ライフサイエンスコーパス: CDR3

1 d (CDR1 and CDR2) or somatically rearranged (CDR3).

2 he third complementarity determining region (CDR3).

3 ssed mutated IgVH with multiple arginines in CDR3.

4 ortest and most conformationally constrained CDR3.

5 h-affinity TCRs engineered by mutagenesis of CDR3.

6 well as on a distinct amino acid in the IGHV-CDR3.

7 peptide representing Herceptin's heavy chain CDR3.

8 study because of the large diversity of the CDR3.

9 d TCR bearing a conserved residue leucine in CDR3.

10 yet results in an altered conformation of a CDR3.

11 ressing a conserved motif within the TCRbeta CDR3.

12 rogen bonds with CDRs of the Ab other than H CDR3.

13 d in a decrease of 2 to 3 amino acids in the CDR3.

14 negatively charged mutations at the edges of CDR3.

15 strategies, and carries four mutations in VL-CDR3.

16 b" architecture in its ultralong heavy chain CDR3, allowing substitutions of the "knob" domain with p

17 function, single amino acid variants of the CDR3 alpha-chain were generated.

18 Binding of the TCR induced CDR3-alpha-dependent structural changes in the F' roof o

19 V3S1/BV8S2 chains, with remarkably conserved CDR3 amino acid motifs and lengths in both chains.

20 rtoire showed that a majority of NDN-encoded CDR3 amino acid motifs start at CDR3 position four, well

21 Jbeta analyses, we demonstrate selection of CDR3 amino acid motifs, which strongly suggests Ag-drive

22 h alpha-chains with highly diverse VJ usage, CDR3 amino acid sequence, and length.

23 CDR3 amino acid sequences associated with response to in

24 nalysis to nonidentical, but highly similar, CDR3 amino acid sequences revealed a number of other TT-

25 Analysis of identical CDR3 amino acid sequences that were shared by individual

26 ut instead had skewed V-J pairing and skewed CDR3 amino acid use.

27 lthy control subjects but relatively similar CDR3 amino acid use.

28 thermore, minimal changes in surface-exposed CDR3 amino acids, even the addition of a single hydroxyl

29 robable formation of disulfide bonds between CDR3 and CDR1, FW2, or CDR2 was also observed, as descri

30 ted in seven amino acid changes (three in VL-CDR3 and four in VH-CDR3) and gave an approximate 30-fol

31 f positively charged amino acids; and longer CDR3 and maintenance of polyreactive specificities.

32 Randomization of the H-CDR3 and site-directed mutagenesis indicated that change

33 raries with antigen-binding sites built from CDR3 and the former light chain interface.

34 o accommodate large structural variations in CDR3 and, consequently, in the TCR-binding site.

35 cid changes (three in VL-CDR3 and four in VH-CDR3) and gave an approximate 30-fold increase in potenc

36 TCR containing the germline WG motif in the CDR3, and a remarkable sharing of one dominant clonotype

37 tructure; additionally, nurse shark TCRdelta CDR3 are more similar to IgH CDR3 in length and heteroge

38 s are further modulated by the hypervariable CDR3 beta loop, thereby defining a functional interplay

39 and TCR that allows eschewing of traditional CDR3 binding with the associated peptide in favor of MHC

40 unusual paratope consisting predominantly of CDR3 but with significant contributions from framework r

41 e computed backbone entropy loss of only the CDR3, but not all CDRs, correlated significantly with th

42 find that single amino acid mutations in the CDR3 can alter TCR fine specificity, affecting recogniti

43 observed that the third position of Vbeta11 CDR3 can encode an Arg or Ser residue as a result of som

44 interactions were influenced most by the VHH CDR3 (CDR, complementarity-determining region) elements,

45 both BCR and TCR rearrangements, visualizes CDR3 characteristics (length and amino acid usage) and j

46 Moreover, TCRB CDR3 clonotypes expressed by autoantigen-specific CD4(+)

47 veils an exception to the dominant role of H CDR3 commonly observed in Ag recognition.

