ライフサイエンスコーパス: (is|are|was|were) defective in *ing

1 rmore, the spalt/spalt-related null antennae are defective in hearing.

2 on insertions in sprB resulted in cells that were defective in gliding.

3 Protein extracts of c03958 flies were defective in hydrolyzing 3'-DNA-tyrosyl residues, d

4 eIF4GI mutants with defects in binding eIF4A were defective in mediating 48S complex formation even i

5 ls and that IL-21-receptor-deficient T cells are defective in generating a T(H)17 response.

6 This TA(-) mutant was defective in producing a zone of inhibition (ZOI) ag

7 n hemA, hemB, hemL, ubi, cydAB or atp, which were defective in generating a proton motive force (PMF)

8 The csrA mutant was defective in forming actin pedestals on epithelial c

9 lized to focal adhesions (FAs), and APC (m4) was defective in promoting actin assembly at FAs to faci

10 However, YR1m4 is defective in supporting activator-independent transcr

11 ant FANCJ-A349P protein had reduced iron and was defective in coupling adenosine triphosphate (ATP) h

12 ct of the nilD6::Tn5 mutant, and this mutant was defective in colonizing all three nematode host spec

13 The FYF and FFF mutants were defective in phosphorylating all of these molecules

14 similar to those of wild-type controls, but were defective in inhibiting alloreactive Th1 cells in v

15 show that all three of these mutant proteins are defective in translocating along DNA while one mutan

16 e Ama(M109) mutant protein binds to Nrt, but is defective in mediating Ama/Nrt cell adhesion.

17 croglia in the CNS of huGFAP-CCL2hi tg+ mice were defective in expressing amoeboid morphology.

18 estingly, tumor-derived mutants of p53 which are defective in inducing an apoptotic response retain t

19 In support of this, SPL-deficient cells were defective in mounting an effective IFN response whe

20 three genes, rng3(+), rng4(+), and rng5(+), were defective in organizing an actin contractile ring.

21 Although Ku86-deficient mice are defective in coding and signal joint formation, rare

22 ified in bacteriophage P22 coat protein that are defective in folding and cause their folding interme

23 reby creating erbB receptor assemblies which are defective in signaling and do not internalize.

24 t mutants in Spo0J that disrupt DNA bridging are defective in spreading and recruitment of structural

25 The Polg-D257A protein is defective in proofreading and increases mtDNA mutatio

26 binding-defective mutant of IGF1 (R36E/R37E) is defective in signaling and ternary complex formation.

27 The lpp double-knockout mutant was defective in invading and inducing cytotoxic effects

28 Moreover, female BALB/c-IL-17RA(KO) mice were defective in producing anti-P. gingivalis immunoglo

29 Epidermal DC in these mice were defective in presenting antigen in vivo to adoptive

30 dotA/icmWXYZ mutants of L. pneumophila that are defective in inducing apoptosis do not induce caspas

31 a palmitoylation-defective Fas C194V mutant is defective in inducing apoptosis in primary mouse T ce

32 Unexpectedly, p53Ala143 was defective in inducing apoptosis in H1299 cells at 32

33 Bax/Bak(-/-) cells were defective in undergoing apoptosis but were more rad

34 Significantly, CD14(-/-) macrophages in vivo are defective in clearing apoptotic cells in multiple ti

35 acking the phosphatidylserine receptor (PSR) were defective in removing apoptotic cells.

36 Furthermore, ycs4-1 is defective in silencing at the mating type loci at the

37 The mutant was defective in mediating ATP-dependent conformational

38 hat TLR4-activated DCs from lupus-prone mice are defective in repressing autoantibody secretion, coin

39 Primary osteoblasts from mutant mice are defective in supporting B lymphopoiesis in vitro, wh

40 d T cell response to bacterial infection and were defective in clearing bacterial infections.

41 ells failed to reject allogeneic tumors, and were defective in rejecting Balb/C allogeneic skin graft

42 In a screen for mutants that are defective in transitioning between crawl and swim be

43 An asgD null mutant was defective in fruiting body formation and sporulation

44 As a consequence, it is defective in stimulating both unwinding by the helica

45 , it was discovered the Arg(74) mutant of TF was defective in enhancing both the amidolytic and prote

46 Three of four ExbB mutants were defective in supporting both the PMF-dependent form

47 ressing only half of the normal Brd4 levels, were defective in reloading Brd4 onto chromosomes.

