ライフサイエンスコーパス: -defective mutant

1 rotein to show that infection by this PLA(2)-defective mutant can be complemented by coinfection with

2 Finally, both wild type and acetylase-defective mutant p300 proteins associated with MDM2 in n

3 p300, but not its acetylase-defective mutant AT2, stimulated p63gamma-dependent tran

4 Transfection of an acetylation-defective mutant of ChREBP (ChREBP(K672A) ) in HepG2 cel

5 We examined the functions of an acetylation-defective mutant of GATA-1 in maturing erythroid cells.

6 Notably, p53(3KR), an acetylation-defective mutant that fails to induce cell-cycle arrest,

7 ylation-mimetic S6K1 mutant, the acetylation-defective mutant displays higher affinity toward Raptor,

8 Acetylation-defective mutants are capable of interacting with HATs a

9 Mechanistic studies using acetylation-defective mutants showed that SIRT1 deacetylates and inh

10 types of DNA binding-positive but activation-defective mutants are found: those unable to recruit the

11 not in cells expressing the ligase activity-defective mutant.

12 at significantly reduced rates in adaptation-defective mutants.

13 nt of LX by Ku is impaired in an adenylation-defective mutant providing further evidence that LX inte

14 Strain YS and a derived cellulose adhesion-defective mutant strain, AD2, played pivotal roles in de

15 red similar Th17 responses, whereas adhesion-defective mutants of these microbes failed to do so.

16 119 of the PAS domain and found 72 aerotaxis-defective mutants, 24 of which were gain-of-function, si

17 Arabidopsis ago1-25, ago2-1, and zip-1 (AGO7-defective) mutants, respectively.

18 a-toxin-deficient mutant (DU1090), or an Agr-defective mutant (ISP546) deficient in production of mul

19 al patients revealed that recovery of an agr-defective mutant from blood was usually predicted by the

20 us was killed rapidly by daptomycin, but Agr-defective mutants survived antibiotic exposure by releas

21 Furthermore, agr-defective mutants were found in uninfected nasal carrier

22 found to remain essential, since an assembly-defective mutant of HIV CA, M185A, abolished assembly wh

23 , wild-type HCV core did not rescue assembly-defective mutants.

24 ATPase-defective mutant, Mot1(D1408N), which inhibits growth wh

25 Moreover, when the ATPase-defective mutant R635A or R638A is mixed with the Walker

26 The ATPase-defective mutant T123A interfered in trans with the in v

27 enotype seen with two additional Cdc6 ATPase-defective mutants.

28 Overexpression of lethal, ATPase-defective mutants in a wild-type strain resulted in domi

29 The ATPase-defective mutants of Prp16 and Prp22 bound to spliceosom

30 of these nine acid tolerance response (ATR)-defective mutants revealed that mutations in gshB, hepA

31 to identify motility-independent attachment-defective mutants.

32 Autoaggregation-defective mutants from three different pools were identi

33 ants, hook-length control in an autocleavage-defective mutant of flhB, the protein responsible for th

34 cal characterizations of the automethylation-defective mutant and CARM1DeltaE15 reveal overlapping ye

35 The p21waf1/cip1-binding-defective mutant of MDM2 was unable to degrade p21waf1/c

36 sk through the reconstitution of Csk binding-defective mutant of VE-cadherin also diminished Src acti

37 The DNA binding-defective mutant ARID1a subunit is stably expressed and

38 DHX33 overexpression, but not a DNA binding-defective mutant, enhanced 47S rRNA synthesis by promoti

39 nally, wild-type Tal1, but not a DNA binding-defective mutant, rescued the proliferative defect in Ta

40 n resistant ob/ob mouse strain a DNA-binding-defective mutant of XBP-1s, which does not have the abil

41 By contrast, an effector binding-defective mutant of Rnd3 when overexpressed undergoes tu

42 Both LT-IIb-B(5) and a GD1a binding-defective mutant (LT-IIb-B(5)(T13I)) could modestly bind

43 g with GD1a, in contrast to the GD1a binding-defective mutant, which moreover fails to activate TLR2

44 eptor (IGF1R)) and that the integrin binding-defective mutant of IGF1 (R36E/R37E) is defective in sig

45 d when a naturally occurring, ligand binding-defective mutant of TTP was used.

