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1 G1 Abs, demonstrating a functional effect on class switch recombination.
2 deletion of intervening DNA sequences during class switch recombination.
3 ution and impedes B cell differentiation and class switch recombination.
4 tation but defective affinity maturation and class switch recombination.
5 homologous end-joining during immunoglobulin class switch recombination.
6 ects VDJ recombination with minor effects on class switch recombination.
7 plex human B cell phenotypes during antibody class switch recombination.
8 )J recombination, somatic hypermutation, and class switch recombination.
9 ate somatic hypermutation and immunoglobulin class switch recombination.
10 ate of IgG1 transcription, without affecting class switch recombination.
11 ht into the molecular mechanisms involved in class switch recombination.
12 anslocate configured the earliest version of class switch recombination.
13 D-dependent antibody gene diversification by class switch recombination.
14 egulate transcriptional responses needed for class switch recombination.
15 cular events such as V(D)J recombination and class switch recombination.
16 on and joining as measured by immunoglobulin class switch recombination.
17 e AID scaffold compromised hypermutation and class switch recombination.
18 are diversified by somatic hypermutation and class switch recombination.
19 but not alternative end-joining, during IgH class switch recombination.
20 ines in mediating B-cell differentiation and class switch recombination.
21 s endonuclease activity is essential for IgA-class switch recombination.
22 erate double-strand DNA breaks for efficient class switch recombination.
23 , Id3-depleted B cells displayed a defect in class switch recombination.
24 ting Ab production, affinity maturation, and class switch recombination.
25 s recruitment to switch (S) regions leads to class-switch recombination.
26 y diversification: somatic hypermutation and class-switch recombination.
27 delayed-type hypersensitivity responses, and class-switch recombination.
28 and Toll receptor stimuli and undergo normal class-switch recombination.
29 ription 3 phosphorylation and immunoglobulin class-switch recombination.
30 were detectable in plasma, demonstrating IgG class-switch recombination.
31 ver, TET2-deficient B cells showed defective class-switch recombination.
32 tion of B lymphocytes and T cell-independent class-switch recombination.
33 nitiating antibody somatic hypermutation and class-switch recombination.
34 cription-dependent somatic hypermutation and class-switch recombination.
35 ), or enzymes responsible for immunoglobulin class-switch recombination.
36 h regions, suggesting that they occur during class-switch recombination.
37 e (AID) to undergo somatic hypermutation and class-switch recombination.
38 terminal maturation, and immunoglobulin (Ig) class-switch recombination.
39 somatic hypermutation, gene conversion, and class-switch recombination.
40 d DNA lesions in cells attempting to undergo class-switch recombination.
41 n in vivo, resulted in proliferation but not class-switch recombination.
42 d apoptosis during somatic hypermutation and class-switch recombination.
43 to become Ab-producing cells and to undergo class-switch recombination.
44 over extended regions during immunoglobulin class-switch recombination.
45 in switch (S) regions during immunoglobulin class switch recombination, a physiological, deletion/re
46 , or initiation of somatic hypermutation and class switch recombination (activation-induced cytidine
47 rmal primary humoral responses, encompassing class switch recombination, affinity maturation, and ger
49 l center (GC) reaction where B cells undergo class switch recombination and clonal selection to gener
50 ster (3' regulatory region) are required for class switch recombination and for high levels of IgH ex
52 GC reaction in primary B cells by impairing class switch recombination and memory B and plasma cell
53 ription factor IRF4 regulates immunoglobulin class switch recombination and plasma cell differentiati
54 1 production, whereas in B cells it controls class switch recombination and plasma cell differentiati
58 in gene products crucial for immunoglobulin class switch recombination and somatic hypermutation imp
59 tidine deaminase (AID) is a key regulator of class switch recombination and somatic hypermutation of
60 ase (AID) is a mutator enzyme that initiates class switch recombination and somatic hypermutation of
61 ) is a genome-mutating enzyme that initiates class switch recombination and somatic hypermutation of
62 lack the ability to undergo normal levels of class switch recombination and somatic hypermutation, tw
63 hat targets immunoglobulin genes to initiate class switch recombination and somatic hypermutation.
