ライフサイエンスコーパス: CSR

1 CSR and SHM are regulated by phosphorylation on AID seri

2 CSR and SHM require the essential activity of the DNA ac

3 CSR creates a virtually unique IgH locus in every B cell

4 CSR is preceded by inducible germline (GL) transcription

5 CSR occurs via an intrachromosomal looping out and delet

6 CSR-1 is a germline-expressed C. elegans Argonaute prote

7 s with the 200-kb upstream Smu to generate a CSR centre (CSRC).

8 o IgA results in reduced, but not abolished, CSR.

9 t of AID to S region DNA, thereby abolishing CSR.

10 ping and resting splenic B cells and altered CSR in activated B cells.

11 Although CSR commences upon T cell priming, it is generally consi

12 Although CSR has also been described in patients with heart failu

13 nt pS38 abated AID chromatin association and CSR but not mutation at Myc.

14 B cells severely inhibits AID expression and CSR, whereas deletion of Sox2 increases the frequency of

15 t MR imaging, SII signal intensity index and CSR chemical-shift ratio have high accuracy to distingui

16 worsening heart failure varied with LVEF and CSR.

17 cluding BASELINe), clonality (Change-O), and CSR.

18 mice elicited more robust Ab production and CSR than wild-type (WT) mice.

19 of cells undergoing V(D)J recombination and CSR.

20 line, DSB formation is severely reduced and CSR frequency is impaired.

21 that extends the reach of r-K selection and CSR selection by linking breeder investments in offsprin

22 Although SHM and CSR are fundamentally different, their independent roles

23 generates deletions, indicating that SHM and CSR employ the same mechanism.

24 RGalaxy includes the newly developed SHM and CSR pipeline to analyze SHM and/or CSR in BCR rearrangem

25 ine the independent contributions of SHM and CSR to the generation and persistence of memory in the a

26 mechanism by which AID can initiate SHM and CSR when properly regulated, yet when unregulated can ac

27 und that PTIP functions in transcription and CSR separately from its association with the MLL3/MLL4 c

28 of sterile gamma1 germ-line transcripts and CSR to IgG1.

29 elegans has revealed the essential Argonaute CSR-1 to play key nuclear roles in modulating chromatin,

30 thway that presumably involves the Argonaute CSR-1.

31 the cause of these abnormalities, we assayed CSR in Lig4(R/R) B cells generated via preassembled IgH

32 Divergent functions emerge at CSR, persist through PC terminal differentiation and fur

33 C. briggsae CSR-1-associated small RNAs that we identified by immuno

34 cellent (intraclass correlation coefficient: CSR chemical-shift ratio , 0.893; SII signal intensity i

35 )UNG(-/-) mouse B cells also cannot complete CSR or affinity maturation despite accumulating signific

36 cognition or oligomerization both compromise CSR in splenic B cells.

37 ID localization to S regions and compromises CSR; both defects can be rescued by exogenous expression

38 nt on BCR signaling strength for controlling CSR, B cell homeostasis, and B cell-mediated disorders.

39 Defective CSR was linked to failed NHEJ and residual A-EJ access t

40 tion of Med1 in B cells results in defective CSR and reduced acceptor S region transcription.

41 globulin class-switch recombination defects (CSR-D) are rare primary immunodeficiencies characterized

42 hanism by which 53BP1 facilitates deletional CSR and inhibits inversional switching events remains un

43 r S-region-downstream DSB-end for deletional CSR(12).

44 downstream S region with Smu for deletional CSR.

45 or and acceptor S-region DSBs for deletional CSR.

46 he link with 53BP1 enforcement of deletional CSR.

47 IgH organization in cis promotes deletional CSR.

48 ons routinely participate in such deletional CSR joining(11).

49 that is capable of robust cytokine-dependent CSR to IgA results in reduced, but not abolished, CSR.

50 ID at serine 38 in mismatch repair-dependent CSR and affinity maturation.

51 Despite CSR-1 being preserved among diverse nematodes, the conse

52 IFC was confirmed by measuring the different CSRs for the different types of cells.

53 correlates, and prognostic value of diurnal CSR in upright position.