46 wild-type InsP(3) receptors, but not binding-defective mutant receptors, were polyubiquitinated in a

47 Using the p53 binding-defective mutant of E6 and p53 RNAi, we show that p53 re

48 in was replaced by the polyubiquitin binding-defective mutant, OPTN(D477N/D477N).

49 wild-type PA (WT-PA) and a receptor-binding-defective mutant (Ub-PA) were cleaved to PA63 independen

50 the TNFR-associated factor 6 (TRAF6) binding-defective mutant IRAK2[E525A] or the catalytically inact

51 ombinant TIFA protein, but not TRAF6-binding-defective mutant, can activate IKK in crude cytosolic ex

52 knock-in mice expressing a ubiquitin-binding-defective mutant of ABIN1 (ABIN1[D485N]) develop autoimm

53 Of the five ICAM-1 binding-defective mutants, four had normal or even stronger inte

54 a molecular basis for generating ACK binding-defective mutants of Cdc42 to delineate ACK-mediated sig

55 wild-type Rvs167 but not calmodulin-binding-defective mutants.

56 es, as cyclin-dependent kinase (CDK) binding-defective mutants are capable of stimulating treslin pho

57 p75 to levels observed for chromatin-binding-defective mutants.

58 Cells expressing p185/Cul7-binding-defective mutants of TAg were unable to grow to high den

59 ding to pRb and p53, these p185/Cul7-binding-defective mutants of TAg were unable to transform primar

60 ion induced apoptosis, whereas CXCR4 binding-defective mutants did not.

61 with wild type DEC1 but not its DNA binding-defective mutants.

62 Analysis of binding-defective mutants showed that the Mps3-H2A.Z interaction

63 RNA-binding-defective mutants demonstrate clear separation of functi

64 An isolated S. gordonii::Tn917-lac biofilm-defective mutant contained a transposon insertion in an

65 igation of an S. gordonii::Tn917-lac biofilm-defective mutant isolated by using an in vitro biofilm f

66 An S. gordonii::Tn917-lac biofilm-defective mutant was isolated by using an in vitro biofi

67 formation on polystyrene, a putative biofilm-defective mutant was isolated.

68 We now describe the construction of a BspA-defective mutant of B. forsythus.

69 Cap-defective mutants efficiently produced the leader RNA, b

70 of wild-type USP7 but not its catalytically-defective mutants deubiquitinates Poleta and increases i

71 A checkpoint-defective mutant protein, Rad17(K118E), which has simila

72 A maturation cleavage-defective mutant of FHV, however, did not.

73 nd the reversible properties of the cleavage-defective mutant, N omega V provides an excellent model

74 In the X. nematophila colonization-defective mutant nilD6::Tn5, the transposon is inserted

75 reiterative use of STM, whereby colonization-defective mutants were assembled into virulence-attenuat

76 ehensive, our analysis identified competence-defective mutants with transposon insertions in genes no

77 Complementation-defective mutants exhibited severe defects in ATPase, he

78 on of ligand binding- and G protein coupling-defective mutant receptors did not significantly improve

79 ation in a Drosophila melanogaster crossover-defective mutant, mei-9.

80 Characterization of crossover-defective mutants has contributed much to our understand

81 es are lost in synapsis-proficient crossover-defective mutants, which often retain SYP-1,2 along the

82 We therefore tested three additional cutin-defective mutants for resistance to B. cinerea: att1 (fo

83 x sites and become diminished or lost in DCC-defective mutants, thereby converting the topology of X

84 nt and -independent mechanisms, as deaminase-defective mutants retain significant anti-retroviral act

85 agocytic uptake in the lysosomal degradation-defective mutants via a pathway requiring cytosolic patt

86 ble genes, but a majority were "derepression-defective" mutants.