48 The positions of TBP mutations which are defective in binding BRF suggest that BRF binds to t

49 Nuclear extracts depleted of Urp are defective in splicing, but activity can be restored

50 In addition, PLCgamma2-deficient mice are defective in clearing C. albicans infection in vivo.

51 c6p mutants that allow a reductional mitosis are defective in binding Cdc28p kinase.

52 Both the frzF and frzG mutant strains are defective in directing cell movement through prey co

53 culA null cells are defective in inducing cell-type-specific gene expres

54 he anti-apoptosis proteins Bcl-2 and Bcl-xL, is defective in eliciting cell death.

55 clones expressing the class IV GCSFR, which is defective in signaling cell maturation.

56 antitative syncytia assays showed that JPVTM was defective in promoting cell-to-cell fusion (i.e., sy

57 A sumoylation-deficient mutant was defective in rescuing cell viability in symplekin sm

58 In addition, Nkrp1b(-/-) mice are defective in rejecting cells lacking Clr-b, supporti

59 on of the GCSFR class IV mRNA isoform, which is defective in signaling cellular differentiation.

60 solation of two recombinant SV5 mutants that are defective in preventing chemokine induction will all

61 cells from Hoxa13 mutant homozygous embryos are defective in forming chondrogenic condensations in v

62 dicated that the RING-finger deletion mutant was defective in inhibiting chromosome condensation afte

63 can also activate CAR, and mice lacking CAR are defective in clearing chronically elevated bilirubin

64 , SSB-113, lacks strong affinity for psi and is defective in promoting clamp loading and processive r

65 One class of mutant proteins was defective in forming complexes with Msh6p and also f

66 paka null cells are defective in completing cytokinesis in suspension.

67 inducing cell proliferation and survival but are defective in inducing differentiation.

68 rmed normally in KatG[D137S] but this mutant is defective in forming dioxyheme and lacks catalase act

69 A binding-deficient mutants of ORF50 protein are defective in activating direct targets, they are non

70 We also study a mutant of Sld2 that is defective in binding DNA, sld2-DNA, and find that sld

71 R50E was defective in inducing DNA synthesis, cell proliferat

72 As expected, some J mutants were defective in binding DnaK (Hsc70); other mutants re

73 find that S635A and T637A hydrolyse ATP, but are defective in unwinding duplex RNA and releasing mRNA

74 that cannot undergo lytic viral replication are defective in promoting EBV-mediated lymphoproliferat

75 An orfU mutant was defective in attaching-effacing lesion formation and

76 nable to bind the p85 subunit of PI-3 kinase is defective in potentiating EGFR signaling, confirming

77 The results demonstrate that all mutants are defective in binding either B or B and C subunits.

78 th EpoR mutants that retain JAK2 binding but are defective in mediating Epo-dependent JAK2 activation

79 s, and that structures that failed to rotate were defective in weaving exogenous laminin matrix.

80 Those that escape to the adult stage are defective in wing expansion and cuticle sclerotizati

81 cause a point mutant lacking ATPase function was defective in blocking expansions.

82 viving exposure to superoxide generators, it was defective in surviving exposure to hydrogen peroxide

83 Both mutants were defective in surviving exposure to oxidative stress

84 exhibit abnormal accumulation of F-actin and are defective in producing fertilized eggs.

85 Talin-deficient and talin1(L325R) platelets were defective in retracting fibrin clots.

86 hat an SH2 domain deletion mutant of Bcr-Abl is defective in transforming fibroblasts but remains cap

87 drate partitioning, we isolated mutants that are defective in exporting fixed carbon from leaves.

88 ured ephrin-B2-deficient smooth muscle cells are defective in spreading, focal-adhesion formation, an

89 e the fork arms would separate in the model, is defective in binding fork DNA.

90 l imaging of the AMD mutant revealed that it is defective in inducing formation of stress granules.

91 go mutations that elevate Trh levels in vivo are defective in binding forms of Trh found in Dysfusion

92 icroscopy studies established that env7Delta is defective in maintaining fragmented vacuoles during h

93 shows that SP-D- but not SP-A-deficient mice are defective in clearing free DNA from the lung.

