ライフサイエンスコーパス: CDR3

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

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

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

4 negatively charged mutations at the edges of CDR3.

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

6 ssed mutated IgVH with multiple arginines in CDR3.

7 ortest and most conformationally constrained CDR3.

8 h-affinity TCRs engineered by mutagenesis of CDR3.

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

10 peptide representing Herceptin's heavy chain CDR3.

11 study because of the large diversity of the CDR3.

12 d TCR bearing a conserved residue leucine in CDR3.

13 sidues including those in close proximity to CDR3.

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

15 Likewise, CDR3 alone did not discriminate against MHC binding, sug

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

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

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

19 lating the probability of generating a given CDR3 amino acid sequence or motif, with or without V/J r

20 CDR3 amino acid sequences associated with response to in

21 MS patients, there was a cluster of related CDR3 amino acid sequences observed for 18 out of 34 MS p

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

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

24 While no clones that shared the same CDR3 amino acid sequences were seen in either HC or MS p

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

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

27 f complementarity determining three regions (CDR3 amino acids) ranged from 4.3% to 77.6% with preproc

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

31 fier, we extracted 4-mers from every TCRbeta CDR3 and represented each 4-mer using biophysicochemical

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

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

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

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

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

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

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

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

43 oire found that these rearrangements possess CDR3 characteristics highly similar to canonical TCRdelt

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

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

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

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

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

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

50 2A1 and an additional ligand recognized in a CDR3-dependent manner.

51 pecific regulation by BTNL/BTN molecules and CDR3-dependent, antibody-like interactions mediating ada

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

53 susceptibility of tryptophan in heavy chain CDR3 did not linearly correlate to higher solvent access

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

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

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

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

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

59 ) and complementarity of IDH1 mutants to the CDR3 domain of the T-cell receptor beta chain (TRB).

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

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

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

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

64 at the complementarity-determining region 3 (CDR3) elements of V2A11 and V8E6 penetrate RTA's active

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

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

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

68 t blood Vgamma9Vdelta2 T cells, including in CDR3 features important for phosphoantigen reactivity.

69 Next, we showed that most of these key adult CDR3 features were already present in the postnatal thym

70 creased frequency of conserved MCC-preferred CDR3 features.

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

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

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

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

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

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

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

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

84 Complementarity-determining region 3 (CDR3) is the most variable part of the TCRalpha and -bet

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

86 However, it remains unclear how the CDR3 landscape is shaped by individual MHC context durin

87 of how MHC-II shapes the naive CD4(+) T cell CDR3 landscape, which essentially defines adaptive respo

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 of MHC-specific TCR is restricted by both CDR3 length and specific amino acid usage.

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

93 ats and humans including gene segment usage, CDR3 length distributions, class switch recombination, s

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

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

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

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

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

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

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

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

102 and characterized by skewed distributions of CDR3 lengths.

103 xtracellular domains and used this to screen CDR3 libraries for clones with increased pMHC affinity.

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

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

106 MHC-restriction disfavors TCR with CDR3 longer than 13 amino acids, limits positively charg

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

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

109 The nature and CDR3 loop composition of the TCRbeta chain played a domi

110 The lack of bound Zn(2+) also made the CDR3 loop highly flexible, as observed in all-atom simul

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

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

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

114 olution revealed a unique feature within its CDR3 loop, which harbors a Zn(2+)-binding site that subs

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

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

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

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

119 y of TCRs and confirms the importance of the CDR3 loops for the adoption to MHC.

120 ain surface. Notably, somatically recombined CDR3 loops implicated in P-Ag recognition were uninvolve

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

122 HV4 loops, but not in somatically recombined CDR3 loops, drastically diminished binding and T cell re

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

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

125 nteractions with a broad range of permissive CDR3 loops.

126 s guided by direct interactions with the TCR CDR3 loops.

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

128 al lead antibody using random mutagenesis of CDR3 loops.

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

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

131 ng structure elements around the heavy chain CDR3 may also be involved.

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

133 A second involves CDR3-mediated gammadelta TCR interaction with diverse li

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

135 treated mice revealed a more closely related CDR3 motif than those of top clonotypes from persistentl

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

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

138 Homologous CDR3 motifs have been reported in other autoimmune disea

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

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

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

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

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

144 nd bound hybridomas expressing the conserved CDR3 motifs.

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

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

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

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

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

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

151 ring an N-glycosylation site, except for the CDR3 of the H chain.

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

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

154 BTN2A1 through the regions between CDR2 and CDR3 of the TCR gamma chain and modulated by the affinit

155 To address this issue, we analyzed the CDR3 of the TCR of human blood and thymic Vgamma9Vdelta2

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

157 ntially used amino acid trimers in alphabeta CDR3 of tTreg.

