ライフサイエンスコーパス: CDR2

1 ate in complementarity-determining region 2 (CDR2).

2 uon in complementarity-determining region 2 (CDR2).

3 their complementarity determining region 2 (CDR2).

4 umors that express a neuronal antigen termed cdr2.

5 C3, perhaps by affecting the conformation of CDR2.

6 alpha chain responsible for these effects is CDR2.

7 within CDR1 and occurs with complete loss of CDR2.

8 ted that Ssp1 promotes mitotic entry through Cdr2.

9 r degeneration breast/ovarian cancer antigen cdr2.

10 sing VH1-46 Abs to Dsg3 reactivity reside in CDR2.

11 e describe that such a screen has identified cdr2(+), a gene that has an important role in the mitoti

12 We have found that cdr2, a cytoplasmic protein harboring a helix-leucine zi

13 cell cycle progression by activating the ARK Cdr2 according to cell growth signals.

14 t manner, but how the Pom1 gradient inhibits Cdr2 activity during cell growth is unknown.

15 Genetic evidence suggests that cdr2(+) acts as a mitotic inducer, functioning through w

16 nthetically lethal with cdc25, nim1/cdr1, or cdr2, all of which are unable to activate the p34cdc2 ki

17 The sequences in the CDR1 alpha and CDR2 alpha correlate with differential expression in CD4

18 tarity determining regions (CDR) 1 alpha and CDR2 alpha residues.

19 A few CDR1 and CDR2 amino acids dominated the most crossreactive TCR in

20 his recognition is dependent upon the shared CDR2 amino acids.

21 specifically blocked the interaction between cdr2 and c-Myc in vitro.

22 Movements of the CD8alpha CDR2 and CD8beta CDR1 and CDR2 loops as well as the flex

23 eptor function, whereas mutations in CD8beta CDR2 and CDR3 loops abolish CD8alphabeta coreceptor acti

24 06 with the N-terminal domain of TG2 via the CDR2 and CDR3 loops of the heavy chain and the CDR2 loop

25 of CD8beta tilts away from its corresponding CDR2 and CDR3 loops.

26 The CDR1, CDR2 and CDR4 peptides were each able to block prolifera

27 in the CDR1 loop and mutations spanning the CDR2 and DE loops had no effect.

28 Affinity mutations were generated in CDR2 and FR3 residues, yielding improvements in affinity

29 ments for particular side chains in CDR1 and CDR2 and in their relative binding contributions among d

30 d express the drug efflux determinants CDR1, CDR2 and MDR1.

31 ursor nodes organized by the SAD-like kinase Cdr2 and Mid1/anillin through an unknown mechanism.

32 am kinase and similar phosphorylation sites, Cdr2 and Ssp2 have distinct regulatory input cues and di

33 anti-Id were located in heavy chain CDR1 and CDR2 and were peripheral to the residues within the Lewi

34 C binding as a result of mutations in either CDR2 and/or CDR3 loops, that bound to the MHC or peptide

35 We have cloned cdr2(+) and have found that it encodes a putative serine

36 ing to complementarity-determining region 2 (CDR2) and CDR3 of the immunizing MBP-reactive T cell clo

37 utants and identified mutations in the CDR1, CDR2, and CDR3 loops that decreased binding to MHC class

38 nes-Hua, Hub, Huc, Hud, Nova1, Nova2, Natpb, Cdr2, and Cdr3.

39 s in complex with QL9-L(d) showed that CDR1, CDR2, and CDR3beta conformations and docking orientation

40 ing indicates not only that residues in FR1, CDR2, and FR3 are involved but also that the three regio

41 complementarity-determining region 1 (CDR1), CDR2, and framework region 3 (FR3) are predicted to be m

42 the database of canonical forms for CDR1 and CDR2, and has implications for antigen recognition by TC

43 plementarity-determining region 1 (CDR1) and CDR2, and less than two replacements in the framework re

44 e found that the mRNA levels of ERG11, CDR1, CDR2, and MDR1, the candidate fluconazole resistance gen

45 sively bearing VDJ rearrangements with CDR1, CDR2, and nearly intact DH segments in germline configur

46 bitory kinases Cdr1 (also known as Nim1) and Cdr2, and the anillin-like protein Mid1.