64 uced cytidine deaminase (AID), the enzyme of class switch recombination and somatic hypermutation; th
65 of B cells involves the sequential events of class switch recombination and somatic hypermutations ch
66 ts or (ii) deletion of enhancer elements for class switch recombination and transcription, or (iii) a
67 dergone the affinity-maturation processes of class switch recombination and, possibly, somatic hyperm
69 maturation, but have also been implicated in class-switch recombination and B cell lymphoma survival.
70 ous end-joining (NHEJ) during immunoglobulin class-switch recombination and consequently impairs immu
72 together with previously reported defects in class-switch recombination and memory immune response, u
74 idine deaminase (AID), which is required for class-switch recombination and somatic hypermutation, ar
76 bility, confirming that these AHAs underwent class-switch recombination and somatic hypermutation.
77 negatively regulatory function regarding Ab class switch recombination, and blockade of PI3K can str
78 e in B cell development, allelic regulation, class switch recombination, and chromosomal looping.
79 ir functionality, somatic mutational status, class switch recombination, and oncogenic Ig translocati
80 o B cells to facilitate affinity maturation, class switch recombination, and plasma cell differentiat
81 ate the involvement of local IgE production, class switch recombination, and receptor revision in NP.
82 nase (AID), initiates somatic hypermutation, class-switch recombination, and gene conversion of Ig ge
83 inase (AID) initiates somatic hypermutation, class-switch recombination, and gene conversion of immun
84 Upregulation of IgE by sCD23 occurs after class-switch recombination, and its effects are isotype-
85 ls, IRF4 controls germinal center formation, class-switch recombination, and the generation of plasma
87 ing transcription, alternative splicing, and class switch recombination are required to facilitate de
88 ich accumulates in the nucleus and increases class switch recombination as well as chromosomal transl
89 al and plays an important role in regulating class switch recombination as well as in the selection o
90 pair, V(D)J recombination and immunoglobulin class switch recombination, as well as innate immune and
92 me is required for somatic hypermutation and class switch recombination at the immunoglobulin locus.
93 ficiency in immunoglobulin hypermutation and class switch recombination, both AID-dependent mechanism
94 osphatidylcholine prevents proliferation and class switch recombination but leads to unfolded protein
96 ells and revealed that the inhibition of IgE class switch recombination by IL-21 was attenuated by CD
97 region and Aicda locus, E-proteins regulated class switch recombination by inducing both Igh germline
98 tant role in repairing DSBs generated during class switch recombination by promoting the classical NH
100 deaminase (AID) that abolish immunoglobulin class-switch recombination, causing an accumulation of I
102 inability of CCTalpha-/- B-cells to undergo class switch recombination correlated with a proliferati
103 rt that RNF8 deficiency results in defective class switch recombination (CSR) and accumulation of unr
104 ls, including DSBs generated during antibody class switch recombination (CSR) and DSBs generated by i
105 are severely compromised for 53BP1-dependent class switch recombination (CSR) and fusion of dysfuncti
106 hat PTIP accumulation at DSBs contributes to class switch recombination (CSR) and genome stability in
107 eaminase that initiates Ig heavy chain (IgH) class switch recombination (CSR) and Ig somatic hypermut
108 tiates immunoglobulin (Ig) heavy-chain (IgH) class switch recombination (CSR) and Ig variable region
110 n-induced cytidine deaminase (AID) initiates class switch recombination (CSR) and somatic hypermutati
111 ase (AID) catalyzes two of these mechanisms: class switch recombination (CSR) and somatic hypermutati
112 re B cells diversify their antibody genes by class switch recombination (CSR) and somatic hypermutati
113 immunoglobulin locus of B lymphocytes during class switch recombination (CSR) and somatic hypermutati
114 ed deaminase (AID) is an enzyme required for class switch recombination (CSR) and somatic hypermutati
115 Activation-induced deaminase (AID) catalyses class switch recombination (CSR) and somatic hypermutati
118 o immunoglobulin (Ig) loci promotes antibody class switch recombination (CSR) and somatic hypermutati
119 uced cytidine deaminase (AID) initiates both class switch recombination (CSR) and somatic hypermutati
120 mphocytes use two DNA alteration mechanisms, class switch recombination (CSR) and somatic hypermutati
121 ing (V(D)J) recombination and immunoglobulin class switch recombination (CSR) are key processes in ad
122 tion through somatic hypermutation (SHM) and class switch recombination (CSR) are similarly initiated
123 d the mechanisms underlying abnormalities in class switch recombination (CSR) associated with the hum
124 D) initiates somatic hypermutation (SHM) and class switch recombination (CSR) by deaminating cytidine
125 n this study, we show that Ab production and class switch recombination (CSR) depend on autocrine C3a
128 hypermutation (SHM) and immunoglobulin (Ig) class switch recombination (CSR) enable B cells to produ
129 ismatch repair (MMR) protein is critical for class switch recombination (CSR) events that occur in mi
133 in joining DSBs during Ig heavy chain (IgH) class switch recombination (CSR) in activated B lymphocy
134 recombination in developing lymphocytes and class switch recombination (CSR) in antigen-stimulated B
135 on-induced deaminase (AID) triggers antibody class switch recombination (CSR) in B cells by initiatin
136 ernative-end-joining (Alt-EJ) pathway during class switch recombination (CSR) in B cells, and HMCES d
141 e fidelity functions of 53BP1 coevolved with class switch recombination (CSR) in the immune system.
