ライフサイエンスコーパス: Ig gene

1 C partner gene (immunoglobulin [IG] or a non-IG gene).

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

3 any other known somatically hypermutated non-Ig gene.

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

5 roduced by copying short segments from other Ig genes.

6 pertoire and heterochromatin localization to Ig genes.

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

8 point mutations into variable regions of the Ig genes.

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

10 -coupled deamination of cytosine residues in Ig genes.

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

12 peripheral blood and examine their expressed Ig genes.

13 responsible for triggering hypermutation of Ig genes.

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

15 uses gene conversion to diversify rearranged Ig genes.

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

17 to ineffective Ab production from expressed Ig genes.

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

19 an evolutionary precursor of modern TCR and Ig genes.

20 s also required for somatic hypermutation of Ig genes.

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

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

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

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

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

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

27 ant for somatic mutation of endogenous mouse Ig genes.

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

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

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

31 ugh next-generation sequencing of rearranged Ig genes.

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

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

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

35 sis observed during somatic hypermutation of Ig genes.

36 t molecular modifications of immunoglobulin (Ig) genes.

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

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

39 in somatic hypermutation of immunoglobulin (Ig) genes.

40 vectors exhibit deletion of immunoglobulin (Ig) genes.

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

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

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

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

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

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

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

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

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

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

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

52 onstrated the successful expression of human Ig genes and antibodies.

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

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

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

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

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

58 To characterize Ig genes and specificities of antral mucosal iNOS(+) and

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

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

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

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

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

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

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

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

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

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

69 asma cell subsets, somatic hypermutations in Ig genes, and in vitro proliferation and antibody produc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 of T cell receptor (TCR) and immunoglobulin (Ig) genes by V(D)J recombination generates the antigen r

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

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

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

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

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

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

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

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

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

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

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

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

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

118 Ig gene diversification is initiated by deamination of c

119 Secondary Ig gene diversification relies on activation-induced cyt

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

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

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

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

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

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

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

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

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

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

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

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

132 3 (V(H)3) is the predominant immunoglobulin (Ig) gene family used in human antibodies to pneumococcal

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

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

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

136 avy- and light-chain sequences of rearranged Ig genes from multiple descendants of the same naive B c

137 H. pylori infection, we sequenced rearranged Ig genes from single cell-sorted PC from biopsy specimen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

153 , as shown by somatic hypermutation of their Ig genes in adaptive immune receptor repertoire sequenci

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

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

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

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

158 Ig genes in cartilaginous fish are encoded by multiple i

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

160 During somatic hypermutation (SHM) of Ig genes in germinal center B cells, lesions introduced

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

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

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

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

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

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

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

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

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

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

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

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

173 g RGYW/WRCY hotspot motifs in the individual Ig genes, indicating T cell-dependent maturation.

174 Rearrangement of Ig genes initiates before typical lymphoid lineage patte

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

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

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

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

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

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

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

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

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

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

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

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

187 Uracils in the Ig gene loci can be recognized by uracil DNA glycosylase

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

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

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

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

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

193 Ig genes must be transcribed for diversification to occu

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

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

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

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

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

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

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

201 repertoire by modifying the immunoglobulin (Ig) genes of mature B cells directly using genome editin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 an algorithm designed to fully characterize Ig gene rearrangements and oncogenic translocations from

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 and oncogenic translocations are

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

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

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

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

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

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

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

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

251 comprising the entire human immunoglobulin (Ig) gene repertoire in the germline configuration was in

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

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

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

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

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

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

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

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

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

261 e demonstrate that hypermutation requires no Ig gene sequences.

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

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

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

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

266 artly resembled that of MALT B cell lymphoma Ig genes, suggestive of a mechanism in which a progressi

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

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

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

270 deaminase (AID) generates U:G mismatches in Ig genes that can be converted into untemplated mutation

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

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

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

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

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

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

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

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

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

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

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

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

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

284 Rearranged Ig genes undergo diversification in sequence and structu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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