94 esidues located at positions 5, 7, 10 and 11 are defective in packaging full-length STMV, but can pac

95 tations that assemble into 30 S subunits but are defective in forming functional ribosomes.

96 Since 14-3-3sigma(-/-) cells are defective in maintaining G(2) arrest, they enter M p

97 ls deficient in the Y-family polymerase REV1 are defective in replicating G-quadruplex DNA.

98 GAP-defective RGS4 mutants invariably were defective in binding G alpha subunits in their tran

99 in, BubR1(+/-) murine fibroblast cells (MEF) were defective in undergoing G(2)/M arrest.

100 line (Mrt) mutants in Caenorhabditis elegans are defective in maintaining genome integrity, resulting

101 Ifnb-/- neurons lacked PD-L1 and were defective in inducing glioma cell death; this effec

102 sidue that structurally supports Switch III, are defective in binding GRK2.

103 of each of these residues, yields GAPs that are defective in stimulating GTP hydrolysis.

104 Worms lacking dma-1 were defective in sensing harsh touch.

105 The shuS mutant was defective in utilizing heme as an iron source.

106 three-hybrid assays suggesting that PIE125K is defective in forming higher order complexes of MADS p

107 ion of the N and CB domains (coupler region) were defective in resolving HJs.

108 Nonpigmented Yersinia pestis (pgm) strains are defective in scavenging host iron and have been used

109 Resulting mutants that make HS but are defective in generating HS(act) were single-cell-clo

110 d Hsp70 binding to receptor, but all mutants were defective in supporting Hsp90-receptor interactions

111 e-capping function in vitro and in vivo, yet are defective in binding human telomerase.

112 ormal L1-CAM-mediated cell aggregation, they are defective in stimulating human epidermal growth fact

113 that elicit morphogenic switching, vph1Delta was defective in forming hyphae whereas stv1Delta was no

114 cannot synthesize arginine, BWP17 and SN152, were defective in making hyphae inside the macrophages,

115 although the mutant still bound to IGF1R, it was defective in inducing IGF1R phosphorylation, AKT and

116 s and of B171, a nonflagellated EPEC strain, were defective in inducing IL-8 release, a phenotype tha

117 substitutions of the 103 buried nonalanines were defective in folding in vivo at 37 degrees C.

118 teresting because we demonstrate that NOD DC are defective in eliciting iNKT cell function, but their

119 ;G129E) has protein phosphatase activity yet is defective in dephosphorylating inositol 1,3,4,5-tetra

120 demonstrated that BAF250a-ablated stem cells are defective in differentiating into fully functional m

121 cursors developed normally in the thymus but were defective in migrating into the skin.

122 iphtheriae and Corynebacterium ulcerans that are defective in acquiring iron from heme and hemoglobin

123 demonstrate that mycobacteria lacking Esx-3 are defective in acquiring iron.

124 , we constructed mutant hCycT1 proteins that are defective in binding its kinase partner, Cdk9, or TA

125 tants retained the ability to bind Hsc70 but were defective in stimulating its ATPase activity.

126 RTA mutants that are defective in inducing K-RBP degradation cannot activ

127 These variant species are defective in binding ligand; however, because their

128 ells, and mice with NFATc1-deficient T cells are defective in controlling Listeria infection.

129 CheA(F214A) was defective in mediating localization of CheY-YFP to t

130 uce long flaps and of dna2Delta mutants that are defective in cutting long flaps.

131 However, the leucine-rich repeat is defective in promoting lysosomal down-regulation of M

132 Unlike their parents, these variants are defective in killing macrophages and lack a major ce

133 served, suggesting that this virus construct was defective in producing mature capsids.

134 Finally, a Gag derivative that is defective in inducing membrane curvature appeared les

135 PAK but not POR1, induced JNK activation but was defective in inducing membrane ruffling and transfor

136 vity; however, Escherichia coli alkB mutants are defective in processing methylation damage generated

137 Microsomes derived from these mutants are defective in exporting misfolded secretory proteins.

138 plate-primer suggest that the mutant enzymes are defective in switching mismatched primer from the po

139 we show that AR-JP-causing parkin mutations are defective in supporting mitophagy due to distinct de

140 s that rescue a Flp variant, Flp(Y60S), that is defective in establishing monomer-monomer interaction

141 is demonstrates that cells disrupted for ptr are defective in altering motility in response to light,

142 tive to the peptide antibiotic sublancin and are defective in swarming motility.