54 During CSR, the IgH locus undergoes dynamic three-dimensional s

55 eviously hypothesized to regulate BER during CSR, as the AID phosphorylation mutant, AID(S38A), canno

56 in promoting AID-mediated DNA breaks during CSR.

57 promoting cNHEJ repair pathway choice during CSR.

58 anner in resolving switch region DSBs during CSR.

59 ong DNA overhangs generated by Alt-EJ during CSR.

60 S regions and the IgH locus enhancers during CSR and their transcriptional activation.

61 the emergent functions of RNA exosome during CSR, SHM, and other chromosomal alterations in B cells,

62 ollateral damage to the B-cell genome during CSR and SHM, AID induces unwanted (and sometimes oncogen

63 illuminating AID targeting mechanisms during CSR and SHM.

64 us enhancers and the acceptor regions during CSR and that their knockdown in CH12 cells results in im

65 MLL4 complex to mediate transcription during CSR.

66 B cell-specific PTEN overexpression enhances CSR.

67 ntrapericardial alpha,beta-meATP also evoked CSR response in vagus-intact rats.

68 3), but not P2Y receptors, powerfully evokes CSR responses through activation of cardiac spinal affer

69 hat activation of cardiac P2 receptor evokes CSR responses by stimulating cardiac sympathetic afferen

70 siological range, AID and Blimp1 expression, CSR, somatic hypermutation and plasma cell differentiati

71 ectly on Il17ra (+) GC B cells to facilitate CSR-related base excision repair genes during the dark z

72 tensity index and 100%, 96.7%, and 0.849 for CSR chemical-shift ratio .

73 showed that Rad54 was neither essential for CSR, RCR nor RDR, and it had no significant influence on

74 Significant correlation was found for CSR chemical-shift ratio (r = -0.761) and SII signal int

75 SReport will provide a unified framework for CSR junction studies.

76 of sequences from our HTS-based protocol for CSR junctions, thereby facilitating and accelerating the

77 est that 3'RR is not absolutely required for CSR and, thus, is not essential for targeting activation

78 tis establishes a conserved nuclear role for CSR-1 and highlights its key role in germline gene regul

79 on-Gurwitz et al. now demonstrate a role for CSR-1 and its slicer activity in downregulating the leve

80 ignificant correlation with age was seen for CSR chemical-shift ratio (r = 0.702, P < .001) but not S

81 m BRCT domain of PTIP that is sufficient for CSR and identified PA1 as its main functional protein pa

82 of C region (CH) loci that are targeted for CSR in a cytokine-dependent fashion in mature B lymphocy

83 , as emphasized by the significantly greater CSR reduction in Rad52(-/-) versus Rad52(+/+) B cells on

84 ted a profound influence on LDC-mediated IgA CSR.

85 cancer growth through modulation of the IgA CSR process.

86 IgD CSR is a rare event, and its regulation is poorly unders

87 IgD CSR occurred via both alternative nonhomologous end-join

88 Microbiota-dependent IgD CSR also was detected in nasal-associated lymphoid tissu

89 signal via Toll-like receptors to elicit IgD CSR.

90 of secreted IgD resulting from increased IgD CSR exclusively within B cells of mucosa-associated lymp

91 gand-deficient mice results in impaired IgG1 CSR and accumulation of IgM-secreting plasma cells.

92 Exome sequencing in 2 immunoglobulin CSR-D patients identified variations in the INO80 gene.

93 atients affected by defective immunoglobulin CSR.

94 However, many immunoglobulin CSR-Ds are still undefined at the molecular level.

95 sess the function of INO80 on immunoglobulin CSR.

96 Impaired CSR can be rescued by ectopic expression of Mbd4 Mbd4 de

97 knockdown in CH12 cells results in impaired CSR.

98 l as its partners Reptin and Pontin impaired CSR.

99 of healthy subjects, revealing that impaired CSR does not interfere with the peripheral B cell tolera

100 However, impairing CSR-1 has very little effect on the accumulation of its

101 germinal center B cell formation and impairs CSR and SHM.

102 -glycosylase (UNG) deficiency, which impairs CSR but not SHM.

103 In CSR-activated primary B cells, I-promoter transcription

104 G4 recognition and oligomerization of AID in CSR.

105 sic role of Lsh in B cell development and in CSR providing a potential target for immunodeficiency th

106 endonuclease and redox functions of APE1 in CSR.