48 beta (variable region beta) gene usage and a CDR3 (complementarity-determining region 3) sequence to

49 ide variant, p5E, shows major changes in the CDR3 contacts compared with wild-type, yet the TCR V-reg

50 stricted TCRbeta usage and nearly monoclonal CDR3 containing novel conserved amino acids.

51 that single amino acid modifications in TCR CDR3 could enhance TCR sensitivity through focal interac

52 ons within ANA V regions, including those in CDR3, could be unequivocally identified.

53 of germ-line-encoded TCR-MHC interactions by CDR3 demonstrates that these interactions possess suffic

54 Y) derivative compound of designation red 3 (CDr3), developed through a high throughput/content scree

55 of libraries of synthetic V(H) domains with CDR3 diversities unconstrained by structural demands.

56 al and computational approach to measure TCR CDR3 diversity based on single-molecule DNA sequencing,

57 on, we determined Treg T-cell receptor (TCR) CDR3 diversity before and after HSCT in patients with ju

58 ct alphabeta pairs, direct assessment of TCR CDR3 diversity has not proved amenable to standard capil

59 ans evolved with greater nontemplate-encoded CDR3 diversity than did mice.

60 islets revealed focused Jbeta usage and less CDR3 diversity than did transcripts from peripheral Vbet

61 aturation of existing hotspot regions (e.g., CDR3) does not majorly influence intrinsic SHM in unmuta

62 ire, which is substantially regulated by the CDR3 domains of individual gamma9delta2TCRs.

63 that the reported molecular requirements of CDR3 domains to interact with target cells shape the phy

64 To understand CDR3 editing at the atomic level, we determined the stru

65 rily selected contacts between TCR and MHC ("CDR3 editing").

66 h CDR1 and CDR2 encoded by the V segment and CDR3 encoded by the V(D)J junction region.

67 HLA-DQ8-glia-alpha1 contacts mediated by the CDR3-encoded arginine were almost identical between TRBV

68 man scFv phage display library that included CDR3 engineered to optimize antibody binding sites.

69 creased frequency of conserved MCC-preferred CDR3 features.

70 ture of these alpha TCRs was the presence of CDR3 fitting to an AGA(G(n))GG-like amino acid motif.

71 rincipal component of a naturally derived VH CDR3 following affinity maturation.

72 rate the complementary determining region 3 (CDR3) for antigen contact.

73 s expected, the third hypervariable segment (CDR3), formed by the rearrangement of the Vgamma and Jga

74 zing the complementary determining region 3 (CDR3) gene sequence, we found no significant differences

75 The resulting CDR3-grafted HC was paired with a CDR-grafted light chai

76 We found that the CDR3(H) from HED-ID B cells were abnormally long, as a r

77 1, 2, 6, 8.1, 8.2, and 8.3, and that the TRB CDR3 had conserved sequence motifs which were shared acr

78 ithin the 258 IgH, we identified heavy chain CDR3 (HCDR3) motifs encoded by certain unmutated IGHD an

79 BV2, and these TRAV12-1/TRBV2 TCRs displayed CDR3 homology.

80 shark TCRdelta CDR3 are more similar to IgH CDR3 in length and heterogeneity than to other TCR chain

81 Packing of the long Valpha CDR3 in the domain-domain interface is found to be influ

82 rticular complementary-determining region 3 (CDR3) in response to encounters with microbes, especiall

83 TCRB complementarity-determining region 3s (CDR3), in all cell subsets, introduced by increased dele

84 -chain complementarity determining region 3 (CDR3) inserts into the receptor binding pocket on HA1, m

85 the interface is dominated by the TCR Vbeta CDR3 interaction with the p7 lysine.

86 These studies indicate that H-CDR3 is critical for pathogenicity of a human autoantibo

87 matic function might be necessary for normal CDR3 junctional diversity.

