ライフサイエンスコーパス: synthetic lethal

1 complex, and mutations in the two genes are synthetic lethal.

2 sting of the proteins Hsl1 and Hsl7 (histone synthetic lethal 1 and 7), which are targeted by the mor

3 y the Saccharomyces cerevisiae HSL7 (histone synthetic lethal 7) gene.

4 Here we develop MiSL (Mining Synthetic Lethals), an algorithm that mines pan-cancer h

5 l phosphoinositide PI4,5P(2), we have used a synthetic lethal analysis, which systematically combined

6 nteractions was undertaken using large-scale synthetic lethal analysis.

7 thods for investigating gene interactions by synthetic lethal analysis.

8 y pooled dual-knockout libraries to identify synthetic lethal and buffering gene pairs across multipl

9 gs establish that Rb1 and Skp2 deletions are synthetic lethal and suggest how this lethal relationshi

10 -selection balance conditions for X-autosome synthetic lethals and steriles.

11 The importance of synthetic lethals and, more generally, of synthetic dele

12 e first clinically implemented examples of a synthetic lethal approach for cancer treatment.

13 Thus, our synthetic lethal approach identified USP11 as a componen

14 e for BRCA-PARP synthetic lethality, how the synthetic lethal approach is being assessed in the clini

15 This provides the basis for a novel synthetic lethal approach to cancer therapy.

16 TR inhibitor response and represents a novel synthetic lethal approach to targeting tumour cells.

17 in triple-negative breast cancers by using a synthetic-lethal approach dependent on cyclin-dependent

18 This provides the basis for a novel "synthetic lethal" approach to cancer therapy.

19 In the laboratory, the success of synthetic lethal approaches suggests another possible di

20 ing chemotherapeutic agents, are amenable to synthetic lethal approaches that exploit defects in DSB/

21 Here, we provide an overview of the synthetic lethal approaches that have been employed to s

22 Synthetic lethal approaches to cancer treatment have the

23 delivers rational combinatorial targets for synthetic lethal approaches with a high potential to pre

24 Synthetic lethals are variants at different loci that ha

25 Here we develop a synthetic lethal chemical screen in isogenic KRAS-mutant

26 pos5 utr1 is a synthetic lethal combination rescued by plasmid-borne co

27 ent sporadic tumors to be susceptible to the synthetic lethal combination with PARP inhibitors.

28 pment of JNK inhibitors in DLBCL, ideally in synthetic lethal combinations with inhibitors of chronic

29 Applying the synthetic lethal concept to target non-BRCA-mutant cance

30 Each strain is unable to grow under synthetic lethal conditions when exogenous long-chain fa

31 ng another Z-ring interacting protein, had a synthetic lethal division effect.

32 press both LOF mutations in pha-1 as well as synthetic-lethal double mutants, including lin-35; ubc-1

33 n suppressing chromosomal instability and in synthetic lethal drug combinations inspire optimism that

34 Furthermore, a synthetic lethal drug screen revealed that antagonists o

35 Identifying genetic biomarkers of synthetic lethal drug sensitivity effects provides one a

36 argets in K562 leukemia cells and identified synthetic lethal drug target pairs for which correspondi

37 nexpectedly, rec-1; him-5 double mutants are synthetic-lethal due to a defect in meiotic double-stran

38 Clinical ATR inhibitors (ATRi) elicited a synthetic lethal effect in SS tumor cells and impaired g

39 that have modest SRP deficiencies produced a synthetic lethal effect, suggesting that SecA and SRP mi

40 In contrast to the synthetic lethal effects of hypomorphic ATR suppression,

41 Silencing of FAK or LAMB3 recapitulated the synthetic lethal effects of miR-1298 expression in KRAS-

42 e combined into higher-order strains without synthetic lethal effects.

43 novel and established synthetic enhancers or synthetic lethals for KRAS(MUT) colorectal cancer, inclu

44 We identify BUD31 as a MYC-synthetic lethal gene in human mammary epithelial cells,

45 predictive ability for our reference list of synthetic lethal gene interactions (R = 0.159).

46 nce the accumulation of mutations can expose synthetic lethal gene interactions and oncogene-driven c

47 similar to those that characterize the known synthetic lethal gene pairs.

48 ntification of Wilms tumor 1 (Wt1) as a Kras synthetic-lethal gene in a mouse model of lung adenocarc

49 de RNA interference screen to search for Myc-synthetic lethal genes and uncovered a role for the SUMO

50 Among the strongest synthetic lethal genes, polarity defects are more appare

51 Synthetic lethal genetic analysis has identified MAT2A a

52 ary for vegetative Nam8 function in multiple synthetic lethal genetic backgrounds.

