ライフサイエンスコーパス: suppressor mutation

1 e proliferation marker Ki-67, or a p53 tumor suppressor mutation.

2 the tumor suppressor fat, and a novel tumor-suppressor mutation.

3 ght act in synergy with VX-809 or the R1070W suppressor mutation.

4 extent with T7 DNA polymerase harboring the suppressor mutations.

5 y be disrupted in the presence of additional suppressor mutations.

6 ively, were obtained only in the presence of suppressor mutations.

7 interaction with IQGAP1 was restored by the suppressor mutations.

8 lar chemical conditions that demand specific suppressor mutations.

9 ased approach was used to design second-site suppressor mutations.

10 orming a large-scale analysis of spontaneous suppressor mutations.

11 ntent per cell was common to all three known suppressor mutations.

12 pressor activity and were interspersed among suppressor mutations.

13 hy1 null mutants carrying extragenic nuclear suppressor mutations.

14 s to understand the mechanism of second-site suppressor mutations.

15 e, which we exploited to isolate second-site suppressor mutations.

16 election for isolates containing second-site suppressor mutations.

17 n the So and T* cores are indeed second-site suppressor mutations.

18 vel base changes in the So and T* cores were suppressor mutations.

19 se resulted in the appearance of spontaneous suppressor mutations.

20 ctivated by the incorporation of second-site suppressor mutations.

21 ns can revert to nonmucoidy in vitro through suppressor mutations.

22 ay can be lethal in the absence of secondary suppressor mutations.

23 rough alternative interactions formed by the suppressor mutations.

24 that are 100% conserved and those altered by suppressor mutations.

25 umvented by the acquisition of certain tumor suppressor mutations.

26 mitigated to varying extents by second-site suppressor mutations.

27 n of spherical cells and the accumulation of suppressor mutations.

28 with small molecule correctors or intragenic suppressor mutations.

29 erature, and the introduction of second site suppressor mutations.

30 We show that lptE6 and both suppressor mutations affect the assembly of the LptD/E c

31 Because multiple suppressor mutations alleviate the constraint imparted b

32 The suppressor mutations allowed export of the native Esheri

33 The alterations resulting from the suppressor mutations also provide insight into the molec

34 R together with the already recognized I539T suppressor mutation, also in the structurally diverse re

35 nactivation were alleviated by a second-site suppressor mutation and which exhibited restricted iron

36 sorder is not restored by stabilizing global suppressor mutations and thus leads to an evolutionary c

37 Like classical tumor suppressors, mutations, and/or loss of GRIM-19 expressio

38 Plants with these intragenic suppressor mutations appear similar to wild-type plants,

39 The suppressor mutations appear to be reduction-of-function

40 Using homology modeling, we show that the suppressor mutations appear to map on one face of the CB

41 diminished if cells with only oncogene/tumor suppressor mutations are also present in the population,

42 at BRCA1 is required for cell proliferation, suppressor mutations are believed to modify BRCA1 phenot

43 All suppressor mutations are extragenic and map to either rp

44 The suppressor mutations are in MSS51, a gene previously imp

45 The suppressor mutations are located in the second and third

46 In some cases, second-site suppressor mutations are needed to confer near-normal be

47 Eighteen of the suppressor mutations are new alleles of spe-6, a previou

48 However, techniques for mapping suppressor mutations are not available for most bacteria

49 Suppressor mutations are used widely to assess protein i

50 Surprisingly, new ahpC suppressor mutations arose in a DeltagshA DeltatrxB stra

51 ined by genetic (terminase-portal intergenic suppressor mutations), biochemical (column retention of

52 Spontaneous suppressor mutations blocking lamotrigine activity mappe

53 While this suppressor mutation broadly impeded SecB-dependent secre

54 Finally, none of these suppressor mutations bypassed fl uG loss-of-function mut

55 Our findings illustrate how tumor suppressor mutations can modulate the immune milieu of t

56 Further, suppressor mutations can then be easily acquired to rest

57 Many of the suppressor mutations caused constitutive receptor activi

58 in close proximity and that the second-site suppressor mutations cluster to one region of the transp

