ライフサイエンスコーパス: class switch recombination

1 plex human B cell phenotypes during antibody class switch recombination.

2 )J recombination, somatic hypermutation, and class switch recombination.

3 ate somatic hypermutation and immunoglobulin class switch recombination.

4 ate of IgG1 transcription, without affecting class switch recombination.

5 ht into the molecular mechanisms involved in class switch recombination.

6 anslocate configured the earliest version of class switch recombination.

7 D-dependent antibody gene diversification by class switch recombination.

8 egulate transcriptional responses needed for class switch recombination.

9 cular events such as V(D)J recombination and class switch recombination.

10 on and joining as measured by immunoglobulin class switch recombination.

11 e AID scaffold compromised hypermutation and class switch recombination.

12 are diversified by somatic hypermutation and class switch recombination.

13 but not alternative end-joining, during IgH class switch recombination.

14 ines in mediating B-cell differentiation and class switch recombination.

15 emulate R-loop structures that arise during class switch recombination.

16 ely defective for immunoglobulin heavy-chain class switch recombination.

17 or a crucial role of Blm in the mechanism of class switch recombination.

18 activation-induced cytidine deaminase and Ig class switch recombination.

19 , Id3-depleted B cells displayed a defect in class switch recombination.

20 ting Ab production, affinity maturation, and class switch recombination.

21 G1 Abs, demonstrating a functional effect on class switch recombination.

22 deletion of intervening DNA sequences during class switch recombination.

23 ution and impedes B cell differentiation and class switch recombination.

24 tation but defective affinity maturation and class switch recombination.

25 homologous end-joining during immunoglobulin class switch recombination.

26 erate double-strand DNA breaks for efficient class switch recombination.

27 ects VDJ recombination with minor effects on class switch recombination.

28 ription 3 phosphorylation and immunoglobulin class-switch recombination.

29 were detectable in plasma, demonstrating IgG class-switch recombination.

30 tion of B lymphocytes and T cell-independent class-switch recombination.

31 nitiating antibody somatic hypermutation and class-switch recombination.

32 cription-dependent somatic hypermutation and class-switch recombination.

33 ), or enzymes responsible for immunoglobulin class-switch recombination.

34 h regions, suggesting that they occur during class-switch recombination.

35 e (AID) to undergo somatic hypermutation and class-switch recombination.

36 terminal maturation, and immunoglobulin (Ig) class-switch recombination.

37 somatic hypermutation, gene conversion, and class-switch recombination.

38 n in vivo, resulted in proliferation but not class-switch recombination.

39 d apoptosis during somatic hypermutation and class-switch recombination.

40 le for V(D)J recombination but essential for class-switch recombination.

41 n as AICDA)-induced breaks in immunoglobulin class-switch recombination.

42 over extended regions during immunoglobulin class-switch recombination.

43 s recruitment to switch (S) regions leads to class-switch recombination.

44 y diversification: somatic hypermutation and class-switch recombination.

45 delayed-type hypersensitivity responses, and class-switch recombination.

46 and Toll receptor stimuli and undergo normal class-switch recombination.

47 in switch (S) regions during immunoglobulin class switch recombination, a physiological, deletion/re

48 , or initiation of somatic hypermutation and class switch recombination (activation-induced cytidine

49 ucidate intrinsic B lymphocyte defects in Ig class switch recombination, activation-induced cytidine

50 of cytokines, including IL-21, and inhibited class switch recombination and B cell activation.

51 l center (GC) reaction where B cells undergo class switch recombination and clonal selection to gener

52 ster (3' regulatory region) are required for class switch recombination and for high levels of IgH ex

53 ne deaminase (AID), which is known to induce class switch recombination and Ig somatic hypermutation.

54 f hs3b and hs4 had a dramatic effect on both class switch recombination and IgH gene transcription; d

55 ismatch repair activity and displayed normal class switch recombination and meiosis.