87 A dimerization-defective mutant of Nef failed to interact with either C

88 s of cells expressing the JAM-A dimerization-defective mutant proteins revealed diminished beta1 inte

89 e, expression of Snapin-C66A, a dimerization-defective mutant with impaired interactions with SNAP-25

90 rced expression in MEL cells of dimerization-defective mutant Ldb1, as well as wild-type Ldb1, signif

91 In contrast, the Y146S/Y154S dimerization-defective mutant displays a severe dNTPase defect in vit

92 Moreover, dimerization-defective mutants could be initiation-defective without

93 In four non-allelic dorsiventrality-defective mutants in tomato, wiry, wiry3, wiry4 and wiry

94 Finally, certain DSB-defective mutant alleles generated in this study conferr

95 n of wild-type Cdc34p, but not that of an E2-defective mutant of Cdc34p, increased repRNA accumulatio

96 xpression of wild-type c-IAP1, but not an E3-defective mutant, resulted in TRAF2 ubiquitination and d

97 t sufficient because we found three elicitor-defective mutants in which there was a high level of pro

98 adient, which fails to develop in elongation-defective mutants.

99 An embryo-defective mutant of Arabidopsis thaliana was isolated th

100 characterize the Arabidopsis thaliana embryo-defective mutant increased size exclusion limit2 (ise2).

101 s assay system was used to screen for embryo-defective mutants, designated increased size exclusion l

102 efore escape detection in screens for embryo-defective mutants.

103 requently missed in prior screens for embryo-defective mutants.

104 sed the most tolerant accessions with embryo-defective mutants disrupted in chloroplast ribosomal pro

105 In contrast, the endocytic-defective mutant was able to prevent sprout formation in

106 This endocytic-defective mutant was unable to rescue the loss of TEER a

107 EPS-defective mutants or pure MAMPs, such as the flagellin p

108 dified type III LTPs or in transformed exine-defective mutant plants.

109 observed with previously studied exonuclease-defective mutants of the Pol delta.

110 n Xenopus oocytes, both wild-type and export-defective mutant hNMD3 proteins bind to newly made nucle

111 over, p53 null cells that coexpressed export-defective mutants of p53 and HDM2 retained partial compe

112 A farnesylation-defective mutant of Rheb co-immunoprecipitated with and

113 biological activity because a farnesylation-defective mutant of Rheb stimulated S6K1 activation less

114 In contrast, a farnesylation-defective mutant of SpRheb (SpRheb-SVIA) is incapable of

115 Specifically, a fengycin-defective mutant of B. subtilis GS67 lost inhibitory act

116 The flowering-defective mutants fca-1, stm-4, and co-1 showed almost u

117 Here we used a folding-defective mutant of human A1-adenosine receptor as a sen

118 absent in cells transfected with the folding-defective mutant DNA.

119 Folding-defective mutants of the human dopamine transporter (DAT

120 ies to remedy disorders arising from folding-defective mutants of human DAT and of other related SLC6

121 n the N terminus of EBV gH results in fusion-defective mutant gH/gL complexes is striking and points

122 The ARF-GEF-defective mutants gnom-like 1 (gnl1-1) and gnom (van7) a

123 2GPI, P. gingivalis W83, or an arg-gingipain-defective mutant of P. gingivalis (HF18).

