ライフサイエンスコーパス: Ig gene

1 eir frequency, type, and location within the Ig gene.

2 any other known somatically hypermutated non-Ig gene.

3 cial insert are all seen in the unselectable Ig gene.

4 +)IgD(+)CD27(+) B cells that express mutated Ig genes.

5 point mutations into variable regions of the Ig genes.

6 ely, yet inefficient, mechanism for mutating Ig genes.

7 -coupled deamination of cytosine residues in Ig genes.

8 SHM) and class switch recombination (CSR) of Ig genes.

9 unique Abs from a limited number of germline Ig genes.

10 ugh next-generation sequencing of rearranged Ig genes.

11 peripheral blood and examine their expressed Ig genes.

12 responsible for triggering hypermutation of Ig genes.

13 ain access to the 5' and constant regions of Ig genes.

14 uses gene conversion to diversify rearranged Ig genes.

15 cers, are also required for transcription of Ig genes.

16 to ineffective Ab production from expressed Ig genes.

17 tion (SHM) and class-switch recombination of Ig genes.

18 an evolutionary precursor of modern TCR and Ig genes.

19 s also required for somatic hypermutation of Ig genes.

20 are preferentially found in the V regions of Ig genes.

21 o those of other non-Ig genes but lower than Ig genes.

22 tion and class switch recombination (CSR) of Ig genes.

23 TLA-4 using transgenic mice expressing human Ig genes.

24 racteristic pattern found in Ig and most non-Ig genes.

25 of cytidines in the V and switch regions of Ig genes.

26 ant for somatic mutation of endogenous mouse Ig genes.

27 ion (CSR) and somatic hypermutation (SHM) of Ig genes.

28 permutation (SHM) of variable (V) regions of Ig genes.

29 wed the presence of ongoing mutations in the Ig genes.

30 ther the mutation machinery also targets non-Ig genes.

31 ion of surface Ig, CD5, B220, and rearranged Ig genes.

32 nvolved in somatic gene conversion of rabbit Ig genes.

33 tated Abs toward PC using a broad variety of Ig genes.

34 mechanism underlying the diversification of Ig genes.

35 The mutation pattern was similar to that of Ig genes.

36 ess that targets mutations to the rearranged Ig genes.

37 ortions of AID hot spots similar to those in Ig genes.

38 sis observed during somatic hypermutation of Ig genes.

39 pertoire and heterochromatin localization to Ig genes.

40 ing V-segments of rearranged immunoglobulin (Ig) genes.

41 t molecular modifications of immunoglobulin (Ig) genes.

42 ithin the variable region of immunoglobulin (Ig) genes.

43 in somatic hypermutation of immunoglobulin (Ig) genes.

44 vectors exhibit deletion of immunoglobulin (Ig) genes.

45 to edit the mouse and human immunoglobulin (Ig) genes.

46 acquired rearranged and somatically mutated Ig genes.1,2 Despite their B-cell origin, the malignant

47 for somatic hypermutation of immunoglobulin (Ig) genes, a key process in the development of adaptive

48 nversion appears to be rare among endogenous Ig genes, Ab H chain transgenes undergo isotype switchin

49 While our analyses of nonfunctional Ig genes accurately predicts regional mutation preferenc

50 Upon recruitment to Ig genes, AID deaminates cytidines at switch (S) recombi

51 tically engineered to be humanized for their Ig genes allow for human antibody responses within a mou

52 manization involves mice humanized for their Ig genes, allowing for human antibody responses within a

53 e an opportunity to infer the association of Ig genes along the chromosomes.

54 to activate transcription of immunoglobulin (Ig) genes, although the mechanisms underlying their role

55 Ig gene analysis showed that 7 of 13 HmAbs used the V(H)

56 gulated, yet when unregulated can access non-Ig genes and cause cancer.

57 However, somatic hypermutation of Ig genes and heavy-chain CDR3 size distribution of IgM(+

58 )-deficient and wild-type mice in endogenous Ig genes and in an Ig transgene.

