) is instigated by activation-induced cytidine deaminase, which converts cytosines in switch r
293 ation (CSR) is induced by activation-induced cytidine deaminase, which initiates a cascade of events
295 e host enzymes in the APOBEC3 (A3) family of cytidine deaminases, which act on CC (APOBEC3G) and TC (
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
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