59 ains, we identified colonies which contained suppressor mutations (cmp) which bypassed the requiremen

60 These suppressor mutations concomitantly cause initiation inhi

61 Thirteen of these suppressor mutations confer phenotypes of their own and

62 The cytoplasmic suppressor mutations conferred SDS sensitivity and parti

63 However, intragenic suppressor mutations could be isolated that bypass the r

64 Suppressor mutations (cxs) were isolated that bypass the

65 The suppressor mutation (D79A) appears to partly alleviate t

66 The suppressor mutations define new alleles of ACT1 and TPM1

67 Four suppressor mutations disrupted the Rho-specific guanine-

68 in the viral chromosome; (ii) the extragenic suppressor mutation does not affect neurovirulence; and

69 Two suppressor mutations, E1 A78T and NS3 Q221L, were furthe

70 Furthermore, we show how a second suppressor mutation (E247Q) cooperates with H80R in prot

71 The suppressor mutations either directly changed packing aro

72 These intragenic suppressor mutations, either alone or in combination, re

73 A suppressor mutation, encoding a substitution of threonin

74 irus following intracranial inoculation, the suppressor mutation enhanced virus growth in the cornea,

75 One suppressor mutation, F119S, in the GAF domain restores i

76 ing the NS1 RQ10NK mutation, we identified a suppressor mutation (F86C) in NS4B, a virally encoded tr

77 We propose that these novel suppressor mutations function by decreasing the efficien

78 ectious mutant (K(6)A/K(7)A) that produced a suppressor mutation (G(1)R) and a novel 2B^2C(ATPase) cl

79 be partially rescued by the addition of two suppressor mutations (glutamine 227 to arginine [Q227R]

80 Strains carrying the ACC1 suppressor mutation have reduced Acc1 activity in vitro

81 Analyses of suppressor mutations have been extremely valuable in und

82 Strikingly, the suppressor mutations highlight that restoration of commu

83 The vast majority of the suppressor mutations, however, unexpectedly occurred in

84 n of DeltaF508 was mitigated by each of five suppressor mutations, I539T, R553M, G550E, R555K, and R1

85 n analysis in a visR mutant and isolation of suppressor mutations, identified three diguanylate cycla

86 Further, a suppressor mutation in a glycopeptidolipid synthesis gen

87 ne, thus presenting an example of an in vivo suppressor mutation in a mammalian model.

88 Here we characterize a growth suppressor mutation in eIF2beta that prevents eIF5 GDI a

89 lethality rate is modified, we identified a suppressor mutation in MOA-1/R155.2, a receptor-protein

90 s and that this block could be released by a suppressor mutation in NS3.

91 mutation and enhance the growth defect of a suppressor mutation in RRM2 of Prp24.

92 itive revertant which was found to contain a suppressor mutation in the crp gene was selected.

93 Here we report isolation of a compensatory suppressor mutation in the lower 50 kDa sub-domain (myo2

94 A temperature-sensitive second-site suppressor mutation in the NTD, A38V, restores infectivi

95 The suppressor mutation in the revertant has been mapped to

96 Suppressor mutations in a putative dibasic ER retention

97 Most importantly, the identification of suppressor mutations in both 2C(ATPase) and the capsid d

98 Although the suppressor mutations in cdc55 affect reductional chromos

99 The cells adapt by acquiring suppressor mutations in cell-division genes or by acquir

100 acps2I mutants contained different secondary suppressor mutations in cps2E, indicating that the initi

101 Suppressor mutations in ctrA bypass the conditional cell

102 d this affinity is partially restored by the suppressor mutations in DNA polymerase.