124 On the other hand, glyoxalase-defective mutants of Hsp31 were found highly compromised

125 7 or UL21a can partially complement a growth-defective mutant virus lacking both UL21a and UL97, with

126 We found that the expression of a GTPase-defective mutant, DLP1-K38A, in cultured cells led to th

127 fferent Dyn2 forms, when expressed as GTPase-defective mutants, exert markedly different inhibitory e

128 function by ectopic expression of its GTPase-defective mutants causes both halves of the first meioti

129 licensing, because a histone acetylase (HAT)-defective mutant of HBO1 bound at origins is unable to l

130 show that both wild-type WRN and a helicase-defective mutant bind with exceptionally high specificit

131 discerned by the stability of Irr in a heme-defective mutant strain.

132 atory role of HOS1 in hypocotyl growth, HOS1-defective mutants exhibited elongated hypocotyls in the

133 The HRM-defective mutant IrrC29A degraded in the presence of iro

134 udy, we developed a screen to identify Hsp90-defective mutants in E. coli.

135 of wild-type TGase-2 and the GTP hydrolysis-defective mutant was sustained.

136 networks constructed with Arp2/3 hydrolysis-defective mutants were more resistant to disassembly by

137 An initiation-defective mutant form of cosB sponsored efficient proces

138 Initiation-defective mutants of the HCV polymerase can increase de

139 An interaction-defective mutant, dbf4DeltaC, phenocopies fkh alleles in

140 n as DeltaANK-ClipR-59, an AS160 interaction-defective mutant, failed to promote AS160 phosphorylatio

141 and the phosphoinositide lipids interaction-defective mutant antagonize cell proliferation.

142 Expression of a beta-Pix interaction-defective mutant of Pak2 rescued filopodia formation but

143 ot its catalytically inactive or interaction-defective mutants, reduces the ubiquitinated forms of XP

144 pic expression of K13, but not its NF-kappaB-defective mutant or a structural homolog, protected plas

145 pic expression of K13, but not its NF-kappaB-defective mutant or other vFLIPs, strongly stimulated th

146 pic expression of K13, but not its NF-kappaB-defective mutant, suppressed the expression of CXCR4.

147 In contrast, a kinase-defective mutant CDK11(p46M) did not inhibit translation

148 Finally, a kinase-defective mutant of IKKepsilon effectively abrogated NF-

149 were prevented by the expression of a kinase-defective mutant or RNA interference knockdown of Syk.

150 Purified recombinant Plk3, but not a kinase-defective mutant, efficiently phosphorylates PTEN in vit

151 Purified recombinant Plk3, but not a kinase-defective mutant, phosphorylated HIF-1alpha in vitro, re

152 Pharmacological (Go6976) or genetic (kinase-defective mutant) inhibition of PKCalpha markedly inhibi

153 IKKbeta, but not its kinase-defective mutant IKKbeta-K44A, led to this observed stab

154 T cell line with a dominant negative, kinase-defective mutant of Rho kinase diminished Jurkat cell pr

155 Expression of wild-type Plk1 but not kinase-defective mutant promotes the binding of Cdc6 to Cdk1.

156 vitro by His(6)-Plk3, but not by the kinase-defective mutant His6-Plk3(K52R), GST-p53 was recognized

157 e Plk3 in HCT116 p53-/- cells and the kinase-defective mutant Plk3(K91R) in p53+/+ cells induced dela

158 t followed by apoptosis, although the kinase-defective mutant was less effective.

159 nd more moderately with wild type and kinase-defective mutants of TbetaRII.

160 stably transfected with two distinct kinase-defective mutants of c-src.

161 of caspofungin-hypersensitive protein kinase-defective mutants.

162 ach of the stable cell lines in which kinase-defective mutants of c-Src were expressed had reduced le

163 Here we show that the egg laying-defective mutant egl-6(n592) carries an activating mutat

164 Analysis of egg-laying-defective mutants has provided insight into a number of

165 reover, expression of Smurf2CG, an E3 ligase-defective mutant of Smurf2, suppresses the above metasta

166 ear functions because a nuclear localization-defective mutant BMI1 rescued several bioenergetic defec

167 Further characterization of one localization-defective mutant protein [FtsQ(V92D)] revealed an unexpe

168 les that restored plaque formation for lysis-defective mutants of Rz and Rz1 were selected.

