ライフサイエンスコーパス: hypermutation

1 A mutations in HIV-1 plus-strand DNA (termed hypermutation).

2 -A mutations and (to a lesser extent) G-to-A hypermutation.

3 fine-tuning of BCR specificities by somatic hypermutation.

4 switch recombination and, possibly, somatic hypermutation.

5 larities in evolutionary dynamics leading to hypermutation.

6 rwent class-switch recombination and somatic hypermutation.

7 G1 memory B cells without additional somatic hypermutation.

8 nd lower frequency and complexity of somatic hypermutation.

9 tiate class switch recombination and somatic hypermutation.

10 and T-bet, and exhibits evidence of somatic hypermutation.

11 ycosylation sites that emerge during somatic hypermutation.

12 ugh clonal selection, expansion, and somatic hypermutation.

13 lass-switch recombination (CSR), and somatic hypermutation.

14 ry B cells showed increased rates of somatic hypermutation.

15 d immunoglobulin class-switching and somatic hypermutation.

16 e DNA sequences were defective due to G-to-A hypermutation.

17 lar defense mechanism called APOBEC-mediated hypermutation.

18 ity of binding at such low levels of somatic hypermutation.

19 tential N-glycosylation sites during somatic hypermutation.

20 munoglobulin variable regions during somatic hypermutation.

21 ir use of D genes and propensity for somatic hypermutation.

22 pe coverage and strong signatures of somatic hypermutation.

23 iled to produce IgG1 and had reduced somatic hypermutation.

24 onally distinct and exhibit enhanced somatic hypermutation.

25 ched antibodies and the frequency of somatic hypermutation.

26 onses, including class switching and somatic hypermutation.

27 long CDR H3, and limited subsequent somatic hypermutation.

28 their BCR repertoires or patterns of somatic hypermutation.

29 binding to group 1 subtypes through somatic hypermutation.

30 nisms that generate long ssDNA vulnerable to hypermutation.

31 by lower viral titres, lower infectivity and hypermutation.

32 -switched Abs and decreased rates of somatic hypermutation.

33 fidelity DNA polymerases to generate somatic hypermutation.

34 vents occurred prior to the onset of somatic hypermutation.

35 redicted by the mutation profiles of somatic hypermutation.

36 double-strand DNA breaks and pro-metastatic hypermutation.

37 s in B cells are off-target sites of somatic hypermutation.

38 of naive B cells that subsequently underwent hypermutation.

39 ne cells, ABCs displayed significant somatic hypermutation.

40 d IgG4 transcripts were analyzed for somatic hypermutations.

41 ely diversified by somatic recombination and hypermutations.

42 and IgA1 transcripts showed reduced somatic hypermutations.

43 explained by the Neuberger model of somatic hypermutation: 1) across multiple data sets there is sig

44 ad large internal deletions, 174 (23.7%) had hypermutations, 15 (1.4%) had small internal deletions,

45 We delineate two main pathways to hypermutation: a de novo pathway associated with constit

46 l N-glycosylation motifs acquired by somatic hypermutation (ac-Nglycs) within Ig H chain V region (IG

47 nths of emergence of the lineage and somatic hypermutations accumulated at key contact residues.

48 the germinal center, B cells undergo somatic hypermutation, affinity-based clonal expansion, and diff

49 Somatic hypermutation after immunization indicates that engineer

50 these clusters there was a range of somatic hypermutations along the IGHV germline segment-derived p

51 ght chain variable domains shaped by somatic hypermutation and affinity maturation of B cells in the

52 Somatic hypermutation and affinity maturation take place in germ

53 cases (9.6%), all of which displayed somatic hypermutation and AID-mRNA expression.

54 B cells cycle between proliferation/somatic hypermutation and antigen-driven selection.

55 nal dose boosting increased antibody somatic hypermutation and avidity and sustained high protection

56 -69 polymorphism on V-segment usage, somatic hypermutation and B cell expansion that elucidates the d

57 iven BCR affinity maturation through somatic hypermutation and cellular selection in germinal centres

58 the expression of AID and increased somatic hypermutation and chromosomal translocation frequency to

59 Germinal center somatic hypermutation and class switch recombination machineries

60 d cytidine deaminase (AID) initiates somatic hypermutation and class switch recombination of the immu

61 n-dependent locus remodeling (global somatic hypermutation and class switch recombination to major is

62 Somatic hypermutation and class-switch recombination of the immu

63 ocesses in antibody diversification: somatic hypermutation and class-switch recombination.