103 Naturally arising suppressor mutations in dnaC restore strains carrying th

104 n cells) associated with oncogenic and tumor suppressor mutations in EGFR pathway genes in human canc

105 The suppressor mutations in gene 5 are necessary and suffici

106 We have focused on the suppressor mutations in gene 5 encoding the T7 DNA polym

107 bacter sp., affords a powerful selection for suppressor mutations in genes required for upstream cata

108 We identified binding site and second site suppressor mutations in HIF-2alpha and HIF-1beta, respec

109 the 2009 H1N1 virus has acquired second-site suppressor mutations in its PB2 polymerase subunit that

110 Suppressor mutations in MCM2, which suppress the tempera

111 Suppressor mutations in Mdv1 that restored Dnm1-Mdv1 int

112 ormation/progression in the context of tumor suppressor mutations in mice and possibly in humans.

113 gella rotated freely by Brownian motion, and suppressor mutations in MotA that were immune to MotI in

114 Here, we report on the isolation of suppressor mutations in MTF which compensate for the for

115 etermined the influence of known second-site suppressor mutations in NBD1 on the conformation of this

116 Suppressor mutations in nsP1, nsP2, and nsP3 that restor

117 In contrast to the suppressor mutations in PRP8, loss-of-function mutations

118 igmaB activity in several RsbX- strains with suppressor mutations in rsbT or -U was high during growt

119 ere unstable and readily accumulated primary suppressor mutations in spxB or its positive regulator,

120 nstrate here that sup-39 is a U1 snRNA gene; suppressor mutations in sup-39 are compensatory substitu

121 sfaA1 also differs from other suppressor mutations in that it cannot suppress a fl bA

122 Analysis of the suppressor mutations in the absence of the pathogenic mu

123 Additional suppressor mutations in the acetyl-CoA binding site of p

124 We isolate two separate suppressor mutations in the Art1 C-terminal domain that

125 We previously described suppressor mutations in the dnaA and dnaN genes that had

126 We identified two amino acid suppressor mutations in the first cytoplasmic loop of Ta

127 Conversely, three suppressor mutations in the first nucleotide binding dom

128 ect of inosine can be rescued by second-site suppressor mutations in the genes responsible for the co

129 growth caused by Yki overexpression or tumor suppressor mutations in the Hpo pathway.

130 Here we report that suppressor mutations in the lpdA gene, which encodes the

131 In this work, we identified suppressor mutations in the M1 protein which complement

132 in CFTR folding, a series of misfolding and suppressor mutations in the nucleotide binding and trans

133 Suppressor mutations in the prfB and prfC genes encoding

134 induced by PcrA depletion can be overcome by suppressor mutations in the recombination genes recFOR.

135 we identified spontaneously arising dominant suppressor mutations in the RFC3 gene.

136 Likewise, second site suppressor mutations in the RNA chaperone Hfq elevated t

137 Suppressor mutations in the synthase domain of the bi-fu

138 report the isolation and characterization of suppressor mutations in the Tat translocase that allow e

139 ombinations of prlA and prlG signal sequence suppressor mutations in these genes.

140 t for the predominance of the reversions and suppressor mutations in tumor proviruses by analyzing wh

141 Second-site intragenic suppressor mutations in wee-1.3(gf) restore self-fertili

142 All three revertants carry an R658H suppressor mutation, in one allele of revertants RH1-26

143 The suppressor mutations increased CBF binding in vitro and

144 These suppressor mutations increased secY expression, and this

145 Strikingly, all suppressor mutations increased the hydrophobicity of the

146 of both AcrA and TolC, two-hybrid assays and suppressor mutations indicate that this interaction occu

147 Accordingly, the Switch I and domain II suppressor mutations induce Switch II to adopt a conform

148 Introduction of the V510D misfolding suppressor mutation into CFTRDeltaF508 modestly increase

149 Transduction of these suppressor mutations into wild-type backgrounds confers

150 This suppressor mutation is a substitution of leucine for glu

151 ype phenotypes suggesting that an extragenic suppressor mutation is able to overcome the loss of fimL

152 uing results reveal that the effect of these suppressor mutations is transmitted to the polymerase do

153 One suppressor mutation isolated also exhibited a far-red-sp

154 yck1Delta yck2-ts suppressor mutations isolated within the YCK3 gene ident

155 In combination with studies on second-site suppressor mutations, it appears that some mutants are i

156 ysis of experimental data collected from the suppressor mutation literature.