169 G2/M-defective mutants of Vpr were not able to deplete MCM10,

170 the community level, we asked whether matrix-defective mutant strains could be coaxed to produce func

171 we show that the infectivity of a maturation-defective mutant of FHV can be restored by viruslike par

172 in SP that restore infectivity to maturation-defective mutant viruses led us to hypothesize that SP m

173 In addition, a methylation-defective mutant of DDB2 displayed diminished nuclear lo

174 Methylation-defective mutants of RCC1 have reduced affinity for DNA

175 was previously shown for VSV cap methylation-defective mutants.

176 ide expression analysis of H3K79 methylation-defective mutants identified only a few telomeric genes,

177 ch emerged from a genetic screen for molting-defective mutants sensitized by low cholesterol.

178 A monoubiquitination-defective mutant form of PCNA fails to interact with Pol

179 ys-163 with Arg yielded a monoubiquitination-defective mutant of IKKbeta that retains kinase activity

180 t IN-INI1 complexes, and the multimerization-defective mutant was unable to form these complexes.

181 Multimerization-defective mutants are also defective for mediating the t

182 In a screen for mutagenesis-defective mutants, we isolated a transposon insertion in

183 translated NCS-1, but not its myristoylation-defective mutant, was found associated with recombinant-

184 ivity and replication, but not that of a Nef-defective mutant.

185 Since the GST-mvhs nuclease-defective mutant protein failed to cleave the synthetic

186 In addition, CtIP nuclease-defective mutants are impaired in Alu-IRs-induced mitoti

187 radiation (IR) sensitivity of mre11 nuclease-defective mutants results from the accumulation of IR-in

188 complementation of a cowpox virus occlusion-defective mutant, its role in occlusion was unknown.

189 An oligomerization-defective mutant of IN, V260E, retained the ability to b

190 is often obtained from studying mutants, OM-defective mutants have not been very informative because

191 Wild-type TBSV or p19-defective mutants initially show a similar infection cou

192 dly reduced in assays using a palmitoylation-defective mutant of FCRL4.

193 The palmitoylation-defective mutant (C574A) failed to promote cell migratio

194 ned by labor-intensive screening for pattern-defective mutants.

195 screen designed to recover severe peroxisome-defective mutants, we isolated a viable allele of the pe

196 ation of wild-type PTEN, but not a phosphate-defective mutant of PTEN, induces apoptosis in these cel

197 The phospho-defective mutant PKD-2(S534A) localizes to cilia, wherea

198 A serine 114 phosphorylation-defective mutant, RIIbeta(S114A), did not form these int

199 A phosphorylation-defective mutant of ChrA [ChrA(D50A)] exhibited signific

200 sion in transgenic mice of a phosphorylation-defective mutant of Shc impaired signaling through the p

201 reatment or overexpressing a phosphorylation-defective mutant RARalphaS77A results in the inhibition

202 ally inactive SK1G82D, and a phosphorylation-defective mutant that does not undergo plasma membrane t

203 trated in experiments with a phosphorylation-defective mutant, caPKD-S916A, which is functionally ina

204 e eps15 mutants, including a phosphorylation-defective mutant, inhibited both virus entry and infecti

205 r(69), confirmed by a BIM-EL phosphorylation-defective mutant (S69G) that increased protein stability

206 al overexpression of a HDAC5 phosphorylation-defective mutant (Ser259/Ser498 were replaced by Ala259/

207 t, after endocytosis occurs, phosphorylation-defective mutant receptors traffic to lysosomes with sim

208 by showing that the PKCdelta phosphorylation-defective mutant, PKCdelta-Y311F, is less able to increa

209 e that overexpression of the phosphorylation-defective mutant PGC-1 alpha (S570A) prevents Ang II-ind

210 and protein turnover of the phosphorylation-defective mutant TH S31A was not altered by cdk5 activit

211 Phosphorylation-defective mutants of R-Ras and TC21 are compromised in t

212 agA knockout mutants or CagA phosphorylation-defective mutants failed to increase MMP10 expression.