47 key positions in the VH gene encoding CDR1, CDR2, and the immunoglobulin framework that are critical

48 om1 phosophorylated the C-terminal domain of Cdr2, and this modification reduced Cdr2-T166 phosphoryl

49 n contrast, it has been argued that CDR1 and CDR2 are involved to a greater extent than CDR3s in the

50 ged division response (Cdr) kinases Cdr1 and Cdr2 are negative regulators of Wee1, and we show that t

51 plementarity-determining regions (CDR) 1 and CDR2 are often used to bind exposed areas of the MHC alp

52 t essential for viability, but cells lacking cdr2(+) are elongated relative to wild-type cells, spend

53 regulation exerted by Pom1 on Cdr2 prevents Cdr2 assembly into stable nodes in the cell tip region w

54 del is supported by experiments showing that Cdr2 associates with the N-terminal regulatory domain of

55 In this study, we show that Pom1 modulates Cdr2 association with membranes by phosphorylation of a

56 V beta bias occurred as a consequence of the CDR2 beta loops determining the affinity of the iNKT TCR

57 1 and 2 bind one NA monomer, the light-chain CDR2 binds the neighbouring monomer, whereas HCDR3 inter

58 We demonstrate that the CDR2 can be engineered to express a 12-amino acid peptid

59 BV5S2 complementarity-determining region 2 (CDR2) can boost significantly the frequency of circulati

60 Deletion of cdr2 causes a G2-M delay that is more severe than that c

61 totic entry by regulating Cdk1 through Pom1, Cdr2, Cdr1 and Wee1.

62 s of the CDR region here designated CDR1 and CDR2 (closest to the carboxyl end) each consist of about

63 complementary determining region (CDR)1 and CDR2 coincided with a combination of overlapping AGCT ho

64 g Ag recognition while gene-encoded CDR1 and CDR2 contribute to the fine specificity of the TCR-pepti

65 taining the amino acid sequences of CDR1 and CDR2 (designated bCDR1 and bCDR2) were synthesized, and

66 If the overlapping hotspots in the CDR1 or CDR2 did not undergo mutation, the frequency of mutation

67 e septation initiation network (SIN) induces Cdr2 dissociation from cytokinetic precursors at this st

68 cdr2 down-regulates c-Myc-dependent transcription in cot

69 ty-determining regions (CDRs), with CDR1 and CDR2 encoded by the V segment and CDR3 encoded by the V(

70 mors, whereas other cdr genes are not; thus, cdr2 encodes the PCD tumor antigen.

71 are independent of wee1(+), suggesting that cdr2(+) encodes a second activity involved in cytokinesi

72 ed and implies that residues in the CDR1 and CDR2-equivalent loops of CD8beta are occluded upon bindi

73 Cdr2 establishes the hierarchical localization of other

74 onor T cells into efficient killers of human cdr2-expressing tumor cells.

75 of 9 of these events occurred in the CDR1 or CDR2, following a pattern consistent with selection, and

76 TLs) specific for the PCD onconeural antigen cdr2 found in the blood of patients with PCD are likely

77 includes the solvent-exposed surfaces of 3' CDR2/FR3 and/or FR1.

78 nd suggest a mechanism whereby inhibition of cdr2 function by autoantibodies in PCD may contribute to

79 We have found that the cdr2 gene, which encodes a cytoplasmic leucine zipper pr

80 CDR1, CDR2, or CDR3 of the L chain, the V(H) CDR2 glycan remained high mannose.

81 k proliferation, with the activity of CDR1 > CDR2 > CDR4.

82 mutants carrying one to five mutations in VH CDR2 had reduced or abolished Ag binding, while 10% were

83 ohydrate attached to nearby positions within CDR2 had variable affects on affinity.

84 , a role of mutations at position 53 in V(H) CDR2 has been demonstrated.