157 One of the suppressor mutations maps at 19.8 centisomes and is a re

158 utants shed light on the mechanisms by which suppressor mutations may arise in V. cholerae.

159 remarkably distinct ways through which tumor suppressor mutations may contribute to heterogeneity in

160 The second suppressor mutation N239Y, which is located in close pro

161 V203A/N239Y/N268D containing the second-site suppressor mutations N239Y and N268D, which specifically

162 The suppressor mutation N268D results in an altered hydrogen

163 Furthermore, the suppressor mutations not only restore in vivo activity t

164 Extragenic suppressor mutations occur in several genes encoding enz

165 Furthermore, spontaneous suppressor mutations occurred frequently in stunted subc

166 B8 (YJL124c) gene, initially identified as a suppressor mutation of a poly(A)-binding protein (PAB1)

167 A spontaneous suppressor mutation of albB that restored resistance to

168 First, a suppressor mutation of transposase overproduction killin

169 ing CheZ activity, we isolated 10 intragenic suppressor mutations of cheZ21IT that restored chemotaxi

170 Suppressor mutations of clpX (cxs-1 and cxs-2) were isol

171 We then isolated two classes of intragenic suppressor mutations of hot1-4: loss-of-function mutatio

172 oximately 36% of the euchromatic genome) for suppressor mutations of piwi2 and identified six strong

173 e performed a genetic screen for second-site suppressor mutations of the Arabidopsis thaliana highly

174 pump complex was uncovered through isolating suppressor mutations of the mutant TolC protein that map

175 ations, and spontaneously arising intragenic suppressor mutations on intracellular replication, induc

176 ed the effects of the L234A mutation and the suppressor mutations on the interaction of the two subun

177 Here, we report the identification of two suppressor mutations, one in act1, which encodes the chl

178 Three second-site suppressor mutations, one in the switch 1 region of the

179 Suppressor mutations, only some of which resulted in inc

180 but their phenotypes are bypassed by certain suppressor mutations or by overexpression of MsbA, the i

181 Suppressor mutations outside this domain did not decreas

182 The occurrence of spontaneous suppressor mutations potentially required for viability

183 Surprisingly, we also identified a suppressor mutation predicted to lie within the second p

184 The cps2K mutants containing the suppressor mutations produced low levels of high-molecul

185 In the results described here, we show that suppressor mutations produced strains that are capable o

186 idate a pathogenetic role of a common tumour suppressor mutation profile in human primary GBM and est

187 e additional phenotypes that result from the suppressor mutations provide genetic evidence that NIMX(

188 ongation factor function, the rRNA and eIF5B suppressor mutations provide in vivo evidence supporting

189 Suppressor mutations provide potentially powerful tools

190 Seizure-suppressor mutations provide unique insight into the gen

191 the identification of three such second-site suppressor mutations, R165W, R165M, and Y250D.

192 The suppressor mutations reduce LpdA activity, causing the a

193 These suppressor mutations reduce the ribosome affinity of eIF

194 phenotype and from these derived second-site suppressor mutations relieving dependence.

195 re constructed which, after the emergence of suppressor mutations, replicated well in HeLa cells.

196 hogenic mutation, V168M, six of seven of the suppressor mutations rescued the yeast phenotype.

