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 r degeneration breast/ovarian cancer antigen cdr2.

5 umors that express a neuronal antigen termed cdr2.

6 C3, perhaps by affecting the conformation of CDR2.

7 alpha chain responsible for these effects is CDR2.

8 occurs in cells at cortical nodes formed by Cdr2.

9 within CDR1 and occurs with complete loss of CDR2.

10 rea (SA) due, in part, to the protein kinase Cdr2.

11 s bound endogenous CDR2L, but not endogenous CDR2.

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

13 ted that Ssp1 promotes mitotic entry through Cdr2.

14 erage of 2-3% deamidation in the heavy chain CDR2, 20-25% deamidation in the Fc domain, and 10-15% N-

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

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

17 recruits other CR components to nodes, pulls Cdr2 aberrantly into the CR, and reduces rates of CR mat

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

19 omyces pombe, two SAD kinases (Cdr1/Nim1 and Cdr2) act as upstream inhibitors of Wee1.

20 ncorporates the cytoplasmic kinase Ssp1 as a Cdr2 activator.

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

22 We propose that Cdr2 acts as a dosage-dependent regulator of cell size b

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

24 sion in a manner dependent on the SAD kinase Cdr2, advances the G2/M transition, precociously recruit

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

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

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

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

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

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

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

32 fluid and serum from PCD patients as well as CDR2 and CDR2L antibodies to neuronal tissue, cancer cel

33 kinectin (KTN1) and that double knockout of CDR2 and CDR2L enhances KTN1-dependent ER sheet stacking

34 ines, and cells transfected with recombinant CDR2 and CDR2L to elucidate which is the major antigen o

35 viation from the canonical CDR structures of CDR2 and CDR3 induced by the substitutions.

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

37 06 with the N-terminal domain of TG2 via the CDR2 and CDR3 loops of the heavy chain and the CDR2 loop

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

39 ta2TCR to BTN2A1 through the regions between CDR2 and CDR3 of the TCR gamma chain and modulated by th

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

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

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

43 Mutations in germline-encoded Vgamma4 CDR2 and HV4 loops, but not in somatically recombined CD

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

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

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

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

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

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

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

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

52 y cerebellar degeneration-related protein 2 (CDR2) and its paralog CDR2-like (CDR2L), onconeural anti

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

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

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

56 Pom1 kinase phosphorylates and inhibits Cdr2, and forms cortical concentration gradients from ce

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

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

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

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

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

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

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

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

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

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

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

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

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

70 This work supports the role of Cdr2 as a sizer factor and highlights the importance of

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

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

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

74 tep model for inhibition of Wee1 by Cdr1 and Cdr2 at nodes.

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

76 1 and 2 bind one NA monomer, the light-chain CDR2 binds the neighbouring monomer, whereas HCDR3 inter

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

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

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

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

81 of cell size and growth, including cell SA (Cdr2), cell volume (Cdc25), and time (Cdc13).

82 ells of different widths, we first show that cdr2(+) cells divide at a fixed cell surface area.

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

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

85 CDR2 competes with the eEF1Bbeta subunit of translation

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

87 The protein kinase Cdr2 contributes to this size control system by forming

88 ng cells, consistent with Pom1 inhibition of Cdr2 decreasing with cell growth.

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

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

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

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

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

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

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

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

97 Cdr2 establishes the hierarchical localization of other

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

99 Exogenous CDR2 expression additionally promotes CC1 box-dependent

100 ssion system, we found that a 6x increase in Cdr2 expression caused hyperphosphorylation of Wee1 and

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

102 This overexpressed Cdr2 formed clusters that sequestered Wee1 adjacent to t

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

104 he monoclonal immunoglobulin light chain FR2-CDR2-FR3 was sequenced by database-aided de novo MS/MS a

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

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

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

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

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

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

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

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

113 al pool demonstrates more Pom1 overlaps with Cdr2 in short than long cells, consistent with Pom1 inhi