107 ese findings, we observe a complete block in CSR in AID(S38A/S38A)MSH2(-/-) mouse B cells that correl

108 deficiency leads to a significant defect in CSR.

109 hing to IgG3 and IgG2b, as well as delays in CSR kinetics associated with defective proliferation dur

110 Our results identify BRIT1 as a factor in CSR and demonstrate that multiple BRCT-domain proteins c

111 e establish a critical role for p110alpha in CSR.

112 ed Igh breaks and a significant reduction in CSR in ex vivo activated splenic B cells.

113 d mismatch repair pathways, respectively, in CSR.

114 the CH12F3 cell line to explore its role in CSR.

115 ate immunity, but with no recognised role in CSR.

116 ormal CSR, Rad52(-/-) B cells show increased CSR, fewer intra-Smu region recombinations, no/minimal m

117 f costimulation (e.g., CD40) does not induce CSR; thus, it remains elusive whether and how the BCR in

118 eletion in B cells enables the BCR to induce CSR in the absence of costimulation.

119 ls to show that the BCR's capacity to induce CSR is restrained by B cell-intrinsic checkpoints TRAF3

120 d cultured with IL-4 and anti-CD40 to induce CSR to IgE.

121 ecifically limit the BCR's ability to induce CSR.

122 Similarly, we induce CSR in all human B cell lines tested with high efficienc

123 signaling strength for licensing BCR-induced CSR and whether deficiency of such molecule(s) disrupts

124 TRAF3 deficiency permits BCR-induced CSR by elevating BCR-proximal signaling intensity.

125 more, NF-kappaB2 is required for BCR-induced CSR in TRAF3-deficient B cells but not for CD40-induced

126 ells but not for CD40-induced or LPS-induced CSR, suggesting that TRAF3 restricts NF-kappaB2 activati

127 ains elusive whether and how the BCR induces CSR mechanistically.

128 ontaining the catalytic SET domain, inhibits CSR without affecting either IgH germline transcription

129 at) 6, and demonstrate a failure to initiate CSR to IgG1 with low expression of gamma1 germ-line tran

130 n-induced cytidine deaminase (AID) initiates CSR by promoting deamination lesions within Smu and a do

131 Interestingly, CSR induced by staggered but not blunt, double-stranded

132 CSR in CH12F3 B lymphoma cells, inversional CSR can be activated by insertion of a CTCF-binding elem

133 ative frequency of deletional to inversional CSR junctions has not been measured.

134 se pro-B-cell lines, dispensable for joining CSR-associated DSBs in a cycling mouse B-cell line, and

135 atients with an orthologous mutation, lacked CSR and SHM, and had broad defects in genome-wide AID(G1

136 Mean CSR chemical-shift ratio and SII signal intensity index

137 und that ATM kinase promotes Alt-EJ-mediated CSR by suppressing interchromosomal translocations indep

138 d resection is dispensable for A-EJ-mediated CSR using cNHEJ-deficient B cells.

139 and resection independence of A-EJ-mediated CSR.

140 Furthermore, the P2X receptor-mediated CSR responses were enhanced by intrapericardial naloxone

141 s opioids suppress the P2X receptor-mediated CSR responses.

142 ad52(+/+) counterparts, which display normal CSR, Rad52(-/-) B cells show increased CSR, fewer intra-

143 I3K isoforms is essential to maintain normal CSR.

144 translocation and mutation frequency but not CSR or Ig switch region mutation.

145 We conclude that SHM, but not CSR, regulates peripheral B cell tolerance through the p

146 cNHEJ-deficient cells, a remarkable ~25% of CSR can be achieved by the alternative end-joining (Alt-

147 mokines CCL22 and CCL17 in the activation of CSR.

148 s and high-throughput sequencing analyses of CSR junctions and a chromosomal break repair assay indic

149 ion about the CSR mechanism, and analysis of CSR junctions is useful in basic and clinical research s

150 are program dedicated to support analysis of CSR recombination junctions sequenced with a HTS-based p

151 Dysregulation of CSR can cause self-reactive BCRs and B cell lymphomas; u

152 BRCT-domain protein BRIT1 as an effector of CSR.

153 mutant alleles that separate the effects of CSR and SHM on polyclonal immune responses.