56 GC reaction in primary B cells by impairing class switch recombination and memory B and plasma cell

57 ription factor IRF4 regulates immunoglobulin class switch recombination and plasma cell differentiati

58 1 production, whereas in B cells it controls class switch recombination and plasma cell differentiati

59 This has important implications for class switch recombination and somatic hypermutation and

60 Both class switch recombination and somatic hypermutation are

61 in gene products crucial for immunoglobulin class switch recombination and somatic hypermutation imp

62 ) is a genome-mutating enzyme that initiates class switch recombination and somatic hypermutation of

63 ase (AID) is a mutator enzyme that initiates class switch recombination and somatic hypermutation of

64 tidine deaminase (AID) is a key regulator of class switch recombination and somatic hypermutation of

65 lack the ability to undergo normal levels of class switch recombination and somatic hypermutation, tw

66 munodeficiencies characterized by defects of class switch recombination and somatic hypermutation.

67 hat targets immunoglobulin genes to initiate class switch recombination and somatic hypermutation.

68 uced cytidine deaminase (AID), the enzyme of class switch recombination and somatic hypermutation; th

69 of B cells involves the sequential events of class switch recombination and somatic hypermutations ch

70 ts or (ii) deletion of enhancer elements for class switch recombination and transcription, or (iii) a

71 dergone the affinity-maturation processes of class switch recombination and, possibly, somatic hyperm

72 maturation, but have also been implicated in class-switch recombination and B cell lymphoma survival.

73 Because BAFF promotes B cell class-switch recombination and humoral autoimmunity, we

74 together with previously reported defects in class-switch recombination and memory immune response, u

75 s B-cell differentiation leading to antibody class-switch recombination and secretion.

76 idine deaminase (AID), which is required for class-switch recombination and somatic hypermutation, ar

77 AID(+) GC B cells then undergo class-switch recombination and somatic hypermutation.

78 bility, confirming that these AHAs underwent class-switch recombination and somatic hypermutation.

79 through clonal expansion while they undergo class-switch recombination and somatic hypermutation.

80 negatively regulatory function regarding Ab class switch recombination, and blockade of PI3K can str

81 e in B cell development, allelic regulation, class switch recombination, and chromosomal looping.

82 o B cells to facilitate affinity maturation, class switch recombination, and plasma cell differentiat

83 (GC) B cells undergo somatic hypermutation, class switch recombination, and rapid clonal expansion t

84 ate the involvement of local IgE production, class switch recombination, and receptor revision in NP.

85 lomere maintenance, immunoglobulin (Ig) gene class switch recombination, and somatic hypermutation.

86 IgH locus transcription, VDJ recombination, class switch recombination, and somatic hypermutation.

87 d during DNA replication, transcription, and class switch recombination, and that Ape1 can endonucleo

88 nase (AID), initiates somatic hypermutation, class-switch recombination, and gene conversion of Ig ge

89 inase (AID) initiates somatic hypermutation, class-switch recombination, and gene conversion of immun

90 Upregulation of IgE by sCD23 occurs after class-switch recombination, and its effects are isotype-

91 ls, IRF4 controls germinal center formation, class-switch recombination, and the generation of plasma

92 ating NHEJ at dysfunctional telomeres and in class switch recombination are not identical.

93 ich accumulates in the nucleus and increases class switch recombination as well as chromosomal transl

94 al and plays an important role in regulating class switch recombination as well as in the selection o

95 pair, V(D)J recombination and immunoglobulin class switch recombination, as well as innate immune and

96 nzymatic function of host UNG in an in vitro class switch recombination assay.

97 me is required for somatic hypermutation and class switch recombination at the immunoglobulin locus.

98 ficiency in immunoglobulin hypermutation and class switch recombination, both AID-dependent mechanism

99 osphatidylcholine prevents proliferation and class switch recombination but leads to unfolded protein

100 In addition, class switch recombination, but not somatic hypermutatio

101 region and Aicda locus, E-proteins regulated class switch recombination by inducing both Igh germline

102 tant role in repairing DSBs generated during class switch recombination by promoting the classical NH

103 Loss of PTIP inhibited class switch recombination by suppressing transcription

104 deaminase (AID) that abolish immunoglobulin class-switch recombination, causing an accumulation of I

105 Classical class-switch recombination (cCSR) substitutes the Cmu ge

106 inability of CCTalpha-/- B-cells to undergo class switch recombination correlated with a proliferati