85 , Asp54 isomerization and Met56 oxidation in CDR2 in the heavy chain of mAb1 result in opposing confo

86 e second complementarity-determining region (CDR2) in the light chain, is due to a spatial proximity

87 Pom1 also inhibits Cdr2 interaction with Mid1, reducing its clustering abil

88 Cdr2 is a 775 amino acid protein kinase that is closely

89 Thus, Cdr2 is a novel mitotic control protein that appears to

90 -privileged sites, the expression pattern of cdr2 is compatible with the autoimmune model of PCD path

91 determine whether the expression pattern of cdr2 is consistent with its proposed role in PCD, we hav

92 ly expressed in such tumors, indicating that cdr2 is in fact an important tumor antigen in the genera

93 Cdr2 is inhibited by a spatial gradient of the DYRK kina

94 activation of the conserved mitotic inducer Cdr2 is integrated with an inhibitory spatial gradient t

95 lear, due in part to reports indicating that cdr2 is not expressed in tumors obtained from neurologic

96 first that the tissue-specific expression of cdr2 is regulated at a post-transcriptional level.

97 Cdr2 is regulated by the cell polarity kinase Pom1, sugg

98 e reexamined this question, and we find that cdr2 is widely expressed in such tumors, indicating that

99 cdr2(+) is not essential for viability, but cells lackin

100 the V region, and especially of the CDR1 and CDR2, is highly evolved to recruit mutations to key resi

101 We show that serine 52a, within CDR2, is required for IdHOM expression, homophilic bindi

102 show that Pom1 acts to prevent activation of Cdr2 kinase activity by the CaMKK Ssp1.

103 ring ability, possibly by down-regulation of Cdr2 kinase activity.

104 It shows striking similarity to the Ig CDR2-like C'C'' region of the CD4 first domain D1 that d

105 R2 and CDR3 loops of the heavy chain and the CDR2 loop of the light chain.

106 this hotspot, key germline-encoded CDR1 and CDR2 loop residues and a crucial but commonly coded resi

107 eptibility to papain cleavage in an adjacent CDR2 loop, and the tendency of the newly formed isoAsp t

108 ts of the CD8alpha CDR2 and CD8beta CDR1 and CDR2 loops as well as the flexibility of the H-2D(d) CD

109 C) was mainly recognized by the TCR CDR1 and CDR2 loops in an MHC-centric manner.

110 e major contacts with the peptide, while the CDR2 loops interact primarily with the MHC.

111 omplementarity-determining region (CDR)1 and CDR2 loops of TCR and MHC.

112 consistent with the notion that the CDR1 and CDR2 loops of the TCR are responsible for MHC restrictio

113 ionarily selected germline Valpha/Vbeta CDR1/CDR2 loops to create highly MHC/peptide cross-reactive T

114 ons of the Vgamma2Jgamma1.2 CDR3 and Vdelta2 CDR2 loops.

115 on state using the germline-encoded CDR1 and CDR2 loops.

116 between cell polarity proteins and the Cdr1-Cdr2 module might underlie the coordination of cell grow

117 Within the brain, both the cdr2 mRNA and immunoreactivity are confined primarily to

118 We have found that cdr2 mRNA is expressed in almost all tissues, whereas th

119 24% (8 of 33), a frequency twice that of VH CDR2 mutants.

120 of this property, upon nitrogen deprivation cdr2(+) mutants do not arrest in G1, but rather undergo

121 the Vbeta8.2-SEC3 complex suggests that the CDR2 mutations act by disrupting Vbeta main chain intera

122 Their GC progeny were rapidly selected for CDR2 mutations that blocked 72% of antigen-binding sites

123 iable region, including framework, CDR1, and CDR2 mutations.

124 sidue (Thr166) in the activation loop of the Cdr2 N-terminal kinase domain both in vitro and in cells

125 studies are consistent with a model in which Cdr2 negatively regulates Wee1.