64 n all adults and progressive introduction of hypermutation and class-switching as animals age.

65 ng antibodies display high levels of somatic hypermutation and cross-react with circulating HCoVs, su

66 cell clones had high frequencies of somatic hypermutation and encoded broadly cross-reactive monoclo

67 viruses (MuLVs) does not appear to be G-->A hypermutation and is unclear.

68 ated 385 pancreatic cancer genomes to define hypermutation and its causes.

69 strains with only approximately 11% somatic hypermutation and no insertions or deletions.

70 ved breadth with only 10% nucleotide somatic hypermutation and no insertions or deletions.

71 three lineages had modest levels of somatic hypermutation and normal antibody-loop lengths and were

72 nge, AID and Blimp1 expression, CSR, somatic hypermutation and plasma cell differentiation.

73 d significantly lower frequencies of somatic hypermutation and predominantly encoded strain-specific

74 er cyclic selection of cells in GCs, somatic hypermutation and proliferation were maintained.

75 k BCL2:IGH translocation enables AID-induced hypermutation and propagates clonal evolution toward mal

76 nd removing their self-reactivity by somatic hypermutation and selection in germinal centers (GCs).

77 programs must balance proliferation, somatic hypermutation and selection to both provide effective hu

78 lones expand and undergo immunoglobulin gene hypermutation and selection.

79 These antibodies had low levels of somatic hypermutation and showed a strong enrichment in VH1-69,

80 s" process is a major contributor to somatic hypermutation and therefore Ig diversification in mice a

81 tients have acquired lower number of somatic hypermutation and used focused IGHV repertoire with over

82 h expressed protein-coding fusions, breakend hypermutation, and acral, but not cutaneous, melanomas.

83 Cognate T cell help, somatic hypermutation, and affinity maturation within germinal c

84 variable region transcription before somatic hypermutation, and antibody heavy chain production, but

85 ling, increased rounds of productive somatic hypermutation, and B-cell selection strength are among t

86 ria, including V gene usage, rate of somatic hypermutation, and CDR-H3 length and composition.

87 e class-switched antibodies, undergo somatic hypermutation, and differentiate into memory B cells.

88 al centers (GC), underwent extensive somatic hypermutation, and differentiated into memory B cells.

89 sing natural diversity introduced by somatic hypermutation, and screened half-antibodies for increase

90 immunity is driven by the expansion, somatic hypermutation, and selection of B cell clones.

91 ctions that support class switching, somatic hypermutation, and the generation of high-affinity Abs.

92 l repertoire, including kataegis and somatic hypermutation, and their relative contribution changes o

93 pproach to the detection of APOBEC3-mediated hypermutation, and use it to compare SFV sequences from

94 y stable as per heavy chain isotype, somatic hypermutations, and clonal composition.

95 Fortunately, the required CH235-lineage hypermutation appeared substantially guided by the intri

96 with oxidative DNA damage and local somatic hypermutation appeared to contribute to this signature i

97 We find that both cell division and hypermutation are directly proportional to the amount of

98 reaks in V regions that arise during somatic hypermutation are poorly understood.

99 e whether the extent of clonal expansion and hypermutation are regulated during interzonal GC cycles.

100 Only a few somatic hypermutations are required for broad antiviral activity

101 breast cancers, which seems to be related to hypermutation arising in A3B(del) carriers.

102 Using somatic hypermutations as a molecular clock, we discovered that

103 Hypermutation at diagnosis or at recurrence associated w

104 The observation that hypermutation at GBM recurrence was rare (8%) and not co

105 plete transcript, and the process of somatic hypermutation at individual nucleotides.

106 Fifteen percent of tumors present hypermutation at relapse in highly expressed genes, with

107 enerally exhibit very high levels of somatic hypermutation, both in their CDR and framework-variable

108 negative GC B cells displayed normal somatic hypermutation but defective affinity maturation and clas

109 onal signatures and a signature of localized hypermutation called kataegis.