154 ves the way for the label-free evaluation of CSR after various cell manipulations and treatments on t

155 was associated with decreased expression of CSR-related novel base excision repair genes that were o

156 ining is a programmed mechanistic feature of CSR as it is for V(D)J recombination and, if so, how thi

157 Amount and structural features of CSR junctions reveal valuable information about the CSR

158 In both groves, the hypothesis of CSR was rejected for all tests performed including quadr

159 as; understanding the timing and location of CSR is therefore important.

160 id organs revealed that the vast majority of CSR events occurred prior to the onset of somatic hyperm

161 ate the mediator complex in the mechanism of CSR and are consistent with a model in which mediator fa

162 y EEG electrode arrays in the mouse model of CSR where mice underwent 18-h sleep deprivation per day

163 y important roles in the DNA repair phase of CSR.

164 t genes between species, we defined a set of CSR-1 target genes with conserved germline expression, e

165 ated tool able to analyze large data sets of CSR junction sequences produced by high-throughput seque

166 rt was assessed using simulated data sets of CSR junctions and then used for analysis of Smu-Salpha a

167 T1-deleted B cells increases the severity of CSR defect over what is observed upon loss of either pro

168 The ligation step of CSR is usually mediated by the classical nonhomologous e

169 M193), this mark is ectopically deposited on CSR-1 target genes.

170 e, we demonstrate a direct effect of PTEN on CSR signaling by acute deletion of Pten specifically in

171 Depletion of SAMHD1 impaired not only CSR but also IgH/c-Myc translocation.

172 d SHM and CSR pipeline to analyze SHM and/or CSR in BCR rearrangements.

173 tosis with XY male-to-female sex reversal or CSR.

174 hyperplasia from tumors, although overlapped CSR chemical-shift ratio values can occur in early adult

175 78H) (Lig4(R/R)) mice exhibit only a partial CSR block, producing near normal IgG1 and IgE but substa

176 for mutagenic NHEJ but not for physiological CSR.

177 Productive CSR must occur in a deletional orientation by joining th

178 itive DNA end-processing enzyme and promotes CSR and aberrant genomic rearrangements by suppressing t

179 g evidence that 3'RR has a role in promoting CSR that is unique from enhancing S region transcription

180 es, the endo-siRNA-binding Argonaute protein CSR-1, has recently been ascribed with the ability to li

181 s overlaid on a completely spatially random (CSR) background, before every point is scrambled by its

182 e hypothesis of complete spatial randomness (CSR) of CBS infected trees within the groves.

183 Cell survival rate (CSR) is a very important parameter in biological and med

184 Antibody class-switch DNA recombination (CSR) is initiated by AID-introduced DSBs in the switch (

185 tely enhance class-switch DNA recombination (CSR), while decreasing at higher doses over a broad phys

186 Class-switch recombination (CSR) alters the Ig isotype to diversify antibody effecto

187 during antibody class switch recombination (CSR) and DSBs generated by ionizing radiation.

188 for Flt3 in IgG1 class-switch recombination (CSR) and production.

189 ) initiates both class switch recombination (CSR) and somatic hypermutation (SHM) in antibody diversi

190 AID mediates class-switch recombination (CSR) and somatic hypermutation (SHM) in B cells, but the

191 enzyme-mediating class-switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin g

192 tion mechanisms, class switch recombination (CSR) and somatic hypermutation (SHM), to re-engineer the

193 romotes antibody class switch recombination (CSR) and somatic hypermutation (SHM), whereas AID target

194 ntibody genes by class switch recombination (CSR) and somatic hypermutation (SHM), which are both dep

195 d immunoglobulin class switch recombination (CSR) are key processes in adaptive immune responses that

196 abnormalities in class switch recombination (CSR) associated with the human homozygous Lig4 R278H mut

197 DCs induced IgA class-switch recombination (CSR) by activating B cells through T cell-dependent or -

198 b production and class switch recombination (CSR) depend on autocrine C3a and C5a receptor (C3ar1/C5a

199 Class switch recombination (CSR) diversifies antibodies for productive immune respon

200 tation (SHM) and class-switch recombination (CSR) during transcription of immunoglobulin variable (Ig

201 mature B cells, class switch recombination (CSR) generates different antibody classes by replacing C

202 Class switch recombination (CSR) generates isotype-switched Abs with distinct effect

203 lymphocytes and class switch recombination (CSR) in antigen-stimulated B cells.