126 These data indicate that cdr2 normally sequesters c-Myc in the neuronal cytoplasm

127 Peptides derived from CDR1 of 44aacb, CDR2 of 118.1, and CDRs 1 and 3 of MY904 heavy chains we

128 hat when the anti-dextran V(H) CDR2 replaced CDR2 of an anti-dansyl V(H), the glycosylation site was

129 H genes that use CDR1 of one VH gene and the CDR2 of another are frequently encountered.

130 restored full viral receptor activity to the CDR2 of human CD134 in the context of feline CD134, with

131 CDR2 structure is unique by mutating the VH CDR2 of the anti-PC-protein murine Ab, PCG1-1.

132 he epitope was recognized mainly by CDR1 and CDR2 of the heavy chain, which are highly conserved amon

133 h CDRs were CDR1 of the heavy chain (H1) and CDR2 of the light chain (L2).

134 Previously, we found that the VH CDR2 of the murine T15 Ab is highly sensitive to mutatio

135 lored the sequence requirements for CDR1 and CDR2 of the TCR alpha-chain in a human T cell response c

136 We also show that residue 51 in CDR2 of the TCR alpha-chain interacts with the peptide a

137 rate that single amino acid substitutions in CDR2 of the TCR-alpha chain controlled whether a T cell

138 Mutational analysis of residues in CDR1 and CDR2 of the three Valpha2 regions showed the importance

139 plementarity determining region 1 (CDR1) and CDR2 of the V alpha element can be responsible for deter

140 The complementarity-determining region 2 (CDR2) of the beta-chain and, to lesser extents, CDR1 and

141 ite in the complementary determining region (CDR2) of the heavy chain variable region were elucidated

142 chain complementarity determining region 2 (CDR2) of the phosphocholine-specific T15 Ab can have a d

143 d that complementarity determining region 2 (CDR2) of the Vbeta contributed the majority of binding e

144 in the complementarity-determining region 2 (CDR2) of the VH, and the presence of carbohydrate leads

145 omplementarity determining regions (CDR1 and CDR2) of this Valpha are shorter than the CDRs correspon

146 Combinations of CDR1 peptide with CDR2 or CDR4 peptides allosterically enhanced the abilit

147 that are either germ line-encoded (CDR1 and CDR2) or somatically rearranged (CDR3).

148 en another carbohydrate was present in CDR1, CDR2, or CDR3 of the L chain, the V(H) CDR2 glycan remai

149 ns in the first residue of the Valpha, CDR1, CDR2, or CDR3 were isolated.

150 Most of these V(H)s were with different CDR2 origins (six of seven groups of V(H) germlines) or

151 ce of a cka2 mutant, as expected if CDR1 and CDR2 overexpression is responsible for fluconazole resis

152 ibitor of mitotic entry, working through the Cdr2 pathway.

153 s presenting endogenously loaded MHC class I-cdr2 peptide.

154 l involve a limited set of slightly modified CDR2 peptides from BV genes involved in T cell recogniti

155 S2 peptides were immunized successfully with CDR2 peptides from different BV gene families overexpres

156 east one of three overlapping or substituted CDR2 peptides possessing a core epitope of residues 44-5

157 In contrast, the CDR2 peptides were less immunogenic and contained crypti

158 Of the CDR2 peptides, the substituted (Y49T)BV5S2-38-58 peptide

159 that the dual regulation exerted by Pom1 on Cdr2 prevents Cdr2 assembly into stable nodes in the cel

160 w here that SIN-dependent phosphorylation of Cdr2 promotes its interaction with the 14-3-3 protein Ra

161 n was blocked by heavy chain residues in the CDR2 region and appeared to lack part of the canyon wall

162 g of QS4120 an antibody directed against the CDR2 region of CD4.

163 sly created by saturation mutagenesis of the CDR2 region of T15.

164 ite, amino acid residue Asn55 located in the CDR2 region of the heavy chain, is of particular interes

165 t recognize a TCR peptide from the conserved CDR2 region of the TCR Vbeta8.2-chain in the context of

166 y occurring somatic mutations in the H chain CDR2 region that conferred a markedly prolonged off-rate

167 ltiple mutations must be introduced into the CDR2 region to create a nonbinder phenotype.

168 acts with some portion of the Valpha CDR1 or CDR2 region.

169 ng the structure and the interactions of the CDR2 region.