110 ic and adult patients, including tumors with hypermutation caused by chemotherapy, carcinogens, or ge

111 ts of class switch recombination and somatic hypermutations characteristic of germinal center reactio

112 -induced deaminase (AID) involved in somatic hypermutations/class switch recombination, in primary hu

113 IgG contained equivalent numbers of somatic hypermutations compared with all other VHs, a characteri

114 nal mutational burden of MMBIR consisting of hypermutation confined to the locus and manifesting as S

115 Two tumors had hypermutation consistent with mismatch repair deficiency

116 es, which exhibited a high degree of somatic hypermutation, consistent with chronic antigen exposure.

117 lted in reduced GC sizes and reduced somatic hypermutation coupled with a failure to control chronic

118 iomas(1-5); however, the mechanisms by which hypermutation develops and whether it predicts the respo

119 trics that incorporate the biases of somatic hypermutation do not outperform simple Hamming distance.

120 We identified high rates of somatic hypermutations, especially targeting RGYW/WRCY hotspot m

121 The ADAR1-mediated biased hypermutation events are consistent with the protein kin

122 he diversity of which is expanded by somatic hypermutation following antigen exposure(1).

123 IDH1-wild-type primary GBMs rarely developed hypermutation following temozolomide (TMZ) treatment, in

124 eatment, indicating low risk for TMZ-induced hypermutation for these tumors under the standard regime

125 Consistent with AID, comparable somatic hypermutation frequencies and class-switching indicated

126 of this interaction varies, since a range of hypermutation frequencies are observed in HIV-1 patient

127 s that displayed significantly lower somatic hypermutation frequencies than their counterparts with C

128 pressing clones and showed decreased somatic hypermutation frequencies.

129 es CSP-specific antibody avidity and somatic hypermutation frequency in CSP-specific B cells, demonst

130 uch as large deletions and APOBEC3G-mediated hypermutation, from the majority of proviruses that have

131 e (AID) protein is known to initiate somatic hypermutation, gene conversion or switch recombination b

132 We show that these cells exhibit somatic hypermutation, gene expression characteristic of signali

133 Somatic hypermutation generates a myriad of Ab mutants in Ag-spe

134 CIN), which is often mutually exclusive from hypermutation genotypes, represents a distinct subtype o

135 ody-mediated selection, suggesting localized hypermutation has evolved to facilitate host persistence

136 omes are intact, lack APOBEC-3G/F-associated hypermutations, have limited genome truncations, and ove

137 d overusage of the IGHV4-34 gene and somatic hypermutation in 71/79 (89.8%) IGHV-IGHD-IGHJ gene rearr

138 change the frequency or spectrum of somatic hypermutation in Ab genes, indicating that DNA repair an

139 but not ibrutinib, showed increased somatic hypermutation in AID off-targets.

140 iota) is an attractive candidate for somatic hypermutation in antibody genes because of its low fidel

141 which supports the critical role of somatic hypermutation in broadening the bnAb response.

142 play an important role in generating somatic hypermutation in cancers as well as in noncancerous cell

143 oire diversity, clonal expansion and somatic hypermutation in cells from mice immunized with a vaccin

144 chain intron enhancers efficiently stimulate hypermutation in chicken cells.

145 ing genome-wide increase in aberrant somatic hypermutation in EBV-positive tumors, supporting a link

146 The striking amount of somatic hypermutation in HIV bnAbs led to the hypothesis that T

147 o had significantly reduced rates of somatic hypermutation in IgG (P = .003) but not IgA or IgM heavy

148 pectedly, we discover high levels of somatic hypermutation in infants as young as 3 months old.

149 , indicating the possible absence of somatic hypermutation in lungfish LAs.

150 Furthermore, a comparison of hypermutation in mouse B cells, AID-induced kataegis in

151 rallels and differences in the mechanisms of hypermutation in prostate cancer compared with other MSI

152 e breadth through moderate levels of somatic hypermutation in response to emerging viral variants.

153 ns are restriction factors that induce G-->A hypermutation in retroviruses during replication as a re

154 tralization activity on the level of somatic hypermutation in the Ab framework, we applied a computat

155 ight zone (LZ) and proliferation and somatic hypermutation in the dark zone (DZ).

156 iterative interzonal cycles of division and hypermutation in the GC dark zone followed by migration

157 d light chain contact with HIV Env, and less hypermutation in the heavy chain, compared with antibodi

158 ell death and increased frequency of somatic hypermutation in the immunoglobulin VH locus.