213 anistic investigations using phosphorylation-defective mutants revealed that KAP1 Ser473 phosphorylat

214 pili remains uncertain, largely because pili-defective mutants also have cytochrome defects.

215 d appears to be a specific feature of pollen-defective mutants with impaired membrane trafficking.

216 site, by comparison with another polymerase-defective mutant enzyme, namely, R668A DNA polymerase.

217 We previously showed that primase-defective mutants failed to recruit the polymerase catal

218 ed in silico were examined, and a processing-defective mutant was created to explore P30 maturation f

219 The processing-defective mutant exhibited reduced gliding velocity and

220 Processing-defective mutants of Hh are degraded by the same ERAD co

221 ning the impaired Hh signaling of processing-defective mutants, such as those causing human holoprose

222 Using processing-defective mutants of type III NRG1, we demonstrate that

223 a genetic screen for germ-line proliferation-defective mutants, we identified mutations in rpl-11.1 (

224 unrepaired DNA damage, causing recombination-defective mutant mice to be sterile.

225 atocyte elimination, different recombination-defective mutants manifest distinct responses, providing

226 rses a similar membrane pathway as recycling-defective mutant B2ARs.

227 Coexpression of recycling-defective mutant B2ARs also enhanced proteolytic degrada

228 le functioning, restore growth to this redox-defective mutant.

229 In a screen for DNA repair-defective mutants in the fungus Ustilago maydis, a gene

230 ver and suppress the sterility of DSB repair-defective mutants.

231 ph2-and previously characterized PSII repair-defective mutants-exhibited reduced growth under fluctua

232 strain, dl5-29, and other HSV-2 replication-defective mutant strains to protect against genital chal

233 Replication-defective mutants were typed as class I (blocked at inte

234 method to identify intracellular replication-defective mutants.

235 nation by expressing a series of replication-defective mutants of BMV RNA3 in (+) or (-) polarity.

236 Finally, the identification of replication-defective mutants with normal viral assembly phenotypes

237 The replication-defective mutants showed defects in both early and late

238 Two replication-defective mutants (429DA and 460EA) were grossly impaire

239 Of the 42 rereplication-defective mutants analyzed, we were able to clone comple

240 We discovered that resection-defective mutants fail to stop transcription around a DS

241 n-rescue experiments show that a respiration-defective mutant of SOD1 is also impaired in its ability

242 However, other respiratory-defective mutants were no less susceptible to Spm implyi

243 nate immune suppression of recombinant RNase-defective mutants in both cell culture and guinea pig mo

244 Two nick sealing-defective mutants were active in ligase adenylylation an

245 -restored mutant L chains with the secretion-defective mutant H chains rescued secretion of the assem

246 This SH3-defective mutant of MLK3 exhibited increased catalytic a

247 The transduction of NPM shuttling-defective mutants or the loss of Npm1 inhibited the nucl

248 n of a binding defective mutant and a signal-defective mutant rescues signal generation to produce cA

249 n of wild-type LAG-3, but not by a signaling-defective mutant.

250 ssion phenotyping of wild-type and signaling-defective mutant plants, including eds3, eds4, eds5, eds

251 BR signaling-defective mutants of Arabidopsis thaliana were hypersens

252 tumors and tumors expressing EphA2-signaling-defective mutants.

253 ns wild type or each of two hyphal signaling-defective mutants (efg1/efg1 and efg1/efg1 cph1/cph1).

254 chromatic regions of wild-type and silencing-defective mutants of the fission yeast Schizosaccharomyc

255 e analyzed in wild-type plants and silencing-defective mutants.

256 bayanus using a genetic screen for silencing-defective mutants.