59 f nucleic acids underlies diversification of Ig genes and inhibition of retroviral infection, and thu

60 generated by disrupting the endogenous mouse Ig genes and simultaneously introducing human Ig transge

61 limits of nucleosome positioning for SHM of Ig genes and suggests that stable nucleosomes may need t

62 gements, the unique cluster organization for Ig genes and the "conventional" translocon organization

63 Because of the cluster organization of shark Ig genes and the paucicopy nature of IgNAR, we were able

64 Occasionally, AID can target non-Ig genes and thereby promote GC B-cell lymphomagenesis.

65 ermutation (SHM) diversifies the V region of Ig genes and underlies the process of affinity maturatio

66 somatic hypermutation of the immunoglobulin (Ig) genes and selection of higher-affinity B cell clones

67 translocations (CTs) between immunoglobulin (Ig) genes and the BCL6 proto-oncogene are frequently ass

68 gate the topographies of the immunoglobulin (Ig) genes and transcripts during B-cell development.

69 ere obtained from endogenous immunoglobulin (Ig) genes and were presumably influenced by selection of

70 teracting proteins that might recruit AID to Ig genes, and allow it to target both DNA strands.

71 and intraclonal variation in the rearranged Ig genes, and one case expressed switched Ig heavy chain

72 umulation of more highly mutated IgM and IgG Ig genes, and persistent clonal B cell populations in th

73 mized for generating mutational diversity in Ig genes, and we discuss how the properties of AID actin

74 matic hypermutation (SHM) of immunoglobulin (Ig) genes appears to involve the generation of double-st

75 SHM) and class-switch recombination (CSR) of Ig genes are dependent upon activation-induced cytidine

76 osome translocations between Ig (Ig) and non-Ig genes are frequently associated with B-cell lymphomas

77 endogenous micro heavy and kappa light chain Ig genes are inactivated and which carry human Ig gene s

78 the mechanism(s) of somatic hypermutation in Ig genes are largely unknown.

79 deaminase (AID) to target Ig and certain non-Ig genes are not understood, although transcription has

80 Cs) through well-defined stages during which Ig genes are rearranged to generate a clonal BCR.

81 on, selection and somatic diversification of Ig genes are regulated in these species, in part, by the

82 nt study attempts to understand how multiple Ig genes are regulated with respect to rearrangement ini

83 ecies because they are proliferating and the Ig genes are somatically diversified.

84 Ig genes are the most highly mutated genes, presumably b

85 g AID activity to the variable (V) region of Ig genes are unknown.

86 why the very 5' and most of the 3' region of Ig genes are unmutated.

87 matic hypermutation (SHM) of immunoglobulin (Ig) genes are initiated by the activation-induced cytosi

88 ARL-derived immunoglobulin (Ig) genes are significantly diversified from germline, s

89 Antibodies (Abs) produced by immunoglobulin (IG) genes are the most diverse proteins expressed in hum

90 he T-cell receptor (TCR) and immunoglobulin (Ig) genes are unique among vertebrate genes in that they

91 s were detected in 55% of the cases, with an IG gene as partner in 18 of 22, in particular with light

92 l features considered essential in mammalian Ig gene assembly and expression.

93 ypothesis that pol eta contributes to SHM of Ig genes at A-T pairs via short patches of low fidelity

94 articipates in hypermutation of A:T bases in Ig genes because humans deficient for the polymerase hav

95 n must have already existed in the ancestral Ig gene, before H and L chain divergence.

96 rmed a comparative analysis of the expressed Ig genes between large sets of EBV-infected and uninfect

97 dividual segmental elements than is found in Ig genes but have undergone fewer changes in gene organi

98 at frequencies similar to those of other non-Ig genes but lower than Ig genes.

99 nearly equivalent as candidates for a given Ig gene, but have different consequences in an analysis.

100 strate that MYC rearrangements (MYC-Rs) with IG genes, but not with other partner genes, have a negat

101 It is customary to estimate Ag selection on Ig genes by assessment of replacement (R) as opposed to

102 exclusion ensures monoallelic expression of Ig genes by each B cell to maintain single receptor spec

103 switch recombination, and gene conversion of Ig genes by the deamination of deoxycytidine, followed b

104 e for the diversification of immunoglobulin (Ig) genes by somatic hypermutation (SHM), class switch r

105 mble a diverse repertoire of immunoglobulin (Ig) genes by the process of V(D)J recombination.