204 ) pathway during class switch recombination (CSR) in B cells, and HMCES deficiency leads to a signifi

205 Antibody class switch recombination (CSR) in B lymphocytes replaces immunoglobulin heavy chai

206 xhibited a lower class-switch recombination (CSR) in the GC B cells, leading to lower serum levels of

207 1 coevolved with class switch recombination (CSR) in the immune system.

208 tation (SHM) and class-switch recombination (CSR) increase the affinity and diversify the effector fu

209 Class-switch recombination (CSR) is a DNA recombination process that replaces the im

210 lymphocytes, Ig class switch recombination (CSR) is induced by activation-induced cytidine deaminase

211 In B cells, Ig class switch recombination (CSR) is initiated by activation-induced cytidine deamina

212 unoglobulin (Ig) class switch recombination (CSR) is initiated by the transcription-coupled recruitme

213 IgH class switch recombination (CSR) occurs through the deliberate introduction of activ

214 tation (SHM) and class switch recombination (CSR) of antibody genes.

215 domas, we induce class-switch recombination (CSR) of the IgH chain to the desired subclass.

216 tation (SHM) and class switch recombination (CSR) pipeline.

217 Class switch recombination (CSR) plays an important role in adaptive immune response

218 tation (SHM) and class-switch recombination (CSR) processes.

219 ulin heavy chain class switch recombination (CSR) requires targeted formation of DNA double-strand br

220 B cells undergo class switch recombination (CSR) to generate antibodies with different isotypes by j

221 low frequency of class switch recombination (CSR) to IgE ex vivo.

222 Immunoglobulin class switch recombination (CSR) to IgE is a tightly regulated process central to at

223 IgH expression, class-switch recombination (CSR), and somatic hypermutation.

224 Following class-switch recombination (CSR), antigen-activated B cells differentiate into extra

225 g immunoglobulin class switch recombination (CSR), are repaired by non-homologous end joining (NHEJ).

226 rmutation (SHM), class-switch recombination (CSR), or both.

227 unoglobulin (Ig) class switch recombination (CSR), somatic hypermutation (SHM), and gene conversion b

228 tation (SHM) and class switch recombination (CSR).

229 eavy chain (Igh) class switch recombination (CSR).

230 eavy Chain (IgH) class switch recombination (CSR).

231 reaks (DSBs) for class-switch recombination (CSR).

232 regulation of Ig class switch recombination (CSR).

233 regulator of Ig class switch recombination (CSR).

234 acity to undergo class switch recombination (CSR).

235 nd breaks during class switch recombination (CSR).

236 n the process of class switch recombination (CSR).

237 bs generated via class switch recombination (CSR); however, stimulating the BCR in the absence of cos

238 pe class switch (class switch recombination [CSR]).

239 eficient B cells, however, undergo (reduced) CSR through an alternative(A)-NHEJ pathway, which introd

240 core component of the NHEJ pathway, reduces CSR efficiency in a mouse B-cell line capable of robust

241 pioids in cardiac sympathoexcitatory reflex (CSR) responses remain unclear.

242 insertion also inactivates upstream S-region CSR and converts adjacent downstream sequences into an e

243 of APE1 appears to play a role in regulating CSR through the interleukin-6 signaling pathway and in p

244 uster-situated (transcriptional) regulators (CSRs) of the biosynthetic genes.

245 formational/stereoselectivity relationships (CSR) between catalysts and substrates provide a framewor

246 ree modes: complementary strand replication (CSR), rolling circle replication (RCR) and recombination

247 Cheyne-Stokes respiration (CSR) is believed to only occur in supine and sleeping co

248 and proportion of Cheyne-Stokes Respiration [CSR]).

249 of E. cyaneus) and cellular stress response (CSR) capacity, potentially causing species-related diffe

250 (lacking the large spacer regions) restores CSR to a level equivalent to or even higher than in wild

251 human and rodent chronic sleep restriction (CSR) studies suggests that NREM delta power is not progr

252 onic ( approximately 5 d) sleep restriction (CSR).