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

159 chain complementarity determining region 3 (CDR3) of mAbs A and B with no significant oxidation foun

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

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

162 in the complementarity determining region 3 (CDR3) of TCRbeta chains.

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

164 in the complementarity-determining region-3 (CDR3) of their TCR repertoire, allowing the usage of sho

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

166 42 peptide segment (Abeta residues 17-42) in CDR3 on the solubility and conformational specificity of

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

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

169 lonally deletes TCRs with cysteines in their CDR3 peptide-binding regions.

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

171 pulation, and differences in V(D)J usage and CDR3 physicochemical properties were found.

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

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

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

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

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

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

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

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

180 8 TCGA breast cancer exomes, the fraction of CDR3 reads was associated with TILs fraction, tumor puri

181 nce of antigen-driven selection and the long CDR3 region (21 amino acids [aa]), we further characteri

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

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

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

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

186 a chain and modulated by the affinity of the CDR3 region of the TCRdelta chain, which was phosphoanti

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

188 , contribute to significant variation in the CDR3 region.

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

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

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

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

193 w that germline-encoded residues in CDR1 and CDR3 regions of TRBV4-1-encoded sequences interact with

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

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

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

197 tinguished by features in their non-germline CDR3 regions, with many pre-selection CDR3 sequences not

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

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

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

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

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

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

204 The CDR3 repertoire diversity reflects clonal composition, t

205 of a fetal-type or adult-type Vgamma9Vdelta2 CDR3 repertoire is determined by the fetal and postnatal

206 We first identified key differences in the CDR3 repertoire of fetal and adult blood Vgamma9Vdelta2

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

208 isotype contained a unique, clonally related CDR3 repertoire.

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

210 sed on overall CDR3 repertoires, classifying CDR3 repertoires by antigen specificity, and distinguish

211 ishing twins from non-twins based on overall CDR3 repertoires, classifying CDR3 repertoires by antige

212 of the complementarity-determining region-3 (CDR3) represented by immune receptors associated with lo

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

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

215 , whereas the other involved only CDRs, with CDR3 restructuring to wedge in between opposing walls of

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

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

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

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

220 five private overrepresented and one public CDR3 sequence (CATWDGPYYKKLF) associated with CMV infect

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

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

223 r F(ab')2 mass, intact LC and Fd masses, and CDR3 sequence coverage enabled determination of heavy ch

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

225 CDR3 sequence length distribution and amino acid conserv

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

227 data for BCR or TCR sequences based on their CDR3 sequence or V3J clonotype.

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

229 te invariant/public cytomegalovirus-reactive CDR3 sequences (TRGV8-TRJP1-CATWDTTGWFKIF, TRDV2-TRDD3-C

230 y, TAIR is one of the largest collections of CDR3 sequences and tissue types, and should serve as an

231 broad range of sequence similarity, matching CDR3 sequences are likely to share specificities.

232 Public CDR3 sequences are shared between mice of different MHC

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

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

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

236 CDR3 sequences from nTregs displayed a divergent pattern

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

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

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

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

241 Finally, we observed a higher frequency of CDR3 sequences matching the TCR sequences of the proinsu

242 rmline CDR3 regions, with many pre-selection CDR3 sequences not compatible with MHC-binding.

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

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

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

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

247 ion of SJL mice, that differed only in their CDR3 sequences were utilized to generate retrogenic mice

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

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

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

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

252 e predictive power that can be obtained from CDR3 sequences, using representative, readily interpreta

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 nd Vbeta gene segments with randomly created CDR3 sequences.

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

260 segment rearrangements and possessed unique CDR3 sequences.

261 immunity when combined with different murine CDR3 sequences.

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

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

264 mplete complementarity-determining region 3 (CDR3) sequences, a prerequisite for cloning/expression o

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

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

267 oire formation using high throughput TCRbeta CDR3 sequencing in immunodeficient mice receiving human

268 e assignments based on high-throughput TCRBV CDR3 sequencing.

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

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

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

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

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

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

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

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

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

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

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

280 ute to complementarity-determining region 3 (CDR3), the region that binds antigen(1).

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

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

283 essibility is a prerequisite for heavy chain CDR3 tryptophan oxidation.

284 CDR3 usage was not skewed in control Vbeta16 CDR3 transc

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

286 ding the complementary-determining region 3 (CDR3), using regular RNA sequencing data such as those f

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

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

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

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

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

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

293 tryptophan in close proximity to heavy chain CDR3 were not susceptible to oxidation.

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

295 Types and length of CDR3 were similar among groups.

296 -chain complementarity determining region 3 (CDR3) were highly overrepresented.

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

298 gh the Complementarity-determining region 3 (CDR3), which is responsible for imparting specific antib

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

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