106 minase (AID) is required for immunoglobulin (Ig) gene class switch recombination (CSR), somatic hyper

107 epair, telomere maintenance, immunoglobulin (Ig) gene class switch recombination, and somatic hypermu

108 gions of DNA, suggesting that at transcribed Ig genes, cleavage may be coordinated with deamination b

109 examine junctional diversity in defined fish Ig genes, comparing productive vs nonproductive rearrang

110 To investigate whether the Ig gene configuration could be characterized using Igkap

111 S gene that is expressed in flowers, but its IGS gene contains a frame-shift mutation that renders it

112 pletes the characterization of its classical Ig gene content (two H chain isotypes, mu and omega, and

113 transcription of the endogenous heavy-chain Ig gene continues in the absence of the core intronic en

114 These results lead to a model in which Ig gene conversion initiates and is completed or nearly

115 Homology-based Ig gene conversion is a major mechanism for Ab diversifi

116 hat is a marker of double-strand breaks, and Ig gene conversion may therefore proceed by a pathway in

117 mutations that render the rearranged TCR and Ig genes defective.

118 Somatic hypermutation (SHM) of Ig genes depends upon the deamination of C nucleotides i

119 Ig genes derived from the IGHV3-11 and IGHV3-74 germline

120 Ig gene diversification is initiated by deamination of c

121 Secondary Ig gene diversification relies on activation-induced cyt

122 r some circumstances, AID mediates efficient Ig gene diversification without the assistance of RPA.

123 Thus, E2A acts in cis to promote Ig gene diversification, and G(1) phase is the critical

124 e that cis-acting elements are important for Ig gene diversification, and we propose that targeting s

125 T40 B cell line, which performs constitutive Ig gene diversification.

126 DNA cleavage in the AID-initiated pathway of Ig gene diversification.

127 esponse to DNA damage and in immunoglobulin (Ig) gene diversification.

128 pendent immune responses in mouse and human, Ig genes diversify by somatic hypermutation within germi

129 matic gene conversion is rarely found within Ig genes during immune responses in mouse and human, we

130 riable segment of rearranged immunoglobulin (Ig) genes during a germinal center reaction.

131 We found that a diverse population of Ig genes encodes for auto-Abs that exclusively recognize

132 ated SMI, expressing unmutated H and L chain Ig genes encoding a low-affinity, polyreactive human (h)

133 Immunoglobulin (Ig) genes expressed in mature B lymphocytes can undergo

134 tion by RA of B cell population dynamics and Ig gene expression in purified splenic mouse B cells sti

135 Allelic exclusion of Ig gene expression is necessary to limit the number of f

136 tical role for Oct-2 not only in maintaining Ig gene expression, but in maintaining the overall genet

137 ing, and, as segregation to B-1 occurs after Ig gene expression, it precedes segregation to the B-1 s

138 3 (V(H)3) is the predominant immunoglobulin (Ig) gene family used in human antibodies to pneumococcal

139 s this question, we cloned and expressed the Ig genes from 177 IgG-producing bone marrow plasma cells

140 roduce a vaccine within hours of cloning the Ig genes from a B-cell tumor.

141 nd somatic hypermutation (SHM) of functional Ig genes from antigen-activated B cells within secondary

142 uman mAbs generated by expression cloning of Ig genes from single plasma cells of the celiac disease

143 ithin hours of amplification of the specific Ig genes from the B-cell tumor.

144 ology to isolate and express immunoglobulin (Ig) genes from joint-derived B cells of active RA patien

145 Unlike AID-induced DSBs in Ig genes, genome-wide AID-dependent DSBs are not restric

146 bly influenced by selection of B cells whose Ig genes had undergone certain mutations.

147 equency of CD27(+) memory B cells, and their Ig genes have a low level of somatic hypermutation (SHM)

148 n mapped to a chromosomal region in which no Ig genes have been identified, with somatic IgH sequence

149 Possibly the variable regions of Ig genes have evolved for low nucleosome stability to en

150 The immunoglobulin (Ig) genes have been extensively studied as model systems

151 because of multiple CAGGTG motifs within the Ig genes, high transcription activity, and the presence

152 The results show unequivocal evidence of non-Ig gene hypermutation in germinal center B cells and pro

153 fication, "gene gating" at the nuclear pore, Ig gene hypermutation, and sister chromosome cohesion ha

154 based on the presence or absence of ongoing Ig gene hypermutation.

155 MYC translocation partner was an IG gene in 24 cases (MYC-IG) and a non-IG gene (MYC-non-

156 f the monotypic plasmablasts, the rearranged Ig genes in 13 patients with KSHV-related MCD, including

157 ) and mb1 (Igalpha, CD79a) occur as often as Ig genes in a broad spectrum of GC- and post-GC-derived

158 Somatic hypermutation (SHM) of Ig genes in B cells is crucial for antibody affinity mat

159 oire by promoting somatic diversification of Ig genes in B cells that have migrated to GALT.