88 Residues in the light chain CDR3 (LCDR3) were assessed to be important.

89 R(2) = 0.97) was observed between increasing CDR3 length and higher cysteine content.

90 amino acid changes in VH and VL and striking CDR3 length and J segment selection among TG2-specific I

91 on broad differences in TCR family usage and CDR3 length between wild-type and TdT-/- mice.

92 Tetramer-specific B cells exhibited skewed CDR3 length distribution and increased mutation frequenc

93 and SW thymus grafts showed similar, normal CDR3 length distributions.

94 clonotype expressing Vbeta14-Jbeta1.2 with a CDR3 length of 7 aa exists in the naive peripheral reper

95 e subset of the TCR repertoire and, based on CDR3 length polymorphisms, have a limited clonality.

96 Using the CDR3 length spectratyping technique, we characterized th

97 fect, we compared TCR V segment utilization, CDR3 length, and sequence diversity of the response to n

98 es with features, in terms of gene usage and CDR3 length, associated with broadly neutralizing antibo

99 e arthritic joint generally made up a single CDR3 length.

100 The complementarity determining region 3 (CDR3) length adjusted for different inherent V-segment a

101 TCR beta-chain CDR3-length distribution analysis using PCR primers spec

102 t subsets or tissues for VH gene mutation, H-CDR3-length, and VH/JH usage, comparing these different

103 s (six of seven groups of V(H) germlines) or CDR3 lengths (ranging from 7 to 24 residues) and could b

104 s in CD127(+) and CD127(-) cells had smaller CDR3 lengths and fewer N-nucleotide insertions than pedi

105 bed nonpolyclonal distributions of TCR Vbeta CDR3 lengths, indicative of Ag-driven T cell responses.

106 participates in rearrangements of differing CDR3 lengths, restricted to multiples of three.

107 and characterized by skewed distributions of CDR3 lengths.

108 is limited to TCR Vbeta1-J2 with homogenous CDR3 lengths.

109 different Vbeta1 genes and also had diverse CDR3 lengths.

110 Crucially, the CDR3-like loop formed an electrostatically distinct surf

111 s, and depends upon specific residues on the CDR3-like loop within the membrane-distal variable domai

112 ino-acid alpha-helix that sits within the VH CDR3 loop at the center of the antigen binding site.

113 tions located within or directly adjacent to CDR3 loop at the dimer interface, which remarkably inclu

114 monstrate unprecedented autonomy of a single CDR3 loop in antigen recognition.

115 able beta and joining region use and average CDR3 loop length.

116 lected with similar efficiency regardless of CDR3 loop sequence.

117 often characterized by pairing dual-charged CDR3 loop sequences with dual-charged PSA.

118 eference for a zwitterionic motif within the CDR3 loop sequences, aligning well with the known requir

119 ly uses BV19 chains with Arg-Ser (RS) in the CDR3 loop.

120 of the complementarity-determining region 3 (CDR3) loop from top clones indicate a lack of specific v

121 ce the complementarity-determining region 3 (CDR3) loop of an antibody light chain and appear to "pro

122 he TCR complementarity-determining region 3 (CDR3) loop.

123 in reveals that stochastic diversity in both CDR3 loops alone almost exclusively accounts for their d

124 contacts the peptide using the hypervariable CDR3 loops as the transition state decays to the bound s

125 e demonstrate that the somatically generated CDR3 loops can markedly alter evolutionarily selected co

126 Nurse shark TCRdelta have long CDR3 loops compared with the other three chains, creatin

127 of naive antibodies with NNK-randomized V(H) CDR3 loops converges upon mutants containing BF when pla

128 o examine the diversity of Vbeta8.2-Jbeta2.3 CDR3 loops from naive T cell repertoires of multiple mic

129 e responsible for MHC restriction, while the CDR3 loops interact solely with the peptide.

130 he N-terminal domain of TG2 via the CDR2 and CDR3 loops of the heavy chain and the CDR2 loop of the l

131 were grafted into the heavy- and light-chain CDR3 loops, respectively.

