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 d immunoglobulin class-switching and somatic hypermutation.

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

4 lar defense mechanism called APOBEC-mediated hypermutation.

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

6 tential N-glycosylation sites during somatic hypermutation.

7 munoglobulin variable regions during somatic hypermutation.

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

9 pe coverage and strong signatures of somatic hypermutation.

10 iled to produce IgG1 and had reduced somatic hypermutation.

11 onally distinct and exhibit enhanced somatic hypermutation.

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

13 ched antibodies and the frequency of somatic hypermutation.

14 onses, including class switching and somatic hypermutation.

15 long CDR H3, and limited subsequent somatic hypermutation.

16 nally expanded Vh7 revealed signs of somatic hypermutation.

17 agenesis, as in the case of in vitro somatic hypermutation.

18 class-switch recombination (CSR) and somatic hypermutation.

19 heavy chain gene class switching or somatic hypermutation.

20 93 cells, and matured using in vitro somatic hypermutation.

21 er-driving genes, especially those masked by hypermutation.

22 dergo class-switch recombination and somatic hypermutation.

23 munoglobulin variable regions during somatic hypermutation.

24 fine-tuning of BCR specificities by somatic hypermutation.

25 ry strategies of bacteria include methods of hypermutation.

26 an generated by recombinatorial diversity or hypermutation.

27 cofactors could also be involved in APOBEC-3 hypermutation.

28 a direct role for DNA polymerase zeta in Ig hypermutation.

29 switch recombination and, possibly, somatic hypermutation.

30 ne cells, ABCs displayed significant somatic hypermutation.

31 larities in evolutionary dynamics leading to hypermutation.

32 rwent class-switch recombination and somatic hypermutation.

33 G1 memory B cells without additional somatic hypermutation.

34 nd lower frequency and complexity of somatic hypermutation.

35 tiate class switch recombination and somatic hypermutation.

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

37 ycosylation sites that emerge during somatic hypermutation.

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

39 ry B cells showed increased rates of somatic hypermutation.

40 ely diversified by somatic recombination and hypermutations.

41 nts and then diversified by numerous somatic hypermutations.

42 d IgG4 transcripts were analyzed for somatic hypermutations.

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

44 and thus time for clonal expansion, somatic hypermutation, affinity maturation, and acquisition of a

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

46 activation markers and had undergone somatic hypermutation, albeit at levels lower than their CD27(+)

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

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

49 Somatic hypermutation and affinity maturation take place in germ

50 After undergoing Ig somatic hypermutation and Ag selection, germinal center (GC) B c

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

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

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

54 -69 polymorphism on V-segment usage, somatic hypermutation and B cell expansion that elucidates the d

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

56 ion, e.g. APOBEC3G, or initiation of somatic hypermutation and class switch recombination (activation

57 own as AICDA) enzyme is required for somatic hypermutation and class switch recombination at the immu

58 Germinal center somatic hypermutation and class switch recombination machineries

59 nd initiates the events that lead to somatic hypermutation and class switch recombination of immunogl

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

61 esentation may have implications for somatic hypermutation and class switching during affinity matura

62 Somatic hypermutation and class-switch recombination of the immu

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

64 key catalyst in initiating antibody somatic hypermutation and class-switch recombination.

65 f AID during transcription-dependent somatic hypermutation and class-switch recombination.

66 n-induced deaminase (AID) to undergo somatic hypermutation and class-switch recombination.

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

68 Somatic hypermutation and clonal selection lead to B cells expre

69 esults implicate APOBEC3B/A in breast cancer hypermutation and give insight into the mechanism of kat

70 itical in normal B cells to initiate somatic hypermutation and immunoglobulin class switch recombinat

71 ne to uracil in viral (-)DNA, which leads to hypermutation and inactivation of the provirus.

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

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

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

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

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

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

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

79 lones expand and undergo immunoglobulin gene hypermutation and selection.

80 of antibody maturation has been that somatic hypermutation and subsequent clonal selection increase a

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

82 however, showed high frequencies of somatic hypermutations and increased usage of downstream IgG sub

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

84 the site of B cell clonal expansion, somatic hypermutation, and affinity-based selection, the combina

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

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

87 obulin genes by V(D)J recombination, somatic hypermutation, and class switch recombination.

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

89 y facilitating isotype switching and somatic hypermutation, and promoting the generation of memory ce

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

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

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

93 re oligoclonal and exhibit extensive somatic hypermutation, and their numbers decrease after rituxima

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

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

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

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

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

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 -induced cytidine deaminase-mediated somatic hypermutation, as shown by comprehensive analysis of enr

104 Hypermutation at diagnosis or at recurrence associated w

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 nfirmed that the data were inconsistent with hypermutation, but consistent with germline selection: m

110 (V) genes of immunoglobulins undergo somatic hypermutation by activation-induced deaminase (AID) to g

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

112 ique mutation spectra, general and inducible hypermutation can analogously influence the ecology and

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

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

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

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

117 Two tumors had hypermutation consistent with mismatch repair deficiency

118 uced infectivity and the virus accrued G-->A hypermutations, consistent with APOBEC3 protein pressure

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

120 he method using tumor karyotypes and somatic hypermutation data sets.

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

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

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 , B-cell subset replication history, somatic hypermutation frequencies, CSR patterns, B-cell repertoi

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 POBEC-1 was overexpressed by adenovirus, the hypermutation frequency of apoB mRNA increased from 0.4%

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

134 icantly shaping pathogenic populations where hypermutation has been most widely observed.