107 rt that RNF8 deficiency results in defective class switch recombination (CSR) and accumulation of unr

108 ls, including DSBs generated during antibody class switch recombination (CSR) and DSBs generated by i

109 are severely compromised for 53BP1-dependent class switch recombination (CSR) and fusion of dysfuncti

110 hat PTIP accumulation at DSBs contributes to class switch recombination (CSR) and genome stability in

111 eaminase that initiates Ig heavy chain (IgH) class switch recombination (CSR) and Ig somatic hypermut

112 tiates immunoglobulin (Ig) heavy-chain (IgH) class switch recombination (CSR) and Ig variable region

113 We find that both class switch recombination (CSR) and R-loop formation de

114 n-induced cytidine deaminase (AID) initiates class switch recombination (CSR) and somatic hypermutati

115 mphocytes use two DNA alteration mechanisms, class switch recombination (CSR) and somatic hypermutati

116 ase (AID) catalyzes two of these mechanisms: class switch recombination (CSR) and somatic hypermutati

117 immunoglobulin locus of B lymphocytes during class switch recombination (CSR) and somatic hypermutati

118 ed deaminase (AID) is an enzyme required for class switch recombination (CSR) and somatic hypermutati

119 Activation-induced deaminase (AID) catalyses class switch recombination (CSR) and somatic hypermutati

120 Ig class switch recombination (CSR) and somatic hypermutati

121 Both class switch recombination (CSR) and somatic hypermutati

122 aminase (AID) is required for immunoglobulin class switch recombination (CSR) and somatic hypermutati

123 uced cytidine deaminase (AID) initiates both class switch recombination (CSR) and somatic hypermutati

124 ing (V(D)J) recombination and immunoglobulin class switch recombination (CSR) are key processes in ad

125 tion through somatic hypermutation (SHM) and class switch recombination (CSR) are similarly initiated

126 d the mechanisms underlying abnormalities in class switch recombination (CSR) associated with the hum

127 D) initiates somatic hypermutation (SHM) and class switch recombination (CSR) by deaminating cytidine

128 n-induced cytidine deaminase (AID) initiates class switch recombination (CSR) by introducing lesions

129 Class switch recombination (CSR) diversifies antibodies

130 Class switch recombination (CSR) diversifies antibodies

131 hypermutation (SHM) and immunoglobulin (Ig) class switch recombination (CSR) enable B cells to produ

132 ismatch repair (MMR) protein is critical for class switch recombination (CSR) events that occur in mi

133 s in developing bone marrow B cells, whereas class switch recombination (CSR) exchanges IgH constant

134 In mature B cells, class switch recombination (CSR) generates different ant

135 Class switch recombination (CSR) generates isotype-switc

136 Class switch recombination (CSR) has the potential to ge

137 in joining DSBs during Ig heavy chain (IgH) class switch recombination (CSR) in activated B lymphocy

138 recombination in developing lymphocytes and class switch recombination (CSR) in antigen-stimulated B

139 on-induced deaminase (AID) triggers antibody class switch recombination (CSR) in B cells by initiatin

140 Class switch recombination (CSR) in B lymphocytes is ini

141 Antibody class switch recombination (CSR) in B lymphocytes joins

142 During IgH class switch recombination (CSR) in B lymphocytes, switc

143 during immunoglobulin (Ig) heavy chain (IgH) class switch recombination (CSR) in peripheral B lymphoc

144 Class switch recombination (CSR) involves a DNA rearrang

145 dies through somatic hypermutation (SHM) and class switch recombination (CSR) is a critical component

146 Immunoglobulin heavy chain class switch recombination (CSR) is believed to occur th

147 In B lymphocytes, Ig class switch recombination (CSR) is induced by activatio

148 Immunoglobulin (Ig) class switch recombination (CSR) is initiated by activat

149 In B cells, Ig class switch recombination (CSR) is initiated by activat

150 Immunoglobulin (Ig) class switch recombination (CSR) is initiated by the tra

151 Immunoglobulin (Ig) class switch recombination (CSR) is initiated by the tra

152 Class switch recombination (CSR) is instigated by activa

153 Ig class switch recombination (CSR) is regulated through lo

154 Ig class switch recombination (CSR) occurs in activated mat

155 ant region in the IgH locus, indicating that class switch recombination (CSR) occurs in the absence o

156 IgH class switch recombination (CSR) occurs through the deli

157 to initiate somatic hypermutation (SHM) and class switch recombination (CSR) of antibody genes.