160 ermutation and class switch recombination of Ig genes in B cells.

161 Assembly of Ig genes in B lineage cells involves two distinct DNA re

162 Ig genes in cartilaginous fish are encoded by multiple i

163 ct genetic modification events diversify the Ig genes in germinal center (GC) B cells: somatic hyperm

164 RE11 associates specifically with rearranged Ig genes in hypermutating B cells, whereas APE1, the maj

165 lso contribute to effective transcription of Ig genes in mature and/or activated B cells, bringing bo

166 Our results indicate that Ig genes in mouse and human cells can be edited to obtai

167 s) and concurrent secondary rearrangement of Ig genes in normal peripheral lymphoid organs (receptor

168 ibody production by somatic hypermutation of Ig genes in response to T-independent Ags.

169 atures of the initiation of hypermutation of Ig genes in vivo.

170 n model equation, which is inappropriate for Ig genes in which mutations have four different distribu

171 initiates diversification of immunoglobulin (Ig) genes in B cells, introducing mutations within the a

172 e secondary rearrangement of immunoglobulin (Ig) genes in peripheral lymphoid tissues.

173 to enhance transcription of immunoglobulin (Ig) genes in vitro.

174 ns and a lower frequency of mutations in non-Ig genes, including Pax5 and Rhoh compared with AID(+/+)

175 t harbor somatic mutations in the rearranged Ig genes, indicating origination from naive B cells.

176 Rearrangement of Ig genes initiates before typical lymphoid lineage patte

177 enzyme AID, which converts cytosines (C) in Ig genes into uracils (U).

178 The V kappa10 family of murine light chain Ig genes is composed of three members, two of which (V k

179 nalysis of somatic mutations in V regions of Ig genes is important for understanding various biologic

180 Somatic hypermutation (SHM) of Ig genes is initiated by the activation-induced cytidine

181 Somatic hypermutation of Ig genes is probably dependent on transcription of the t

182 Somatic hypermutation (SHM) of the Ig genes is required for affinity maturation of the humo

183 omatic hypermutation (SHM) of the rearranged Ig genes is required for the affinity maturation of Abs.

184 Mistargeting of AID to non-Ig genes is thought to result in the malignant transform

185 Somatic rearrangement of immunoglobulin (Ig) genes is a key step during B cell development.

186 matic hypermutation (SHM) of immunoglobulin (Ig) genes is initiated by the activation-induced cytidin

187 ase (GPI) were examined in the corresponding Ig gene knock-in mice.

188 monoclonal autoantibodies from combinatorial Ig-gene libraries derived from autoimmune thyroiditis pa

189 the configuration and rearrangements of the Ig gene loci has contributed extensively to our understa

190 f the unrearranged human H chain and L chain Ig gene loci.

191 The processes of Ig gene locus contraction and looping during V(D)J-recom

192 We suggest that a rejoined Ig gene may not merely be a sequence restricting antibod

193 th light chains encoded by several different Ig genes, molecular repairing experiments showed exquisi

194 Ig genes must be transcribed for diversification to occu

195 as an IG gene in 24 cases (MYC-IG) and a non-IG gene (MYC-non-IG) in 26 of 50 evaluable cases.

196 ut DNA sequencing to the study of rearranged Ig genes now makes this possible.

197 -switch recombination of the immunoglobulin (Ig) genes occur in germinal center (GC) B cells and are

198 matic hypermutation (SHM) of immunoglobulin (Ig) genes occur in two steps: the generation of uracils

199 utation and extended CDR3 were observed with Ig genes of several molecularly cloned rabbit MAbs.

200 mutations within rearranged immunoglobulin (Ig) genes of activated B cells, providing genetic divers

201 The rearranged immunoglobulin (Ig) genes of CLL cells may be either germ-line in sequen

202 n can occur at noncanonical RSS sites within Ig genes or at other loci, outside the context of normal

203 Like Ig genes, ORF50, the key regulator of the switch from la

204 Other major differences in Ig gene organization and the mechanisms of somatic diver

205 They possess a unique Ig gene organization consisting of 15 to >50 individual

206 that AID-induced double-strand breaks in non-Ig genes other than c-myc lead to their translocation, a

207 t appear to process U:G base pairs at all in Ig genes outside G1 phase.