253 the predominant mechanism catalyzing robust CSR.

254 ive competitors, stress-tolerants, ruderals (CSR) classification.

255 During constitutive Salpha CSR in CH12F3 B lymphoma cells, inversional CSR can be a

256 l line capable of robust cytokine-stimulated CSR in cell culture.

257 years; 80% men), 195 (34%) presented supine CSR only, 82 (14%) presented supine and upright CSR, and

258 95% CI: 1.54 to 10.46; p = 0.004 vs. supine CSR).

259 e for p110alpha and p110delta in suppressing CSR.

260 munoglobulin heavy chain (Igh) locus targets CSR-associated DNA damage and is promoted by the BRCT do

261 better with SII signal intensity index than CSR chemical-shift ratio .

262 sing confocal microscopy, we then found that CSR but not SD mice show morphological signs of microgli

263 Instead, we found that CSR-1 functions with P granules to prevent MSP and sperm

264 Here, we report that CSR levels are not further reduced by deletion of either

265 We show that CSR is programmed to occur in a productive deletional or

266 e have used multiple approaches to show that CSR is triggered prior to differentiation into GC B cell

267 ctions reveal valuable information about the CSR mechanism, and analysis of CSR junctions is useful i

268 sphorylation of DNA-PKcs does not affect the CSR efficiency.

269 otypic composition of tonsil B cells and the CSR to IgE ex vivo.

270 (WAGO) and 'activating' siRNAs bound by the CSR-1 Argonaute require the DRH-3 helicase, an RdRP comp

271 Caenorhabditis briggsae to characterize the CSR-1 pathway, its targets and their evolution.

272 that the HSIFC can accurately determine the CSR, and the accuracy is comparable to that of flow cyto

273 n-chip label-free method for determining the CSR.

274 e modulated independently, especially in the CSR condition.

275 our hypersensitive sites contain most of the CSR-promoting functions of 3'RR.

276 PIR-1 also regulates the CSR-1 22G-RNA pathway and has critical functions in both

277 sible that APE1 has a role in regulating the CSR through its function as a redox coactivator.

278 opographical NREM sleep EEG responses to the CSR condition, including period-amplitude analysis of in

279 the binding of biosynthetic products to the CSR has been shown to provide negative feedback.

280 Using the CSR-competent mouse B-cell line CH12F3 and a combination

281 Yet, the CSR junctions recovered from DNA-PKcs (5A/5A) B cells re

282 egion of the gene encoding SgcR1, one of the CSRs of lidamycin production.

283 ting cardiac sympathetic afferents and these CSR responses are modulated by endogenous opioids.

284 in supine and sleeping conditions, and thus, CSR treatment is applied to those specific states.

285 late AID expression are of much relevance to CSR and genomic integrity; however, effectors of such re

286 p EEG in different brain regions responds to CSR.

287 ad52 and translesion DNA polymerase theta to CSR.

288 Finally, we show that in B cells undergoing CSR, the dynamic long-range contacts between the IgH enh

289 ost exclusively in those that have undergone CSR.

290 Upright CSR in HF patients is predicted by increased chemosensit

291 only, 82 (14%) presented supine and upright CSR, and 297 patients (52%) had normal breathing.

292 as the only independent predictor of upright CSR (odds ratio: 3.96; 95% confidence interval [CI]: 1.4

293 4.05; p = 0.001) and the presence of upright CSR independently predicted 8-year cardiac death (hazard

294 test to investigate the presence of upright CSR, assessment of chemoreflex response to hypoxia and h

295 Patients with upright CSR had the greatest apnea-hypopnea and central apnea in

296 At 8-year follow-up, patients with upright CSR had the worst outcome (log-rank = 14.05; p = 0.001)

297 mechanism and provide an explanation of why CSR is so reliant on the 53BP1 DSB-response factor.

298 th V(D)J recombination, DSBs associated with CSR can be resolved in NHEJ-deficient cells (albeit at a

299 suppress genomic instability associated with CSR.

300 onal regulation, and by (2) functioning with CSR-1 to limit the domain of sperm-specific expression a