158 hRNA screen to identify factors required for class switch recombination (CSR) of antibody loci.

159 ine, and the somatic hypermutation (SHM) and class switch recombination (CSR) pipeline.

160 Class switch recombination (CSR) plays an important role

161 Immunoglobulin heavy chain (IgH) class switch recombination (CSR) replaces the initially

162 Immunoglobulin heavy chain class switch recombination (CSR) requires targeted forma

163 We hypothesize that MMSET also regulates class switch recombination (CSR) through its effect on 5

164 gE(+) cells in vivo and the low frequency of class switch recombination (CSR) to IgE ex vivo.

165 Immunoglobulin class switch recombination (CSR) to IgE is a tightly reg

166 ity maturation and DNA breakage for antibody class switch recombination (CSR) via transcription-depen

167 Here, we studied immunoglobulin (Ig) class switch recombination (CSR), a physiological proces

168 B cell function with age is decreased in class switch recombination (CSR), activation-induced cyt

169 d mice and humans, including decreases in Ig class switch recombination (CSR), activation-induced cyt

170 transcriptional program, immunoglobulin (Ig) class switch recombination (CSR), and plasma cell develo

171 ) in the IgH gene (Igh) to stimulate isotype class switch recombination (CSR), and widespread breaks

172 uch as those occurring during immunoglobulin class switch recombination (CSR), are repaired by non-ho

173 globulin switch (S) regions is essential for class switch recombination (CSR), but no molecular funct

174 ial for both somatic hypermutation (SHM) and class switch recombination (CSR), two processes involved

175 n to DNA double-strand break (DSB) repair in class switch recombination (CSR), we ablated Rev3, the c

176 duced cytidine deaminase (AID)-dependent IgH class switch recombination (CSR).

177 cytes hypersecrete IgM and do not undergo Ig class switch recombination (CSR).

178 ature B cells in the germinal center through class switch recombination (CSR).

179 ld-type 53BP1 with respect to immunoglobulin class switch recombination (CSR).

180 al cellular processes such as immunoglobulin class switch recombination (CSR).

181 ediates in Ig gene rearrangements: V(D)J and class switch recombination (CSR).

182 y to produce somatic hypermutation (SHM) and class switch recombination (CSR).

183 into switch (S) regions, leading to antibody class switch recombination (CSR).

184 (non-coding) transcription (GT) and promote class switch recombination (CSR).

185 Germline transcription precedes class switch recombination (CSR).

186 atory intermediates for Ig heavy chain (Igh) class switch recombination (CSR).

187 diversity) joining [V(D)J] recombination and class switch recombination (CSR).

188 , initiating somatic hypermutation (SHM) and class switch recombination (CSR).

189 deaminase (AID, also known as AICDA) during class switch recombination (CSR).

190 g immunoglobulin light chain and heavy chain class switch recombination (CSR).

191 the gene encoding the Ig H chain C region by class switch recombination (CSR).

192 ions has been implicated in regulation of Ig class switch recombination (CSR).

193 ate antibody somatic hypermutation (SHM) and class switch recombination (CSR).

194 Class-switch recombination (CSR) alters the Ig isotype t

195 Activated B cells undergo immunoglobulin class-switch recombination (CSR) and differentiate into

196 ntigens and cytokines, mouse B cells undergo class-switch recombination (CSR) and differentiate into

197 eviously unappreciated role for Flt3 in IgG1 class-switch recombination (CSR) and production.