143 ls, double-mutant deltacdc13 deltacig2 cells are defective in undergoing multiple rounds of DNA repli

144 Mutant Plin5 that binds Abhd5 but not Atgl was defective in preventing neutral lipid accumulation c

145 nsporter and that truncated isoforms of CHP1 were defective in stimulating NHE1 biosynthetic maturati

146 sactivating alanine, the truncated construct was defective in hydrolyzing non-cognate Ala-AMP.

147 Rpp2-depleted cells are defective in processing of the 5.8S rRNA.

148 RNA metabolism revealed that the slo3 mutant was defective in splicing of NADH dehydrogenase subunit7

149 ck-/-fgr-/-lyn-/- triple mutant cells, which are defective in spreading on fibronectin-coated surface

150 This result suggests that the mutant gonad is defective in choosing on its surface only a single si

151 ant cannot fully induce their expression and is defective in growing on DMSO under anaerobic conditio

152 mnn4 or mnn6 mutants lack phosphomannans and are defective in binding osmotin to the fungal cell wall

153 Mesenchymal cells lacking Shn3 are defective in promoting osteoclastogenesis in respons

154 a single base mismatch; EndoIII mutants that are defective in carrying out DNA/protein CT do not redi

155 Yeast dmc1 mutants are defective in crossing over and synaptonemal complex

156 We show here that the PMS2(R20Q) variant is defective in activating p73-dependent apoptotic respo

157 riant reported in four independent SCZ cases was defective in activating PAK3 as well as MAPK (mitoge

158 29Q and S326C bind to PARP-1, these proteins were defective in activating PARP-1.

159 In addition, the frzZ mutant was defective in swarming, particularly on soft agar (0.

160 promised in ups1 indicating that this mutant is defective in signalling pathways activated in respons

161 Plants tested were defective in signaling pathways (abscisic acid, sal

162 gly, ICSBP(-/-) bone marrow progenitor cells were defective in generating pDCs in the fms-like tyrosi

163 without apparent cell-cell interactions, and were defective in forming permanent attachments.

164 lating and characterizing seven mutants that were defective in regulating pheromone signaling.

165 found a WDR48 somatic mutation (L580F) that is defective in stabilizing PHLPP1 in colorectal cancers

166 t two TSC2 mutants derived from TSC patients are defective in repressing phorbol 12-myristate 13-acet

167 , a mutant of TSC2 derived from TSC patients was defective in repressing phosphorylation of 4E-BP1.

168 oteins bound to PII, while the S227R protein was defective in binding PII.

169 ady-state level of a mutant form of PML that is defective in binding Pin1.

170 Expression of Arf6 mutants that are defective in activating PLD, Arf6N48R and Arf6N48I,

171 oth IE1(1-346) and IE1(L174P) mutants, which are defective in displacing PML from PODs, failed to inh

172 Smurf1(-/-) macrophages are defective in recruiting polyubiquitin, the proteasom

173 MR-/- mice were defective in clearing proteins bearing accessible m

174 ble full-length CCN1 with the D125A mutation is defective in binding purified alphavbeta3 and impaire

175 fling and cell migration, suggesting that it is defective in activating Rac signaling.

176 Moreover, the S516A mutant of Chk2 is defective in ionizing radiation-induced apoptosis, su

177 pliced ASPP2 isoform lacking the N terminus, was defective in binding Ras-GTP and stimulating Raf/MEK

178 isorder of NADPH oxidase in which phagocytes are defective in generating reactive oxidants.

179 In vivo, the Rad50 hook mutants are defective in being recruited to chromosomal DSBs in

180 TFIIH from cells with XPB or XPD mutations was defective in supporting repair, whereas TFIIH from s

181 M variant carrying a mutation in the PIP-box is defective in promoting replication traverse of inters

182 ol, and a RhoGDI mutant, RhoGDI(I177D), that is defective in extracting Rho GTPases off the membrane

183 i-Goutieres syndrome disease-causing mutant, is defective in degrading RNA.