159 IgG and IgA subclasses with limited somatic hypermutation in the initial weeks of infection.

160 Somatic hypermutation in the other CDRs of PGT145 were crucially

161 lvability and help explain the prevalence of hypermutation in various settings, ranging from emergenc

162 stricts HIV-1 replication by inducing G-to-A hypermutation in viral DNA and by deamination-independen

163 ral antibodies that are subjected to somatic hypermutation in vivo.

164 Hypermutations in cancer cells are due to defects in DNA

165 ow, blood B and plasma cell subsets, somatic hypermutations in Ig genes, and in vitro proliferation a

166 iate from the frequent occurrence of somatic hypermutations in Ig sequences.

167 We show that hypermutation independently evolves when different Esche

168 vity revealed a precise targeting of somatic hypermutation indicative of an active, ongoing interacti

169 uired for class switch recombination/somatic hypermutation induction inhibits T1D development in the

170 Similarly, somatic hypermutation is almost negligible at the JH4 intron in

171 h whether the sequence has undergone somatic hypermutation is dependent on the maturation stage at wh

172 , but significantly variable by cancer type (hypermutation is excluded from this study).

173 able binding to AQP4, revealing that somatic hypermutation is required for the generation of anti-AQP

174 a glycan site at N332 on gp120, and somatic hypermutation is required to accommodate the neighboring

175 Hypermutation is restricted to germinal center B cells a

176 A high tumour mutational burden (hypermutation) is observed in some gliomas(1-5); however

177 ocess that generates these lineages, somatic hypermutation, is biased by hotspot motifs which violate

178 inhibit viral replication by inducing G-to-A hypermutation, it is not known whether they are copackag

179 butions, class switch recombination, somatic hypermutation levels and in features of V(D)J recombinat

180 clonal lineage analysis reveals that somatic hypermutation levels are increased in both infants and t

181 lls showed reduced proliferation and somatic hypermutation levels, whereas these were normal in CD27(

182 pertaining to the hypothesis that localised hypermutation (LH) compensates for fitness losses caused

183 RISPR-X, a strategy to repurpose the somatic hypermutation machinery for protein engineering in situ.

184 which impaired apoptosis and ongoing somatic hypermutation may lead to an increased risk of lymphoma

185 ersification in infants and toddlers.Somatic hypermutation of antibodies can occur in infants but are

186 iates class switch recombination and somatic hypermutation of antibodies in jawed vertebrates.

187 rmore, we provided statistical evidence that hypermutation of cancer driver genes on inactive X chrom

188 volved in mutagenic processes during somatic hypermutation of immunoglobulin genes.

189 or of class switch recombination and somatic hypermutation of immunoglobulin in B cells, yet its role

190 h APOBEC3 protein and used them to show that hypermutation of proviral DNAs from seven patients was i

191 3 family of cytidine deaminases cause lethal hypermutation of retroviruses via deamination of newly r

192 Studies on somatic hypermutation of the antigen binding region, receptor ex

193 ide protection against HIV-1Deltavif through hypermutation of the viral genome, inhibition of reverse

194 ells are Ag experienced, as shown by somatic hypermutation of their Ig genes in adaptive immune recep

195 NA production and cytidine-to-uridine-driven hypermutation of this cDNA.

196 uced (cytosine) deaminase to promote somatic hypermutation on both DNA strands to generate double-str

197 either point mutations in V exons in somatic hypermutation or deletion of intervening DNA sequences d

198 ed into untemplated mutations during somatic hypermutation or DNA double-strand breaks during class s

199 autoantibodies showed low numbers of somatic hypermutations or were unmutated.

200 ed that J9 and J8 followed divergent somatic hypermutation pathways, and that a limited number of mut

201 match repair identified in cell lines with a hypermutation phenotype.