208 The activity of Ig gene promoters and enhancers is regulated by two rela

209 as determined by 1) the restoration of V(H) Ig gene rearrangement and 2) the appearance of immature

210 Given that abnormalities in Ig gene rearrangement and DNA damage repair are hallmark

211 ot its catalytic activities, is required for Ig gene rearrangement and production of B cell receptors

212 that E-protein activity regulates secondary Ig gene rearrangement at the immature B cell stage and c

213 naling, we show that PI3K signaling inhibits Ig gene rearrangement by suppressing the expression of t

214 V(H) genes; however, Pax5 did not induce any Ig gene rearrangement in the absence of Ikaros.

215 Together, our results suggest that ordered Ig gene rearrangement is regulated by distinct activitie

216 Receptor editing or secondary Ig gene rearrangement occurs in immature, autoreactive B

217 exhibit the skewed Ig V gene repertoire and Ig gene rearrangement patterns associated with these spe

218 Moreover, sequencing of Ig gene rearrangement products showed that a diverse rep

219 tumors arose at high incidence and displayed Ig gene rearrangement with downregulated expression of B

220 the induction of the machinery that mediates Ig gene rearrangement.

221 nship between CD127 expression/signaling and Ig gene rearrangement.

222 phocyte-associated genes and immunoglobulin (Ig) gene rearrangement occurred before CD45R acquisition

223 al or oligoclonal pattern of immunoglobulin (Ig) gene rearrangement.

224 e (MRD) by real-time PCR directed to TCR and Ig gene rearrangements allows a refined evaluation of re

225 mice succumbed to lymphoid tumors containing Ig gene rearrangements and immunophenotypes characterist

226 review the data currently available on both Ig gene rearrangements and protein patterns seen in myel

227 e that occurred concomitantly with decreased Ig gene rearrangements and rag-1 transcripts.

228 o programmed cell death due to nonproductive Ig gene rearrangements are cleared from the bone marrow

229 omparative analysis of platelet-reactive Fab Ig gene rearrangements from each patient suggested that

230 The amplification of nonproductive Ig gene rearrangements from HED-ID B cells reflects the

231 B in human V(D)J recombination, we amplified Ig gene rearrangements from individual peripheral B cell

232 ive analysis of productive and nonproductive Ig gene rearrangements from transgenic mice engineered t

233 In addition to this, the analysis of Ig gene rearrangements in B-cell neoplasms provides info

234 We found intact Ig gene rearrangements in immunoglobulin heavy (IgH) and

235 pment and Ab selection in humans we analyzed Ig gene rearrangements in pro-B cells from two patients

236 Analysis of Ig gene rearrangements indicates monoclonality or oligoc

237 tance of EBF1 in regulating target genes and Ig gene rearrangements necessary for B cell lineage spec

238 lerance mechanism that operates by secondary Ig gene rearrangements to change the specificity of auto

239 Interestingly, they possess Ig gene rearrangements, but lack Ig molecule expression

240 the confines of the bone marrow by secondary Ig gene rearrangements.

241 breaks (DSBs) are essential intermediates in Ig gene rearrangements: V(D)J and class switch recombina

242 Immunoglobulin (Ig) gene rearrangements are used to define clonality of

243 DCs with a lymphoid past were identified in Ig gene recombination substrate reporter mice treated wi

244 ion patterns shows that DNA lesions at shark Ig genes recruit DNA repair factors with a species-speci

245 e positioning sequence (MP2) into a variable Ig gene region to assess its impact on SHM in vivo.

246 r interactions that are likely important for Ig gene regulation in B cells.

247 RIL proteins delivered survival, activation, Ig gene remodeling, and differentiation signals by stimu

248 established with the mechanisms that lead to Ig gene remodeling, including V(D)J recombination, isoty

249 cells in thymus were mature and displayed an Ig gene repertoire that was similar to pediatric bone ma

250 We therefore studied the Ig gene repertoires and reactivity to autoantigens of si

251 up through their surface Igs, data on thymic Ig gene repertoires are limited and reactivity to autoan

252 matic hypermutation (SHM) of immunoglobulin (Ig) genes requires activation-induced cytidine deaminase

253 in DNA repair and programmed mutagenesis of Ig genes, requiring it to act on sparsely or densely spa