170 is study shows that residues in the CDR1 and CDR2 regions are primary determinants for MHC class disc

171 eptides, and moderately diverse TCR CDR1 and CDR2 regions contact moderately diverse MHC alpha-helice

172 ouse Vbeta8 family, has amino acids in their CDR2 regions that consistently bind a particular site on

173 ly, we found that when the anti-dextran V(H) CDR2 replaced CDR2 of an anti-dansyl V(H), the glycosyla

174 panel of Abs with which to test 17 of the 19 CDR2 residues.

175 on was still dependent on the conserved CDR1/CDR2 residues.

176 very TCR mutant, including those in CDR1 and CDR2, retained remarkable peptide specificity.

177 CDR2 sequences, whereas high IF clan I J558 CDR2 sequences are diverse.

178 odies, whereas the germline-encoded CDR1 and CDR2 sequences are much more cross-reactive.

179 Finally, alanine scanning of CDR1 and CDR2 sequences of TRBV4-1 revealed two unique residues,

180 te in the first 6 weeks have unique CDR1 and CDR2 sequences, permitting each to be identified using s

181 n II/III V(H)s share more positively charged CDR2 sequences, whereas high IF clan I J558 CDR2 sequenc

182 ding and secretion may be common outcomes of CDR2 somatic mutation.

183 These mice were used to clone high-avidity cdr2-specific CD8(+) T cells that recognize human tumor

184 panded populations of MHC class I-restricted cdr2-specific CTLs in the blood of 3/3 HLA-A2.1+ PCD pat

185 We suggest that activated cdr2-specific CTLs in the CSF contribute to Purkinje deg

186 rolimus also reduced the number of activated cdr2-specific CTLs in the peripheral blood, but did not

187 PCD patients harbor cdr2-specific CTLs in their peripheral blood, and these

188 In PCD, peripheral activation of cdr2-specific CTLs is likely to contribute to the subseq

189 ic and contained cryptic determinants as the CDR2-specific T cell lines did not recognize autologous

190 ell receptor (TCR) alpha and beta genes from cdr2-specific T cells; electroporation of RNA encoding t

191 Cloned cdr2-specific TCR genes provide a clinically relevant me

192 Here we test whether the T15 VH CDR2 structure is unique by mutating the VH CDR2 of the

193 a conserved residue in the activation loop (Cdr2-T166 and Ssp2-T189).

194 omain of Cdr2, and this modification reduced Cdr2-T166 phosphorylation by Ssp1.

195 In contrast, Cdr2-T166 phosphorylation is regulated by protein phosph

196 This leads to an immune response to cdr2 that is associated with tumor immunity and autoimmu

197 Whereas cdr2 therefore appears to be the target of an effective

198 The CDR1 and CDR2 therefore represent new canonical forms that could

199 body response to the tumor and brain antigen cdr2, this humoral response has not been shown to be pat

200 We found that Ssp1 activates Cdr2 through phosphorylation of a conserved threonine re

201 ring precursors organized by the SAD kinase Cdr2 to pre-define the division plane [5-8]; then, massi

202 cka2 mutants overexpress CDR1 and CDR2, two fluconazole efflux transporter genes, and a cd

203 To evaluate the immunogenicity of CDR2 vs other regions of the TCR, we vaccinated seven MS

204 sulfide bonds between CDR3 and CDR1, FW2, or CDR2 was also observed, as described in camelids.

205 cdr2(+) was identified in a screen for regulators of mit

206 mplementarity-determining region 1 (CDR1) or CDR2 were sufficient to change selection from the CD4 su

207 Two fluconazole efflux pumps, CDR1 and CDR2, were upregulated in the in vivo biofilm-associated

208 plementarity-determining region 1 (CDR1) and CDR2, which exhibited higher replacement-to-silent ratio

209 to the conserved cell cycle kinases Cdr1 and Cdr2, which localize to a set of cortical nodes in the c

210 tumors express an onconeural antigen termed cdr2, which normally is expressed in cerebellar Purkinje

211 on in fission yeast is the SAD family kinase Cdr2, which organizes a set of cortical nodes in the cel

212 D-induced mutations primarily in the AGCT in CDR2, which was also the most frequent site of mutation

213 placing the overlapping hotspots in CDR1 and CDR2 with neutral or cold motifs resulted in a reduction