198 6, must process the deoxyuridine to initiate class-switch recombination (CSR) and somatic hypermutati

199 an immune response and is essential for both class-switch recombination (CSR) and somatic hypermutati

200 DA in humans) is critical for immunoglobulin class-switch recombination (CSR) and somatic hypermutati

201 the diversification of the Ig locus through class-switch recombination (CSR) and somatic hypermutati

202 AID mediates class-switch recombination (CSR) and somatic hypermutati

203 tidine deaminase (AID), the enzyme-mediating class-switch recombination (CSR) and somatic hypermutati

204 ed cytidine deaminase (AID) is essential for class-switch recombination (CSR) and somatic hypermutati

205 CD103(+) and CD24(+)CD11b(+) DCs induced IgA class-switch recombination (CSR) by activating B cells t

206 y initiating somatic hypermutation (SHM) and class-switch recombination (CSR) during transcription of

207 Class-switch recombination (CSR) ensures that these Abs

208 n require Ig somatic hypermutation (SHM) and class-switch recombination (CSR) for high-affinity respo

209 nduced cytidine deaminase (AID) initiates Ab class-switch recombination (CSR) in activated B cells re

210 that trigger immunoglobulin G (IgG) and IgA class-switch recombination (CSR) in B cells by engaging

211 Somatic hypermutation (SHM) and class-switch recombination (CSR) increase the affinity a

212 idine deaminase (AID) to efficiently mediate class-switch recombination (CSR) is dependent on its pho

213 Ig class-switch recombination (CSR) is directed by the long

214 Somatic hypermutation (SHM) and class-switch recombination (CSR) of Ig genes are depende

215 M(+) mouse B cells and hybridomas, we induce class-switch recombination (CSR) of the IgH chain to the

216 ymphocytes perform somatic hypermutation and class-switch recombination (CSR) of the immunoglobulin l

217 enes through somatic hypermutation (SHM) and class-switch recombination (CSR) processes.

218 Immunoglobulin heavy chain (IgH) class-switch recombination (CSR) replaces initially expr

219 Ig heavy chain (IgH) class-switch recombination (CSR) replaces the IgH C mu c

220 Immunoglobulin class-switch recombination (CSR) requires activation-ind

221 ls activated to undergo Ig heavy-chain (IgH) class-switch recombination (CSR) to be reprogrammed into

222 mologous end-joining (NHEJ) factors, Ab gene class-switch recombination (CSR) uses an alternative end

223 atory functions that control IgH expression, class-switch recombination (CSR), and somatic hypermutat

224 lity to perform somatic hypermutation (SHM), class-switch recombination (CSR), or both.

225 During immunoglobulin class-switch recombination (CSR), the cytidine deaminase

226 e Igh locus plays a major role in regulating class-switch recombination (CSR), the process by which a

227 ctivation-induced deaminase during IgH (Igh) class-switch recombination (CSR).

228 the mechanism by which BATF controls in vivo class-switch recombination (CSR).

229 IgH switch (S) region DNA breaks (DSBs) for class-switch recombination (CSR).

230 insights into the process of immunoglobulin class-switch recombination (CSR).

231 t for V(D)J recombination and immunoglobulin class-switch recombination (CSR); however, little is kno

232 inal maturation and Ig isotype class switch (class switch recombination [CSR]).

233 ncy patients into subgroups and identified a class-switch recombination defect caused by an UNG mutat

234 Immunoglobulin class-switch recombination defects (CSR-D) are rare prim

235 to lower expression of L-selectin and failed class-switch recombination due to impaired upregulation

236 genes that undergo somatic hypermutation and class switch recombination during B cell activation in r

237 Thus, we find that the dramatic induction of class-switch recombination during Ag-driven differentiat

238 ell differentiation and guide B cell isotype class-switch recombination during host defense against P

239 region super-enhancer and leads to decreased class switch recombination efficiency.

240 We find that AhR negatively regulates class-switch recombination ex vivo by altering activatio

241 s required for humoral memory, and underwent class-switch recombination following Ag encounter.

242 The dramatic reduction in class switch recombination for all H chain genes and the

243 Ig class-switch recombination (Ig-CSR) deficiencies are rar

244 e functionality of AID by evaluating in vivo class switch recombination in 52 MCL cases; and sought f

245 Consistent with this, we show that class switch recombination in Aplf(-/-) B cells is biase

246 se (AID) initiates somatic hypermutation and class switch recombination in B cells by deaminating C -

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 r enzyme that initiates somatic mutation and class switch recombination in B lymphocytes by introduci

250 S phases of the cell cycle, interferes with class switch recombination in B lymphocytes, and leads t

251 ese allowed direct simultaneous detection of class switch recombination in both immunoglobulin-heavy

252 omatic hypermutation and immunoglobulin (Ig) class switch recombination in germinal center (GC) B cel

253 c stability in mouse fibroblasts, and in IgH class switch recombination in mature B cells.