202 Similarities included the presence of two hypermutation phenotypes, as defined by signatures for d

203 ium, Plantago, and Silene indicate localized hypermutation, potentially induced by a higher level of

204 omas, is an off-target of the normal somatic hypermutation process taking place in GC B cells in both

205 nalyses both V(D)J segment usage and somatic hypermutation profiles, we elucidate physiological BCR r

206 We show that VH gene repertoires and somatic hypermutation rates of atypical and classical MBCs are i

207 Somatic hypermutation rates point to a CSF antigen-driven activa

208 rsistent antibodies displayed higher somatic hypermutation relative to transient serum antibodies det

209 had several 'unusual residues' (rare somatic hypermutations, rSHM, with positional frequency of <1%)

210 Somatic hypermutation (SH) generates point mutations within rear

211 However, somatic hypermutation (SHM) and affinity maturation can take pla

212 ion occurs when Ig V regions undergo somatic hypermutation (SHM) and affinity-based selection toward

213 lobulins (Igs) during the process of somatic hypermutation (SHM) and also Ig class switching, can hav

214 ulin (Ig) genes to initiate antibody somatic hypermutation (SHM) and class switch recombination (CSR)

215 rts cytosine into uracil to initiate somatic hypermutation (SHM) and class switch recombination (CSR)

216 d cytidine deaminase (AID) initiates somatic hypermutation (SHM) and class switch recombination (CSR)

217 immune repertoire pipeline, and the somatic hypermutation (SHM) and class switch recombination (CSR)

218 Somatic hypermutation (SHM) and class-switch recombination (CSR)

219 deletions in antibody genes through somatic hypermutation (SHM) and class-switch recombination (CSR)

220 y diversity in B cells by initiating somatic hypermutation (SHM) and class-switch recombination (CSR)

221 Somatic hypermutation (SHM) and immunoglobulin (Ig) class switch

222 hese plasmablasts had high levels of somatic hypermutation (SHM) and recognized the HA stem region of

223 ve antibodies, B cells undergo rapid somatic hypermutation (SHM) and selection for binding affinity t

224 class switch recombination (CSR) and somatic hypermutation (SHM) by deaminating cytosine residues in

225 ed adults and exhibit high levels of somatic hypermutation (SHM) due to years of affinity maturation.

226 d nucleotide motif: the signature of somatic hypermutation (SHM) enzyme, Activation Induced Deaminase

227 ed cytidine deaminase (AID)-mediated somatic hypermutation (SHM) following neurotropic coronavirus in

228 initiates antibody variable (V) exon somatic hypermutation (SHM) for affinity maturation in germinal

229 idine deaminase (AID) initiates both somatic hypermutation (SHM) for antibody affinity maturation and

230 sual traits of bnAbs, including high somatic hypermutation (SHM) frequencies and in-frame insertions

231 Somatic hypermutation (SHM) generates much of the Ab diversity n

232 d as evidenced by elevated levels of somatic hypermutation (SHM) in Ab sequences isolated at the late

233 class switch recombination (CSR) and somatic hypermutation (SHM) in antibody diversification.

234 class-switch recombination (CSR) and somatic hypermutation (SHM) in B cells, but the mechanism by whi

235 xycytidine deaminase (AID) initiates somatic hypermutation (SHM) in immunoglobulin variable (IgV) gen

236 ted the clonal overlap and extent of somatic hypermutation (SHM) in the ASC (effector) and ABC (memor

237 alization associated with increasing somatic hypermutation (SHM) levels over time.

238 d, using laser microdissection, that somatic hypermutation (SHM) occurred efficiently at extrafollicu

239 During somatic hypermutation (SHM) of Ig genes in germinal center B cel

240 class-switch recombination (CSR) and somatic hypermutation (SHM) of Ig genes.

241 induced deaminase (AID) mediates the somatic hypermutation (SHM) of Ig variable (V) regions that is r

242 class-switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes, is essentia

243 During somatic hypermutation (SHM) of immunoglobulin genes, uracils int

244 oad dissemination and high levels of somatic hypermutation (SHM) of most lineages, including tier 2 v

245 hey are not accompanied by extensive somatic hypermutation (SHM) of targeted regions and because repa

246 lymphoma B cells undergo continuous somatic hypermutation (SHM) of their immunoglobulin variable reg

247 germinal center (GC) B cells undergo somatic hypermutation (SHM) of V(D)J exons followed by selection

248 Analyses of somatic hypermutation (SHM) patterns in B cell Ig sequences have

249 egulates both the antigen-stimulated somatic hypermutation (SHM) process and plays a central function

250 ases (107/154) bearing an imprint of somatic hypermutation (SHM) ranging from minimal to pronounced.