132 a result of mutations in either CDR2 and/or CDR3 loops, that bound to the MHC or peptide, respective

133 nteractions with a broad range of permissive CDR3 loops.

134 y is fine-tuned by the somatically generated CDR3 loops.

135 al lead antibody using random mutagenesis of CDR3 loops.

136 as the complementarity determining region-3 (CDR3) loops exclusively mediated contacts with the MHC-I

137 of the complementarity-determining region 3 (CDR3) loops that acted as an 'aromatic-cap' over the com

138 tue of complementarity determining region 3 (CDR3), may also engage with RTB and potentially interfer

139 trates the utility of this novel coiled-coil CDR3 motif as a means for generating stable, potent anti

140 ever, vimentin-reactive FL Igs did not share CDR3 motifs and were not homologous.

141 election induced a limited set of homologous CDR3 motifs at high frequency.

142 Homologous CDR3 motifs have been reported in other autoimmune disea

143 ty from different donors, and that conserved CDR3 motifs help to define the TCR clusters that are oft

144 Our data indicate that a limited set of TCR CDR3 motifs may be important for the pathogenesis of ant

145 Regarding intraindividual variation, the CDR3 motifs of the dominant clones were identical to tho

146 This interchangeability of TCR V regions and CDR3 motifs permits multiple structural solutions to bin

147 ecule, using a restricted number of TRBV and CDR3 motifs that are homologous to T cells isolated from

148 to control subjects, and TRAV12-1 and TRBV2 CDR3 motifs were shared among multiple DR3(+) LS patient

149 e of TRAV24 and TRBV2 variable genes, shared CDR3 motifs, and a high frequency of public clonotypes.

150 nd bound hybridomas expressing the conserved CDR3 motifs.

151 whereas the same VH domains with other polar CDR3 mutations recognize both Abeta conformers.

152 er, Abeta VH domains with negatively charged CDR3 mutations show significant preference for recognizi

153 Mechanistically, CDR3 networks were promoted by MHC-mediated selection, a

154 observed that T cells with identical TCRbeta CDR3 nucleotide sequences were capable of recognizing do

155 al diversity, where poly-Gly/Ala runs in the CDR3 of alpha- and beta-chains might provide high levels

156 lantation and determined the sequence of the CDR3 of immunodominant alloreactive clones; 10 correspon

157 e present a mutational analysis of the Vbeta CDR3 of such a cross-reactive T-cell receptor (TCR), YAe

158 repertoires with an oligoclonal expansion in CDR3 of T cell receptor Vbeta14.

159 ide chimeras of CCR5mim1 and the heavy-chain CDR3 of the antibody PG16.

160 nces between the antibodies, particularly in CDR3 of the heavy chain variable region, are proposed to

161 ibodies with a preponderance of arginines in CDR3 of the Ig variable H chain (IgVH).

162 ted by the non germ line encoded portions of CDR3 of the T cell receptor alpha chain.

163 e at the 101st position (Kabat numbering) in CDR3 of the variable heavy chain (V(H)), having aspartic

164 ve and display very limited diversity in the CDR3 of the Vgamma9 chain gene, where a germline-encoded

165 on the complementarity-determining region 3 (CDR3) of FLCs are critically important determinants of t

166 to the complementarity-determining-region 3 (CDR3) of mature T-cell receptor beta (TCRB) can be used

167 hain complementarity-determining region 3 (H-CDR3) of most pathogenic, but not nonpathogenic, mAbs sh

168 he third complementarity-determining region (CDR3) of the ANA originate from V(D)J recombination or s

169 he third complementarity-determining region (CDR3) of the T-cell receptor (TCR) alpha and beta chains

170 While the hypervariable region CDR3 often mediates much of the specificity of mature an

171 42 peptide segment (Abeta residues 17-42) in CDR3 on the solubility and conformational specificity of

172 a divergent pattern of Jalpha usage, minimal CDR3 overlap (3.4%), and less diversity than did CDR3 se

173 s were identified according to the degree of CDR3 overlap within tumor sample group.