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

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

137 DNA showed extensive APOBEC-mediated G-to-A hypermutation in a donor animal at week 9, corroborating

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

139 ng to TSHR, indicating importance of somatic hypermutation in acquiring TSAb activity.

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

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

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

143 chain intron enhancers efficiently stimulate hypermutation in chicken cells.

144 find candidate genes responsible for somatic hypermutation in germinal center B cells.

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

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

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

148 plication in experimental systems and induce hypermutation in infected patients; however, the relativ

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 Somatic hypermutation in the other CDRs of PGT145 were crucially

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

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

162 egion (CDR) 3 grafting combined with somatic hypermutation in vitro.

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

164 tudies, suggest an expanded role for somatic hypermutation in which both binding affinity and stabili

165 Hypermutations in cancer cells are due to defects in DNA

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

167 it was the finding that the level of somatic hypermutations in rearranged IG heavy-chain genes could

168 ed the induction of high frequency of G-to-A hypermutations in the env genes from HIV-1BaL-infected M

169 APOBEC-3 proteins induce C-to-U hypermutations in the viral genome of various viruses an

170 trict HIV-1 replication in MDDCs by inducing hypermutations in the viral genome.

171 We show that hypermutation independently evolves when different Esche

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

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

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

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

176 Hypermutation is restricted to germinal center B cells a

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 nsable for normal GC cellularity and somatic hypermutation, it is required for the efficient selectio

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

181 NA denaturation PCR at 72-76 degrees C, with hypermutation levels increasing up to 67%.

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

183 to these genome-wide mutational signatures, hypermutation localized to small genomic regions, 'katae

184 ap for Ang2 by harnessing the B cell somatic hypermutation machinery and coupling this to selectable

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

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

187 Diversity arises from somatic hypermutation of an ultralong DH with a severe codon bia

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

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

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

191 However, somatic hypermutation of Ig genes and heavy-chain CDR3 size dist

192 ibute to mutagenesis observed during somatic hypermutation of Ig genes.

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

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

195 is achieved through translocation (~40%) or hypermutation of its promoter (~15%).

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

197 replication by inducing deleterious dC > dU hypermutation of replication intermediates.

198 3 family of cytidine deaminases cause lethal hypermutation of retroviruses via deamination of newly r

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

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

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

202 (including those unable to generate somatic hypermutations of immunoglobulin genes) displayed anti-n

203 , as well as excessive cytidine deamination (hypermutation) of the DNAs that are synthesized.

204 emoval of cold agglutinin self-reactivity by hypermutation, often accompanied by mutations that inact

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

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

207 found that rat APOBEC-1 overexpression had a hypermutation pattern similar to that of APOBEC-3s on it

208 The finding of an APOBEC-3 hypermutation pattern with rat APOBEC-1 suggests that co

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

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

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

212 3 DRMR>A4 mutant proviruses displayed G-to-A hypermutations primarily in GG and GA dinucleotides as e

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

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

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

216 class switch recombination (CSR) and somatic hypermutation requires RNA polymerase II (polII) transcr

217 Somatic hypermutation (SH) generates point mutations within rear

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

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

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

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

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

223 iversification of antibodies through somatic hypermutation (SHM) and class switch recombination (CSR)

224 Antibody diversification through somatic hypermutation (SHM) and class switch recombination (CSR)

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

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

227 sponses to Ag stimulation require Ig somatic hypermutation (SHM) and class-switch recombination (CSR)

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

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

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

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

232 oma (FL) is apparent from studies of somatic hypermutation (SHM) caused by activation-induced deamina

233 Somatic hypermutation (SHM) diversifies the V region of Ig genes

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

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

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

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

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

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

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

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

242 repertoire diversification occurs by somatic hypermutation (SHM) in germinal centers following Ag sti

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

244 germinal centers where they undergo somatic hypermutation (SHM) in V(D)J exons for the generation of

245 Somatic hypermutation (SHM) is an integral process in the develo

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

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

248 Somatic hypermutation (SHM) of Ig genes is initiated by the acti

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

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

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

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

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

254 may also be associated with impaired somatic hypermutation (SHM) of the Ig V regions.

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

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

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

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

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

260 They play major roles in regulating somatic hypermutation (SHM), class switch DNA recombination (CSR

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

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

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

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

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

266 class switch recombination (CSR) and somatic hypermutation (SHM).

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

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

269 ciency and only modestly affects the somatic hypermutation spectrum in vitro.

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

271 LC- and HC-MBL had similar somatic hypermutation status, yet different IGHV gene repertoire

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

273 n with clonal expansion and signs of somatic hypermutation suggest a CD4(+) T lymphocyte-dependent an

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

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

276 strain and exhibited high levels of somatic hypermutation, suggesting they were derived from recall

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

278 ll-associated vDNA revealed extensive G-to-A hypermutation, suggestive of APOBEC-mediated viral restr

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

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

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

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

283 Y. enterocolitica porins to undergo somatic hypermutation to acquire a cross-reactive pathogenic res

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 These data indicate that hypermutation via multiple simultaneous changes in rando

288 Hypermutation was detected in tumor types not previously

289 However, somatic hypermutation was increased specifically on the transcri

290 that DNA polymerase zeta participates in Ig hypermutation, we generated two mouse models of Pol zeta

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

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

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

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

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

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

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