257 Expression of a phosphorylation site-defective mutant of 4EBP1 that constitutively binds the

258 There are several spermatogenesis-defective mutants that cause defects in MO morphogenesis

259 The Z sumo-defective mutants were, however, partially defective for

260 Moreover, a sumoylation-defective mutant of HIPK1 (KR5) localizes to the cytopla

261 Mice expressing a SUMOylation-defective mutant of LRH-1 (LRH-1 K289R mice) developed N

262 ion in co-infection experiments, 19 survival-defective mutants were identified.

263 A novel mating-type switching-defective mutant showed a highly unstable rearrangement

264 at DSBs are being repaired in these synapsis-defective mutants.

265 rget host innate immune mechanisms, and T3SS-defective mutants are cleared more efficiently than T3SS

266 ficantly reduced in cells infected with T6SS-defective mutants of B. cenocepacia, suggesting that the

267 of WT Runx2, but not a subnuclear targeting-defective mutant, induces both p21(WAF/CIP1) and p19(ARF

268 to Ty elements were increased in telomerase-defective mutants, potential dicentric translocations an

269 Trafficking-defective mutant HERG protein is a mechanism for reduced

270 and explored potential rescue of trafficking-defective mutants by pharmacological means.

271 ies will be required to separate trafficking-defective mutants from those that alter channel function

272 ncoding HIV-1 tat (but not a transactivation-defective mutant) into these tumor cells increases NF-ka

273 the growth of an HSV-1 VP16 transactivation-defective mutant virus in an HSV viral DNA cotransfectio

274 tably, introduction of a signal transduction-defective mutant RAGE (DN-RAGE) to microglia attenuates

275 The UR2 transformation-defective mutants were differentially impaired compared

276 of wild-type BNIP3, but not a translocation-defective mutant, activated cardiac myocyte death only w

277 d in a secretion-competent but translocation-defective mutant, the YscFD28AD46A strain (expressing Ys

278 ve and swollen state and of the transmission-defective mutant, P73G, under native conditions.

279 and sequence analyses of one such transport-defective mutant revealed that the transposon insertion

280 unusually high number of severely transport-defective mutants.

281 t is dramatically different in the transport-defective mutants L8P and V10P, where the Ton box is fou

282 The other two transport-defective mutants (Y143C and E146C) exhibited low specif

283 s that permitted the growth of a transporter-defective mutant were identified.

284 We show that Set1 trimethyl-defective mutants can rescue a set1Delta slow growth def

285 A number of DNA unwinding-defective mutants were generated.

286 In the Fe uptake-defective mutant iron-regulated transporter1 (irt1), lat

287 carrying an additional vimA gene and a vimA-defective mutant in a different P. gingivalis genetic ba

288 The vimA-defective mutant (FLL451) in the P. gingivalis ATCC 3327

289 owed a phenotype similar to that of the vimA-defective mutant (FLL92) in the P. gingivalis W83 geneti

290 ture's growth phase, in contrast to the vimA-defective mutant P. gingivalis FLL92, which has increase

291 by the growth phase, in contrast to the vimA-defective mutant P. gingivalis FLL92.

292 ar protein fraction, in contrast to the vimA-defective mutant P. gingivalis FLL92.

293 he membrane of P. gingivalis FLL92, the vimA-defective mutant, demonstrated immunoreactivity only wit

294 e protease activity was observed in the vimA-defective mutant, P. gingivalis FLL92, compared to that

295 associated proteins were altered in the vimA-defective mutants.

296 f both P. gingivalis W83 and FLL93, the vimE-defective mutant.

297 racellular fractions from the vimA- and vimE-defective mutants, a monoclonal antibody (1B5) that reac

298 sugar biogenesis in both the vimA- and vimE-defective mutants.

299 n-competent HIV-1 encoding intact Vpr or Vpr-defective mutants.

300 of HBX are biologically important and the X-defective mutants, possibly as attenuated viruses, are n