174 rtain V(D)J rearrangements encoding specific CDR3 peptides in all adults and progressive introduction

175 matic mutations in the VH CDR and altered VH CDR3 physicochemical properties.

176 NDN-encoded CDR3 amino acid motifs start at CDR3 position four, well within the V region.

177 ion within the V region reveals selection on CDR3 position four.

178 We propose, for the first time, that CDR3 (position 91) affects the stability and fiber forma

179 f side chains associated with turn motifs at CDR3 positions three and four fits with the structural n

180 ody light chain and appear to "probe" the HC CDR3, potentially influencing the selection of the antib

181 ly, Vkappa4-57-1 polymorphisms that confer a CDR3 Pro-Pro motif enhance self-reactivity in VH125Tg/NO

182 by aromatic residues in the 1G2 heavy chain CDR3 protruding into a hydrophobic cleft in the gB antig

183 coded residue in the hypervariable region of CDR3 provide the basis for the substantial bias in the s

184 pecifically, we propose a method to identify CDR3 reads in a breast tumor exome and validate it using

185 8 TCGA breast cancer exomes, the fraction of CDR3 reads was associated with TILs fraction, tumor puri

186 sequence used during humanization, only the CDR3 region from a murine antibody that recognizes the c

187 by short stretches of amino acids within the CDR3 region may determine TcR specificity and define a n

188 e large sequence repertoires of the variable CDR3 region of human CD4+ T-cell receptor beta chains to

189 ne at position 118 of the alpha-chain in the CDR3 region of the TCR improved its functional avidity i

190 We suggest that the unique CDR3 region of the tg-encoded muH chain is responsible f

191 ls (Teff) displayed sequence profiles in the CDR3 region that were characteristic of biased repertoir

192 ity, HPRT mutation, and T-cell receptor beta CDR3 region unique gene sequence also showed a significa

193 of these mutations appears to stabilize the CDR3 region.

194 , contribute to significant variation in the CDR3 region.

195 memory population have significantly longer CDR3 regions and greater divergence from germline sequen

196 metry is strongly associated with monoclonal CDR3 regions by quantitative sequencing and positive TCR

197 TCRs expressed by RTEs are skewed to longer CDR3 regions compared with those of MN T cells, suggesti

198 presence of a larger cavity between the two CDR3 regions could accommodate iGb3 and, in the other, a

199 nized mechanism by which the highly variable CDR3 regions define ligand specificity.

200 Sequencing of the CDR3 regions demonstrated significant interindividual va

201 The CDR3 regions of both the alpha- and beta-chains are enco

202 es largely from the juxtaposed hypervariable CDR3 regions on the TCRalpha and TCRbeta chains, and obt

203 Finally, we found that the TRBV and CDR3 regions used by both murine and human 70-kDa-specif

204 During the past year, the CDR3 regions were found to determine the antigen specifi

205 lly, the sequences of several TCR beta-chain CDR3 regions were homologous to TCR beta-chains identifi

206 ertoire of older individuals also had longer CDR3 regions with increased usage of G/A runs, whose mol

207 show increased numbers of B cells with long CDR3 regions, a trend toward accumulation of more highly

208 ells were confirmed by analysis of TCR Vbeta CDR3 regions.

209 sis of complementarity-determining region 3 (CDR3) regions containing the beta-chain variable region

210 CRbeta complementarity-determining region 3 (CDR3) regions in subjects with a series of immune dysreg

211 eatured shorter complementarity-determining (CDR3) regions relative to those from circulating B cells

212 Vbeta complementarity-determining region 3 (CDR3) regions, a previously inaccessible level of TCR re

213 patients at 10-day intervals and, sequenced CDR3-regions of the TCRB chain by high-throughput sequen

214 The CDR3 repertoire diversity reflects clonal composition, t

215 comparison with humans and mice, the chicken CDR3 repertoire was skewed toward longer sequences, was

216 inding complementarity determining region 3 (CDR3) repertoire of different mice.