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

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

116 ea sensing and supporting the existence of a Cdr2-independent secondary sizer mechanism more closely

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

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

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

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

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

122 ly specified by cell volume, suggesting that Cdr2 is essential for area sensing and supporting the ex

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

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

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

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

127 We demonstrate in human cancer cells that CDR2 is recruited by the integral ER membrane protein ki

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

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

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

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

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

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

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

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

136 lls divide at a threshold size partly due to Cdr2 kinase, which forms nodes at the medial cell cortex

137 ee1, but it has not been known how increased Cdr2 levels might impact Wee1 and cell size.

138 and eEF1Bbeta knockdown increases endogenous CDR2 levels on ER sheets, inducing their centrosome-prox

139 ion-related protein 2 (CDR2) and its paralog CDR2-like (CDR2L), onconeural antigens with poorly under

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

141 The peripheral membrane kinase Cdr2 localizes in clusters (nodes) on the medial plasma

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

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

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

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

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

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

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

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

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

151 igh amino acid diversity of the TCR CDR1 and CDR2 loops, and that such conservation is unlikely to do

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

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

154 It also has not been clear if and how Cdr2 might regulate Wee1 in the absence of the related k

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

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

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

158 The model predicts that a cdr2 mutant in an Ssp1 phosphorylation site (cdr2-T166A)

159 When combined with cdr2 mutants that affect node assembly or disassembly, g

160 Cdr2 mutants that disrupt either kinase activity or clus

161 24% (8 of 33), a frequency twice that of VH CDR2 mutants.

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

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

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

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

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

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

168 Here, we show that the Cdr2 nodal density, which scales with cell size, is used

169 Cdr2 node anchoring at the cell cortex is not fully unde

170 In arf6 mutants, Cdr2 nodes detached from the membrane and exhibited incr

171 In arf6Delta mutants, Cdr2 nodes detached from the membrane and exhibited incr

172 Arf6 stably localized to Cdr2 nodes in its GTP-bound but not GDP-bound state, and

173 To investigate how Cdr2 nodes may sense area, we derive a minimal mathemati

174 Our work identifies a regulated anchor for Cdr2 nodes that is required for cells to sense surface a

175 Pom1 clusters colocalize with Cdr2 nodes, forming a glucose-modulated inhibitory thres

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

200 y restricted autoantigen, with minimal CDR1, CDR2, or HV4 contributions.

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

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

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

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

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

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

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

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

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

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

211 Here, we show that both Cdr1 and Cdr2 promote Wee1 phosphorylation in cells, but only Cdr

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

213 chizosaccharomyces pombe, the protein kinase Cdr2 promotes mitotic entry by organizing cortical oligo

214 ever, Yo antibodies can bind the recombinant CDR2 protein used in routine clinical testing for these

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

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

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

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

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

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

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

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

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

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

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

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

227 id-cell levels, which represent the critical Cdr2-regulating pool.

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

229 eet stacking, reversal of which by exogenous CDR2 requires its dynein-binding CC1 box motif.

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

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

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

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

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

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

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

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

238 Pom1 inhibits Cdr2 signaling to Wee1 specifically in small cells, but

239 the conserved GTPase Arf6 as a component of Cdr2 signaling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

254 cdr2 mutant in an Ssp1 phosphorylation site (cdr2-T166A) [4] should form nodes whose density register

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

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

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

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

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

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

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

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

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

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

265 Our work reveals how Pom1-Cdr2-Wee1 operates in multiprotein clusters at the corte

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

267 ncentrations of either kinase Pom1 or kinase Cdr2 were varied with the nmt1 promoter, the numbers of

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

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

270 ls the timing of mitotic entry by inhibiting Cdr2, which forms stable membrane-associated nodes at mi

271 The heavy chain CDR2, which is the only CDR containing asparagine residu

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

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

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

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

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