251 s difference may be linked to B cell somatic hypermutation (SHM) targeting, including error-prone DNA

252 otably, the frequency of VH with low somatic hypermutation (SHM) was strikingly higher, especially in

253 mportance of affinity maturation via somatic hypermutation (SHM) within the Ig variable H (VH) and va

254 During somatic hypermutation (SHM), activation-induced deaminase (AID)

255 g) class switch recombination (CSR), somatic hypermutation (SHM), and gene conversion by converting D

256 r analysis of replication histories, somatic hypermutation (SHM), and immunoglobulin class-switching

257 and assess their ability to perform somatic hypermutation (SHM), class-switch recombination (CSR), o

258 During somatic hypermutation (SHM), deamination of cytidine by activati

259 class switch recombination (CSR) and somatic hypermutation (SHM), to re-engineer their antibody gene

260 class switch recombination (CSR) and somatic hypermutation (SHM), whereas AID targeting of non-Ig loc

261 class switch recombination (CSR) and somatic hypermutation (SHM), which are both dependent on efficie

262 s-switch DNA recombination (CSR) and somatic hypermutation (SHM), which require activation-induced cy

263 nsions and had significant levels of somatic hypermutation (SHM).

264 s (PCs) from CD lesions have limited somatic hypermutation (SHM).

265 ed livers proliferated and underwent somatic hypermutation (SHM).

266 th severely decreased frequencies of somatic hypermutations (SHMs), but their underlying molecular de

267 ay differ due to the accumulation of somatic hypermutations (SHMs).

268 e B cells were characterized by more somatic hypermutation, shorter CDR3 segments, and less negative

269 vaccines driving immunoglobulin gene somatic hypermutation should be a priority to protect elderly in

270 et composition, replication history, somatic hypermutation status, and class-switch recombination in

271 d immunoglobulin heavy variable gene somatic hypermutation status, we propose a novel hierarchical mo

272 r can trigger the formation of single-strand hypermutation substrates.

273 breadth, and extraordinary level of somatic hypermutation suggested commonalities in maturation amon

274 tract and have higher frequencies of somatic hypermutation, suggesting extensive and serial rounds of

275 EC3 proteins are devoid of detectable G-to-A hypermutations, suggesting one or multiple deaminase-ind

276 nventional GC B cells that underwent somatic hypermutation, survived despite losing antigen reactivit

277 s, creating lineage trees, inferring somatic hypermutation targeting models, measuring repertoire div

278 analysis of a published database of somatic hypermutations that arose in the IGHV3-23*01 human V reg

279 oantibodies after the acquisition of somatic hypermutations that improve affinity for self-antigens.

280 We identified somatic hypermutations that were recurrently selected in such pu

281 c pipeline to detect indels, frameshifts, or hypermutations that would render them defective.

282 me of class switch recombination and somatic hypermutation; the transcription factor E47, crucial for

283 and minor contributions of antibody somatic hypermutations to epitope contacts.

284 ls of class switch recombination and somatic hypermutation, two mutagenic DNA processes used to gener

285 perienced malaria continue to induce somatic hypermutations upon malaria rechallenge.

286 This suggests an important role for biased hypermutation via an adenosine deaminase, RNA-specific (

287 Hypermutation was detected in tumor types not previously

288 However, somatic hypermutation was increased specifically on the transcri

289 ferent rates across the glioma subtypes, and hypermutation was not associated with differences in ove

290 mplex chains of rearrangements and localized hypermutation were detected in almost all cases.

291 efects, we identified six cases of synthetic hypermutation, where the combined effect of the drug and

292 Sequencing revealed 82% with somatic hypermutation, whereas 18% had >98% germ-line identity,

293 body variable (V) regions results in somatic hypermutation, whereas its recruitment to switch (S) reg

294 trand breaks, chromosome rearrangements, and hypermutation, which are all sources of genomic instabil

295 Neutral evolution enables tolerance of hypermutation, which defines a surprisingly large fracti

296 MT expression in pretreated GBM is linked to hypermutation, which in turn contributes to increased ge

297 FeLV-B was subject to G-->A hypermutation with a predominant APOBEC3G signature in p

298 gue plasmablasts had high degrees of somatic hypermutation, with a clear preference for replacement m

299 associated (P < 0.001) with lack of somatic hypermutation within the clonotypic immunoglobulin heavy

300 VDJ rearrangement and somatic hypermutation work together to produce antibody-coding B