254 ated in NP, and there was evidence for local class switch recombination in NP.

255 It directly demonstrated asynchrony of the class switch recombination in the two alleles in structu

256 istent with our data on the decrease seen in class switch recombination in vitro.

257 ro but also trigger antibody production with class switch recombination in vivo.

258 ead to a model for exonuclease 1 function in class switch recombination in which cleavage at activati

259 n history, somatic hypermutation status, and class-switch recombination in 17 children with Down synd

260 receptor participates in the control of IgE class-switch recombination in B cells.

261 e authors show that IgE can be generated via class-switch recombination in IgG1 memory B cells withou

262 ic gene expression, antigen presentation and class-switch recombination in plasmablasts.

263 ase (AID) involved in somatic hypermutations/class switch recombination, in primary human B cells.

264 xpression, germ-line transcription preceding class switch recombination, interactions between targete

265 Ab class switch recombination involves a recombination betw

266 cells class switch in vitro, suggesting that class switch recombination is directed toward specific i

267 Immunoglobulin class switch recombination is governed by long-range int

268 dine deaminase (AID) expression, and blocked class switch recombination, leading to markedly decrease

269 ctivities in cells undergoing immunoglobulin class switch recombination leads to a compound defect in

270 Germinal center somatic hypermutation and class switch recombination machineries were activated, a

271 sured the expression of two miRs crucial for class switch recombination, miR-155 and miR-16, in human

272 ith enhancers involved in the expression and class switch recombination of IgH genes.

273 vents that lead to somatic hypermutation and class switch recombination of immunoglobulin genes.

274 Class-switch recombination of Ab isotype is mediated by

275 Somatic hypermutation and class-switch recombination of the immunoglobulin (Ig) ge

276 ced cytidine deaminase (AID) during antibody class switch recombination or somatic hypermutation.

277 was previously found to be unable to support class switch recombination or to promote radial chromoso

278 ot show any obvious defects in Ab secretion, class switch recombination, or somatic hypermutation.

279 liferation, IgE, IgG1, IgG4, IgA production, class switch recombination, plasma cell differentiation

280 ty of the double-strand break repairs in the class-switch recombination process in vivo.

281 immunoglobulin M (IgM) BCR despite an active class-switch recombination process, and by the introduct

282 in the normal G+C-rich context of mammalian class switch recombination regions, R-loops are obligato

283 hich B lymphocytes undergo clonal expansion, class switch recombination, somatic hypermutation, and a

284 induced cytidine deaminase gene required for class switch recombination/somatic hypermutation inducti

285 ular DNA intermediates, a hallmark of active class switch recombination, suggested that class switchi

286 Beyond class switch recombination, the IgH 3'RR is a central el

287 use AID is required for Ig hypermutation and class switch recombination, these mice lack hypermutated

288 In B cells, STAT6 is required for class switch recombination to IgE and for germinal cente

289 itch circle transcripts reveal ongoing local class switch recombination to IgE.

290 remodeling (global somatic hypermutation and class switch recombination to major isotypes) in activat

291 Class switch recombination to several isotypes was also

292 , which in part impacts the overall level of class switch recombination to targeted C(H) regions.

293 and joining recombination and immunoglobulin class switch recombination, two events requiring nonhomo

294 ersity and joining (V(D)J) recombination and class-switch recombination use overlapping but distinct

295 genes associated with B cell activation and class switch recombination was measured by qRT-PCR.

296 Class switch recombination was partly lost due to a fail

297 Immune responses and in vitro class switch recombination were also altered in Fli-1(De

298 r B cell formation, affinity maturation, and class switch recombination were intact.

299 ese mutations can be attributed to errors in class switch recombination, which facilitate the generat

300 event, supporting somatic hypermutation and class-switch recombination within the salivary follicles