143 dies through somatic hypermutation (SHM) and class switch recombination (CSR) is a critical component
152 ant region in the IgH locus, indicating that class switch recombination (CSR) occurs in the absence o
159 We hypothesize that MMSET also regulates class switch recombination (CSR) through its effect on 5
163 ity maturation and DNA breakage for antibody class switch recombination (CSR) via transcription-depen
165 B cell function with age is decreased in class switch recombination (CSR), activation-induced cyt
166 d mice and humans, including decreases in Ig class switch recombination (CSR), activation-induced cyt
167 transcriptional program, immunoglobulin (Ig) class switch recombination (CSR), and plasma cell develo
168 ) in the IgH gene (Igh) to stimulate isotype class switch recombination (CSR), and widespread breaks
169 uch as those occurring during immunoglobulin class switch recombination (CSR), are repaired by non-ho
170 globulin switch (S) regions is essential for class switch recombination (CSR), but no molecular funct
171 eaminase (AID) initiates immunoglobulin (Ig) class switch recombination (CSR), somatic hypermutation
172 n to DNA double-strand break (DSB) repair in class switch recombination (CSR), we ablated Rev3, the c
194 hat needs isotype-switched Abs generated via class switch recombination (CSR); however, stimulating t
196 Activated B cells undergo immunoglobulin class-switch recombination (CSR) and differentiate into
197 ntigens and cytokines, mouse B cells undergo class-switch recombination (CSR) and differentiate into
199 tidine deaminase (AID), the enzyme-mediating class-switch recombination (CSR) and somatic hypermutati
200 ed cytidine deaminase (AID) is essential for class-switch recombination (CSR) and somatic hypermutati
201 6, must process the deoxyuridine to initiate class-switch recombination (CSR) and somatic hypermutati
202 an immune response and is essential for both class-switch recombination (CSR) and somatic hypermutati
204 CD103(+) and CD24(+)CD11b(+) DCs induced IgA class-switch recombination (CSR) by activating B cells t
205 y initiating somatic hypermutation (SHM) and class-switch recombination (CSR) during transcription of
207 n require Ig somatic hypermutation (SHM) and class-switch recombination (CSR) for high-affinity respo
208 nduced cytidine deaminase (AID) initiates Ab class-switch recombination (CSR) in activated B cells re
209 that trigger immunoglobulin G (IgG) and IgA class-switch recombination (CSR) in B cells by engaging
210 e same, BXD2-p19(-/-) mice exhibited a lower class-switch recombination (CSR) in the GC B cells, lead
213 idine deaminase (AID) to efficiently mediate class-switch recombination (CSR) is dependent on its pho
215 M(+) mouse B cells and hybridomas, we induce class-switch recombination (CSR) of the IgH chain to the
220 ls activated to undergo Ig heavy-chain (IgH) class-switch recombination (CSR) to be reprogrammed into
221 mologous end-joining (NHEJ) factors, Ab gene class-switch recombination (CSR) uses an alternative end
222 atory functions that control IgH expression, class-switch recombination (CSR), and somatic hypermutat
226 e Igh locus plays a major role in regulating class-switch recombination (CSR), the process by which a
231 t for V(D)J recombination and immunoglobulin class-switch recombination (CSR); however, little is kno
233 ncy patients into subgroups and identified a class-switch recombination defect caused by an UNG mutat
235 genes that undergo somatic hypermutation and class switch recombination during B cell activation in r
236 Thus, we find that the dramatic induction of class-switch recombination during Ag-driven differentiat
237 ell differentiation and guide B cell isotype class-switch recombination during host defense against P
242 joining recombination in vivo but not during class switch recombination, for which PAXX appeared to b
243 and joining recombination and immunoglobulin class switch recombination, here, using Cre/lox-specific