184 d markedly reduced ISRE-binding activity and were defective in expressing several type I IFN-inducibl

185 omain 2, and S. coelicolor RbpA mutants that are defective in binding sigma are unable to stimulate t

186 These studies suggest that the mutant MGSA is defective in activating signaling through the recepto

187 quired alphavbeta3 expression, and R36E/R37E was defective in inducing signals in polyHEMA-coated pla

188 during S phase and found that pol30 mutants were defective in establishing silencing at HMR regardle

189 Importantly, the mutant RNAP is defective in binding single strand oligomers of RNA.

190 still recruited to DSB-proximal regions but are defective in tethering sister chromatids and consequ

191 as been previously shown that nhp6ab mutants are defective in expressing SNR6, a Pol III-transcribed

192 We found that macrophages from ICSBP-/- mice were defective in inducing some IFNgamma-responsive gene

193 mutant without the unstructured tail region is defective in mediating spindle assembly checkpoint ac

194 ow that mutants defective for hexamerization are defective in binding ssDNA despite retaining all the

195 Cells with an sspB mutation are defective in degrading ssrA-tagged proteins, demonst

196 While both heterodimers were defective in forming stable complexes with mismatch

197 ing these damage-induced chromatid junctions were defective in resolving stalled forks, restarting re

198 s lethal, and genomes carrying this deletion are defective in directing subgenomic RNA synthesis.

199 t is handicapped in binding to Mdm2 and NPM, were defective in inducing sumoylation of these two targ

200 der of the NADPH oxidase in which phagocytes are defective in generating superoxide and downstream mi

201 Previous studies showed that H2-DM- cells are defective in presenting synthetic peptides to class

202 In vitro, Ox40L-deficient dendritic cells are defective in costimulating T cell cytokine productio

203 POT1(CP)was defective in regulating telomerase, leading to telom

204 in-binding defective IGF1 mutant (R36E/R37E) is defective in inducing ternary complex formation and I

205 in binding-defective IGF1 mutant (R36E/R37E) is defective in inducing ternary complex formation and I

206 of very early elongation intermediates, but is defective in supporting TFIIH action in promoter esca

207 However, it was defective in mediating TGF-beta-stimulated Smad3 act

208 d almost exclusively as heterooligomers that are defective in activating the complement cascade.

209 carcinoma-associated mutant Aalpha subunits are defective in binding the B or B and C subunits.

210 In contrast, mutants that are defective in binding the cellular protein p300 stimu

211 In addition, cells that are defective in initiating the ER stress response, beca

212 unable to establish a symbiosis because they are defective in initiating the production of infection

213 Together, these data suggest that MRL mice are defective in maintaining the developmental arrest of

214 monary vasoconstrictor responses in vivo and are defective in oxygenating the blood.

215 over products, we suggest that htp-1 mutants are defective in preventing the use of sister chromatids

216 thetic pathway indicates that ebp2-1 mutants are defective in processing the 27 SA precursor into the

217 e absence of CD45, natural killer (NK) cells are defective in protecting the host from mouse cytomega

218 COUP-TFII mutants are defective in remodeling the primitive capillary plex

219 settle the thymus, and CCR7(-/-) progenitors are defective in settling the thymus.

220 Compared with the WT peptide, these APLs are defective in stimulating the proliferative responses

221 Mutants were constructed that are defective in stimulating the XPB helicase but still

222 However, chk-2 mutants are defective in triggering the pachytene DNA damage che

223 e ability to cover its surface with L-fucose is defective in colonizing the mammalian intestine under

224 A mutant Fis protein, which is defective in contacting the carboxyl-terminal domain

225 oth amino acid substitutions (A184V + Y271H) is defective in modulating the frequency of initiation f

226 carries the variant allele SCNM1R187X, which is defective in splicing the mutated donor site in the S

227 upports TFIIH action in promoter escape, but is defective in suppressing the frequency of abortive tr

228 e, suggesting that the FtsK44 mutant protein is defective in targeting the septum.

229 The GAS srtA mutant was defective in anchoring the LPXTG-containing proteins

230 Furthermore, a mutant Salmonella strain that was defective in forming the SipC multimer and deficient

231 howed that the mutant RNA polymerase RpoB114 was defective in transcribing the two major promoters of

232 Although these transgenic mice were defective in activating the NF-kappaB pathway in B

233 e conditions revealed that E1A mutants which were defective in binding the pRB family of proteins or

234 ge, and Blimp-1-deficient regulatory T cells were defective in blocking the development of colitis.