217 Importantly, a single, germline-encoded VL-CDR3 residue mediated the key difference between the sta

218 c versus aliphatic variation at a single TCR CDR3 residue.

219 HC contact residues contributed by CDR3, the CDR3 residues buried deep within the V alpha/V beta inte

220 ent cooperative interaction between CDR1 and CDR3 residues that are separated by more than 9 A in the

221 Vbeta expression and deep sequencing of CDR3 revealed that in untreated HIV-1 infection, cycling

222 ic immunogenomic differences concentrated in CDR3's N1-D-N2 region, which allowed the prediction of p

223 rized by more somatic hypermutation, shorter CDR3 segments, and less negative charges.

224 ivation also induced long positively charged CDR3 segments, suggestive of autoreactive Abs.

225 H) domains is essentially independent of the CDR3 sequence and instead derives from mutations that in

226 s the generation probability of any specific CDR3 sequence by the primitive recombination process, al

227 Because any given CDR3 sequence can be produced in multiple ways, the prob

228 ing, and used this approach to determine the CDR3 sequence in millions of rearranged TCRbeta genes fr

229 CDR3 sequence length distribution and amino acid conserv

230 ross-reactivity are controlled by particular CDR3 sequence motifs, which would allow thymic selection

231 By tracking their unique CDR3 sequence, we found that one such polyreactive clone

232 oglobinuria (PNH) patients, in whom specific CDR3 sequences and clonal sizes were determined.

233 Public CDR3 sequences are shared between mice of different MHC

234 ng revealed a significant fraction of shared CDR3 sequences between ALPS DNT and both CD4(+) and CD8(

235 ollected millions of rearranged germline IgH CDR3 sequences by deep sequencing of DNA from mature hum

236 overlap (3.4%), and less diversity than did CDR3 sequences derived from Tconv.

237 CDR3 sequences from nTregs displayed a divergent pattern

238 hat these IgMs have different but related VH/CDR3 sequences from those seen in the class-switched res

239 y-determining region 3 (CDR3), with specific CDR3 sequences highly enriched in acute samples compared

240 ects of selection, we focus on nonproductive CDR3 sequences in T-cell DNA.

241 A significant frequency of TCR CDR3 sequences in the D(b)M(187-195) response have a dis

242 nalloreactive TCR differ specifically in the CDR3 sequences responsible primarily for the peptide spe

243 ublic sequences are enriched for MHC-diverse CDR3 sequences that were previously associated with auto

244 ) beta-chain (Trb, also known as Tcrb) using CDR3 sequences to simultaneously track thousands of uniq

245 In normal T cells, the CDR3 sequences were extremely diverse, without any clono

246 and IgL V(D)J exons, including their unique CDR3 sequences, from progenitor and mature mouse B linea

247 We identified over 600,000 CDR3 sequences, including 15% that were full length.

248 Public CDR3 sequences, relative to private sequences, are two o

249 rent criteria for stereotyped heavy chain VH CDR3 sequences, two of them belonging to subsets previou

250 nd Vbeta gene segments with randomly created CDR3 sequences.

251 gamma1.1(+)Vdelta6.3(+) T cells with diverse CDR3 sequences.

252 immunity when combined with different murine CDR3 sequences.

253 lonal dominance, and selection of particular CDR3 sequences.

254 cross-reactive CD8 T cells use distinct TCRB CDR3 sequences.

255 ons on the basis of their co-occurrence with CDR3 sequences.

256 -21, similarly promoted increased sharing of CDR3 sequences.

257 r, had divergent light-chain and heavy-chain CDR3 sequences.

258 er the complementarity-determining region 3 (CDR3) sequences of tumor-infiltrating T cells in 9,142 R

259 J, and complementarity determining region 3 (CDR3) sequences on the alpha-chain, and displayed restri

260 luding complementarity-determining region 3 (CDR3) sequences, were assessed.