245 e functionality of AID by evaluating in vivo class switch recombination in 52 MCL cases; and sought f
247 PTIP protein in transcription regulation and class switch recombination in B cells, a process that de
248 d break repair protein that is essential for class switch recombination in B lymphocytes and for sens
249 S phases of the cell cycle, interferes with class switch recombination in B lymphocytes, and leads t
250 ese allowed direct simultaneous detection of class switch recombination in both immunoglobulin-heavy
251 protein ATM has long been known to influence class switch recombination in ex vivo-cultured B cells.
252 omatic hypermutation and immunoglobulin (Ig) class switch recombination in germinal center (GC) B cel
255 It directly demonstrated asynchrony of the class switch recombination in the two alleles in structu
257 n history, somatic hypermutation status, and class-switch recombination in 17 children with Down synd
259 e authors show that IgE can be generated via class-switch recombination in IgG1 memory B cells withou
261 ase (AID) involved in somatic hypermutations/class switch recombination, in primary human B cells.
262 underwent efficient V(D)J recombination and class switch recombination, indicating that phosphorylat
263 xpression, germ-line transcription preceding class switch recombination, interactions between targete
265 cells class switch in vitro, suggesting that class switch recombination is directed toward specific i
267 dine deaminase (AID) expression, and blocked class switch recombination, leading to markedly decrease
268 ctivities in cells undergoing immunoglobulin class switch recombination leads to a compound defect in
269 Germinal center somatic hypermutation and class switch recombination machineries were activated, a
270 sured the expression of two miRs crucial for class switch recombination, miR-155 and miR-16, in human
271 l not fully understood where in the body IgE class switch recombination of food allergen-specific B c
272 vents that lead to somatic hypermutation and class switch recombination of immunoglobulin genes.
273 se (AID) initiates somatic hypermutation and class switch recombination of the immunoglobulin genes.
276 n genes encoded proteins contributing to IgE class switch recombination or B-cell receptor signaling.
277 was previously found to be unable to support class switch recombination or to promote radial chromoso
278 in various physiological processes, such as class-switch recombination or crossing-over during meios
279 ot show any obvious defects in Ab secretion, class switch recombination, or somatic hypermutation.
280 liferation, IgE, IgG1, IgG4, IgA production, class switch recombination, plasma cell differentiation
282 immunoglobulin M (IgM) BCR despite an active class-switch recombination process, and by the introduct
283 4 as a regulator of PARP1-dependent NHEJ and class-switch recombination, providing a molecular basis
284 in the normal G+C-rich context of mammalian class switch recombination regions, R-loops are obligato
285 ne segment usage, CDR3 length distributions, class switch recombination, somatic hypermutation levels
286 hich B lymphocytes undergo clonal expansion, class switch recombination, somatic hypermutation, and a
287 induced cytidine deaminase gene required for class switch recombination/somatic hypermutation inducti
288 ular DNA intermediates, a hallmark of active class switch recombination, suggested that class switchi
292 remodeling (global somatic hypermutation and class switch recombination to major isotypes) in activat
294 , which in part impacts the overall level of class switch recombination to targeted C(H) regions.
295 in various basic nuclear processes, such as class-switch recombination, transcription termination an
296 and joining recombination and immunoglobulin class switch recombination, two events requiring nonhomo
299 s attenuated by CD40 signaling, whereas IgG1 class switch recombination was potentiated by IL-21 in t
300 event, supporting somatic hypermutation and class-switch recombination within the salivary follicles