235 owever, naive and convalescent IgA(-/-) mice were defective in reducing the numbers of B. bronchisept

236 e-selection approach to isolate mutants that were defective in regulating the expression of the ADH g

237 loop mutants (12V,35S, 12V,37G, and 12V,40C) was defective in producing this response.

238 meiotic prophase, Ovol1-deficient germ cells were defective in progressing through the pachytene stag

239 nding point mutants (M69E, A70D, L73E, S74D) were defective in binding TLR2 or TLR1 and could not act

240 pRB mutants lacking the LXCXE binding site are defective in binding to adenovirus E1A and human pap

241 MPRs that are defective in binding to GGAs are poorly incorporated

242 trate that SMN mutants found in SMA patients are defective in binding to Sm proteins.

243 ansduced progenitors from CD44-mutant donors are defective in homing to recipient marrow, resulting i

244 in a cis fashion, and myoblasts lacking CDO are defective in responding to recombinant netrin.

245 nim1 (non-inducible immunity) mutants, which are defective in responding to SA and regulation of SAR.

246 We show that C. albicans ash1 mutants are defective in responding to some filament-inducing co

247 Finally, the Rac2Y40C mutant that is defective in binding to all three potential downstrea

248 the affinity of an alphaIIbbeta3 mutant that is defective in binding to beta3-endonexin.

249 One mutant, Srp1-E402Q, is defective in binding to cNLS cargoes that contain two

250 ereas overexpression of a 14-3-3 mutant that is defective in binding to phosphoproteins has no effect

251 not by the K1 mutant of the T antigen, which is defective in binding to RB.

252 , and the ASB2alpha-resistant filamin mutant is defective in targeting to F-actin-rich structures in

253 nd that the 12-amino-acid truncation of FtsZ was defective in binding to FtsA.

254 ituted at position 12 and 40, respectively), was defective in binding to PAK3, a Ste20-related p21-ac

255 One XRCC1 mutant, A482T, that was defective in binding to polynucleotide kinase phosph

256 A mutant of NIPP1 that was defective in binding to PP1 did not have this effect

257 hLigI51D but not hLigI51A was defective in binding to purified RFC and in associat

258 This combined mutant was defective in binding to short single-stranded DNA ol

259 onsisting of the N-terminal 186 amino acids, was defective in binding to the alpha subunit while reta

260 ited normal binding to the alpha subunit but was defective in binding to the theta subunit.

261 A GFP-Glc7-129 fusion was defective in localizing to the bud neck and SPBs.

262 ns in chromosomal genes tc0237 and/or tc0668 was defective in spreading to the mouse gastrointestinal

263 In contrast, the ABE-II mutants were defective in binding to glycocalicin, but displayed

264 eriments revealed that these mutant proteins were defective in binding to host cells and to HAVCR1.

265 gamma 377-411 produced gamma C mutants which were defective in binding to the alpha(M)I-domain.

266 sistant to inhibition by SpoIIAB in vivo and were defective in binding to the antisigma factor in vit

267 sensitive to S. cerevisiae alpha-factor, but were defective in responding to a variant of alpha-facto

268 Two of these were defective in responding to the enhancer binding pro

269 REDD1 mutants that fail to bind 14-3-3 are defective in eliciting TSC2/14-3-3 dissociation and

270 In contrast, non-metabolic glucose analogs are defective in inducing uH2B.

271 ains the ability to form amyloid fibrils but is defective in binding virions and enhancing infection.

272 urthermore, oncogene-transformed fibroblasts are defective in mechanosensing while generating similar

273 are able to promote Wingless signalling, but are defective in repressing Wingless targets.

274 tant of Pyrococcus furiosus (Pfu) RPP29 that is defective in assembling with its binary partner RPP21

275 The resultant core enzyme is defective in associating with TFIIIB and target genes

276 I mutants such as K270A and T409A/S411A that were defective in signaling with triphosphorylated singl

277 BC mutant, but not single or double mutants, was defective in producing wrinkled colonies, a form of