261 ity of complementarity-determining region 3 (CDR3) sequences.

262 ealed a repertoire-encoded VRC01 light-chain CDR3 signature and VRC01-like neutralizing heavy-chain p

263 ic hypermutation of Ig genes and heavy-chain CDR3 size distribution of IgM(+)IgD(+)CD27(+) B cells we

264 showed preferential usage of tumor-reactive CDR3-size lengths, and these cells expressed increased e

265 t Vbeta families that exhibited alloreactive CDR3-size skewing, there was a robust overlap between th

266 eloid leukemia line, MMC6, we used TCR Vbeta CDR3-size spectratype analysis to first show that the Vb

267 his regard, TCR Vbeta repertoire analysis by CDR3-size spectratyping can be a powerful tool for the c

268 TCR Vbeta CDR3-size spectratyping was previously used to analyze C

269 encoded by multiple AV genes with different CDR3 sizes.

270 antigen-specific Vbeta6(+) CD8(+) T cells by CDR3 spectratyping and sequencing indicated that distinc

271 H chain V region genes (V(H)), we performed CDR3 spectratyping of approximately 75-300 rearrangement

272 y of TCRs to accommodate large variations in CDR3 structure and peptide contacts within the constrain

273 but demonstrate that minimal changes in TCR CDR3 structure can promote self reactivity and thereby e

274 e of participation of peptide and associated CDR3 surface.

275 restricted subset of self-associated, public CDR3 TCR sequences, and invite reexamination of the basi

276 We discovered a substantial number of public CDR3-TCRbeta segments that were identical in mice and hu

277 TCR sequencing data, we found that abundant CDR3-TCRbeta sequences were clustered within networks ge

278 s of the complementary determining region 3 (CDR3) (TdT(-/-)) and mice with altered Ab repertoires du

279 to the pMHC contact residues contributed by CDR3, the CDR3 residues buried deep within the V alpha/V

280 bend that positions the remaining portion of CDR3 to interact with the peptide and MHC.

281 CDR3 usage was not skewed in control Vbeta16 CDR3 transcripts.

282 CDR3 usage was not skewed in control Vbeta16 CDR3 transc

283 study, we investigated TCR Vbeta repertoires/CDR3 usage, clonal expansion or dominance, and pulmonary

284 Thus, changing Asn(101) to Asp(101) in CDR3-V(H) of rituximab is responsible for veltuzumab's l

285 s related to the single amino acid change in CDR3-V(H).

286 t included high-throughput sequencing of the CDR3 variable region of the T cell receptor beta-chain a

287 -specific Treg clonotypes share a common TCR CDR3 Vbeta usage with Foxp3+CD4+CD25high and CD4+CD25- T

288 ibrillogenic, the second mutation located at CDR3 (W91A) induced fibrillogenesis.

289 h factor (VEGF) from a library in which only CDR3 was randomized.

290 ormation of each clonal sequence (defined by CDR3), we detected predictive public clone and private c

291 hydrophobic former light chain interface and CDR3, we find that the stability of many in vitro evolve

292 al Valpha and Vbeta genes, differing only in CDR3, we found stark differences in the mechanisms utili

293 tments are both the most enriched for N(-) H-CDR3, we propose a novel direct T1-->MZ pathway and iden

294 Increased somatic mutation and extended CDR3 were observed with Ig genes of several molecularly

295 tibody library in which six residues in V(H) CDR3 were randomized, contains sulfotyrosine and binds g

296 Types and length of CDR3 were similar among groups.

297 arged or asparagine residues at the edges of CDR3, whereas other polar mutations are less effective (

298 CDr3 will be a valuable chemical tool in the study and a

299 ll precursors and found only two examples of CDR3 with D-D rearrangements and one example of a potent

300 inant, complementarity-determining region 3 (CDR3), with specific CDR3 sequences highly enriched in a