197 Second-site suppressor mutations restore filament assembly, but the

198 Intragenic A208V and A382V suppressor mutations restore Met-tRNA(i)(Met) binding af

199 These M1 suppressor mutations restored infectious virus productio

200 tant genotypes, which included a second-site suppressor mutation, restored the ability of Nef to inte

201 A partial suppressor mutation restores flagellar length to the ift

202 Most of the secondary suppressor mutations resulting from loss of these enzyme

203 Genetic mapping and cloning of one of these suppressor mutations revealed a recessive missense mutat

204 Mapping of these suppressor mutations revealed, surprisingly, that suppre

205 ot synthetase activity or with the stringent suppressor mutations rpoB-A532Delta or rpoB-T563P in the

206 whose viability is recovered via second-site suppressor mutation(s).

207 One suppressor mutation, S107-4B, caused a temperature-condi

208 dence is based on results from an intragenic suppressor mutation screen and domain swapping between t

209 r of the EC-accessible Schiff base form, and suppressor mutations shift the equilibrium back toward t

210 The suppressor mutation, sia1-1, identified as an allele of

211 esulted in emergence of multiple second-site suppressor mutations, singly and in combinations.

212 Mapping residue conservation, suppressor mutation sites, binding data, and deletion an

213 A suppressor mutation specific for the C1402U-A1500G mutan

214 t driver mutations (KRAS and EGFR) and tumor suppressor mutations (STK11 and TP53), microarray-based

215 od shape, revertant alleles with second-site suppressor mutations supported lysis events that were pr

216 sml1 suppressor mutations suppress both the accumulation of D

217 T402A mutation, three independent intragenic suppressor mutations (T235M, S269L and E276K) were isola

218 Although this virus contains an extragenic suppressor mutation that confers enhanced growth in tumo

219 We also identified a suppressor mutation that differs from all previously des

220 ring Sply expression or by introduction of a suppressor mutation that diminishes sphingolipid synthes

221 ific activity of the enzyme, we identified a suppressor mutation that increases the turnover rate to

222 ependent signal peptides along with the prlA suppressor mutation that is defective in signal peptide

223 Together with an intragenic suppressor mutation that mimics benzamide binding, the r

224 A spontaneous extragenic suppressor mutation that overcame the stage I block was

225 nsitized genetic background and identified a suppressor mutation that restored replum development.

226 A suppressor mutation that restores Gpd1 homodimerisation

227 urJ biogenesis; by engineering an intragenic suppressor mutation that restores MurJ biogenesis, we fo

228 A second-site suppressor mutation that restores viral spread to lympho

229 In contrast to the srb9 suppressor mutation that we identified, an srb9Delta mut

230 report the isolation and characterization of suppressor mutations that allow export of an ssTor(KK)-G

231 red from infected cells harbored one or more suppressor mutations that allowed growth in the absence

232 pc) mutant, motA-pc1, was used to select for suppressor mutations that alter other proteins in the tr

233 Suppressor mutations that bypass the requirement for Mcm

234 omarker, based on its association with other suppressor mutations that confer worse prognosis in sarc

235 We have analysed a number of the suppressor mutations that correct such growth problems i

236 enetics methods to confirm the identities of suppressor mutations that could compensate for the origi

237 longatus strain and screened for second-site suppressor mutations that could restore normal circadian

238 Intragenic suppressor mutations that disrupt the misfolded helix or

239 The selective pressure imposed resulted in suppressor mutations that eliminated growth defects.

240 technology to identify spontaneously arising suppressor mutations that enabled disruption of rpoE (wh

241 Suppressor mutations that enhanced swarming in the absen

242 GOGAT and GOGAT/AldA double mutants carrying suppressor mutations that increased amino acid uptake fi

243 However, suppressor mutations that lead to RNR overproduction all

244 Suppressor mutations that map to codon 197 in bamD resto

245 rt, were used as parental strains to isolate suppressor mutations that partially restored sugar trans

246 we carried out genetic screens for dominant suppressor mutations that prevented Su(Raf)1 from suppre

247 ance, we used a genetic approach to identify suppressor mutations that reactivate the avrRps4-trigger

248 cholerae rpoE mutants, more than 75% contain suppressor mutations that reduce production of OmpU, V.