254 cells, when antibody synthesis peaks, active Ig genes residing on three different chromosomes exhibit

255 e effect of treatment on somatic mutation of Ig genes, reverse transcriptase-polymerase chain reactio

256 greatly impaired endogenous recombination of Ig gene segments in a Rag2-deficient pro-B cell line and

257 ein complex introduces DNA breaks at Tcr and Ig gene segments that are required for V(D)J recombinati

258 genes are inactivated and which carry human Ig gene segments, with a digoxin-protein conjugate has e

259 Accessibility of immunoglobulin (Ig) gene segments to V(D)J recombination is highly regul

260 e demonstrate that hypermutation requires no Ig gene sequences.

261 Given that isotype class switching and Ig gene somatic hypermutation share molecular mechanisms

262 Unlike Ig genes, somatic hypermutation of TCR V regions is an i

263 of the mutation target sequence, but how the Ig gene specificity of mutations is achieved has remaine

264 In silico analysis of several published IgD genes suggested that this unique splicing mechanism

265 CD83 is a member of the Ig gene superfamily, first identified in activated lymph

266 and find that CD96, which is a member of the Ig gene superfamily, is a promising candidate as an LSC-

267 Like Ig genes, TCR genes are formed by somatic rearrangements

268 lving a group of Immunoglobulin (Ig) and non-Ig genes that are direct targets of AID.

269 (AID) instigates mutations and DNA breaks in Ig genes that undergo somatic hypermutation and class sw

270 at introduces novel point mutations into the Ig gene, the mismatches generated during CSR are process

271 Upon successful assembly of Ig genes, the antigen receptor is expressed on the immat

272 argets double-stranded DNA in sub-regions of Ig genes, the involvement of co-factors and posttranslat

273 point mutations into the variable regions of Ig genes, thereby changing the affinity of antibody for

274 ults in mutations and DNA damage in many non-Ig genes, they act preferentially at Ig loci.

275 nt mutations into the variable region of the Ig gene to generate higher-affinity variants.

276 tidine deaminase mutates the V region of the Ig genes to increase the affinity of Abs.

277 atic hypermutation that diversify rearranged Ig genes to produce various classes of high affinity Abs

278 of T-cell receptor (TCR) and immunoglobulin (Ig) genes to generate a diverse repertoire of antigen re

279 mutator enzyme that targets immunoglobulin (Ig) genes to initiate antibody somatic hypermutation (SH

280 B(-/-) mice showed no apparent deficiency in Ig gene transcription, only cellular immune defects incl

281 ing DNA sequences; or 2) very high levels of Ig gene transcription.

282 Studies showed that Ig gene-transcription levels are positively correlated w

283 Rearranged Ig genes undergo diversification in sequence and structu

284 Here, we evaluated Ig gene usage in patients with anti-myelin-associated gl

285 ts offer improved opportunities to delineate Ig gene usage in the overall B cell repertoire as well a

286 examine the relation between immunoglobulin (Ig) gene usage, clonality, and antigen specificity.

287 arity-determining region than the rearranged Ig genes used by CLL B cells that express V(H)1 genes ot

288 nocked-in a transcription terminator into an Ig gene variable region in DT40 chicken B cell line.

289 uit and activate the mutational machinery at Ig gene variable regions during SHM.

290 mechanisms: recombination of immunoglobulin (Ig) gene variable (V), diversity (D), and joining (J) ge

291 iments, naked DNA containing tsCR1 and tsCR1-Ig genes was injected intramuscularly into the immunized

292 ng(-/-) mice the 5' end and the 3' region of Ig genes was spared from mutations as in wild-type mice,

293 tic gene alterations found in the IG and non-IG genes, we conclude that the FLs and B-LBLs did not de

294 be memory cells based on somatically mutated Ig genes, we found that the reduction was not caused by

295 ontributes to somatic hypermutation (SHM) of Ig genes, we measured the error specificity of mouse pol

296 The resulting uracils in Ig genes were believed to be removed by the uracil glyco

297 and their adjacent flanks in immunoglobulin (Ig) genes, whereas constant regions are spared.

298 cause genetic alterations in immunoglobulin (Ig) genes, which underlie the generation of the secondar

299 eptides, that heteroclitic peptides from the Ig gene with improved binding to human leukocyte antigen

300 AID)-dependent remodeling of immunoglobulin (IG) genes within germinal centers (GCs) to generate memo