249 Suppressor mutations that rescue temperature-sensitive s

250 brlA activation and conidiation, we isolated suppressor mutations that rescued development in strains

251 in beta-lactam resistance, we characterized suppressor mutations that restore cefuroxime resistance

252 is supported by the finding that intragenic suppressor mutations that restore colonization ability t

253 ion mutagenesis, we screened for second-site suppressor mutations that restore colony-forming ability

254 the cyt-18-1 mutation site and are sites of suppressor mutations that restore splicing, but not synt

255 is defect could be rescued upon isolation of suppressor mutations that restored swarming.

256 s the transition of the transporter, whereas suppressor mutations that weaken this association restor

257 lines that were homozygous for the putative suppressor mutation the proportion of plants becoming in

258 The trans-suppressor mutation, threonine 119 --> methionine 119, w

259 The EXA1-1 suppressor mutation thus improves the growth of ssa1 ssa

260 tation, and sequence analysis identified the suppressor mutation to be in dapD, which encodes tetrahy

261 Despite the inability of the suppressor mutation to suppress the avirulent phenotype

262 e describe the identification of second-site suppressor mutations to rescue the activity of 'intolera

263 The striking proximity of two of the prp8 suppressor mutations to the site of the 5'SS:hPrp8 cross

264 by two pairs of intergenic portal-terminase suppressor mutations, two separate regions of the termin

265 to mucoidy in P. aeruginosa CF149 with algU-suppressor mutation via modulation of RpoD.

266 The suppressor mutation was identified, by map-based and can

267 This suppressor mutation was located in the HBO1 zinc finger.

268 The 2A-N32D suppressor mutation was not allele specific and, by incr

269 basis of an unbiased genome-wide search for suppressor mutations, we conclude that this loss of memb

270 In addition to suppressor mutations, we identified frequent secondary m

271 To identify the suppressor mutations, we used genome-wide single-nucleot

272 The majority of suppressor mutations were found to lie within nsrR, whic

273 Allele-specific suppressor mutations were generated at these residues.

274 Two extragenic suppressor mutations were identified as mapping to the p

275 Second-site suppressor mutations were identified following hydroxyla

276 Suppressor mutations were identified in spxA1 mutant cel

277 No suppressor mutations were identified in the F1 region or

278 In addition, dominant suppressor mutations were identified in the RFC1 and RFC

279 Seven suppressor mutations were identified, four of which map

280 Thirty-five different suppressor mutations were identified.

281 Most of the suppressor mutations were in cps2E, which encodes the in

282 All of the suppressor mutations were in vanS but, unexpectedly, man

283 A total of 1326 suppressor mutations were isolated and analyzed.

284 Highly specific suppressor mutations were isolated not only in lptD but

285 Suppressor mutations were isolated that obviate the requ

286 contribute to Ste2p activation, second-site suppressor mutations were isolated that restored functio

287 various SFV-SIN chimeras were isolated, and suppressor mutations were mapped to AU-rich sequences ad

288 Multiple suppressor mutations were mapped to PA0171, PA1121 (yfiR

289 Second-site suppressor mutations were obtained to primary site mutat

290 Ten intragenic wee-1.3 suppressor mutations were recovered and they form an all

291 With each mutant Sdh1, second-site Sdh1 suppressor mutations were recovered in Sdh1 permitting f

292 Second site suppressor mutations which partially restored resistance

293 The 7151 suppressor mutation, which defines the chloroplast-splic

294 s G270P and T287P permitted the isolation of suppressor mutations, which restored wild type growth.

295 was restored by (i) introducing second site suppressor mutations, which trap SERT in the inward faci

296 in proviruses with reversions or second-site suppressor mutations within the core element.

297 Suppressor mutations within the pH sensor rescued channe

298 ted nonrecombinational mechanisms, including suppressor mutations within the tk coding sequence.

299 Here, we describe suppressor mutations within the transplanted BCoV 32-nt

300 A polar suppressor mutation, within zrpA, restored all tested ph