53 mulatory effects on Bni1 activity and have a synthetic lethal genetic interaction in vivo.

54 The yeast synthetic lethal genetic interaction network contains ri

55 When applied to the Saccharomyces cerevisiae synthetic lethal genetic interaction network, we can ach

56 ipl1 cells, and the ipl1-2 mutation exhibits synthetic lethal genetic interaction with sli15 mutation

57 with nim1/cdr1 mutations, suggesting that a synthetic lethal genetic screen could be used to identif

58 The nic96-G3 allele was identified in a synthetic lethal genetic screen with a null allele of th

59 We have used synthetic lethal genetic screens in Schizosaccharomyces

60 ermore, mutants of P32, Nlp, and Nph exhibit synthetic-lethal genetic interactions.

61 NOP12 was identified by complementation of a synthetic lethal growth phenotype in strain YKW35, which

62 Synthetic lethal hits were validated with specific inhib

63 efficiency of CMG disassembly in vivo and is synthetic lethal in combination with a disassembly-defec

64 ian central nervous system, called SLIC, for synthetic lethal in the central nervous system.

65 ing morphogenesis, we performed a screen for synthetic lethals in an unc-34 null mutant background ut

66 Thus, combined loss of Paxx and Xlf is synthetic-lethal in mammals.

67 lymerase (PARP) inhibitors were found to be "synthetic lethal" in cells deficient in BRCA1 and BRCA2

68 significant functional interplay and a novel synthetic lethal interaction among the human RecQ helica

69 significant functional interplay and a novel synthetic lethal interaction among the human RecQ helica

70 ic lethal interactions and compare this with synthetic lethal interaction analysis in Saccharomyces c

71 xt of a transformed genotype may result in a synthetic lethal interaction and the selective death of

72 Here the authors find a synthetic lethal interaction between CDA and the microtu

73 Here, we report a novel synthetic lethal interaction between ctf7 and cdc28.

74 We found a synthetic lethal interaction between cytidine deaminase

75 ic of the genotype e(r)(p1) r(hd1-12) or the synthetic lethal interaction between e(r)(p2) and the No

76 of KRAS-mutant cells, suggesting a druggable synthetic lethal interaction between KRAS and p21(WAF1/C

77 Finally, genetic analyses reveal a synthetic lethal interaction between loss of CDC55 and g

78 We identified and validated a synthetic lethal interaction between MTOR and ponatinib

79 orting tumour cell viability and clarify the synthetic lethal interaction between NUAK1 and MYC.

80 CA1- or BRCA2-defective tumors, based on the synthetic lethal interaction between PARP1 and BRCA1/2-m

81 Here, we describe a synthetic lethal interaction between the C. elegans heli

82 Moreover, there is a synthetic lethal interaction between the disruption of t

83 These results indicate a synthetic lethal interaction between the two terminal re

84 In addition, the method identified a known synthetic lethal interaction between TP53 and PLK1, othe

85 rast, inhibition of MAPK signaling created a synthetic lethal interaction in the setting of menin los

86 Here we identify a synthetic lethal interaction in which H3K36me3-deficient

87 These data uncover a synthetic lethal interaction involving glutathione produ

88 This synthetic lethal interaction is attributable to inhibiti

89 he cohesin complex, STAG2, displays a strong synthetic lethal interaction with its paralog STAG1.

90 non-essential serine-threonine kinase, in a synthetic lethal interaction with MYC.

91 c DNA lesion O(6)-methylguanine and caused a synthetic lethal interaction with the PARP-1 inhibitor o

92 sec34-2 and sec35-1 display a synthetic lethal interaction, a genetic result explained

93 he ATR pathway itself provided the strongest synthetic lethal interaction.

94 53-deficient cancer cells, thus exploiting a synthetic lethal interaction.

95 al, providing mechanistic insights into this synthetic lethal interaction.

96 ious phenotypes, sec and spy mutations had a synthetic lethal interaction.

97 ide reductase subunit, is the target of this synthetic lethal interaction.

98 clinically available drug, revealed a robust synthetic-lethal interaction with native or engineered o

99 Here we demonstrate a "synthetic lethal" interaction between oncogenic BRAF V60

100 -wide RNAi screens in C. elegans to identify synthetic lethal interactions and compare this with synt

101 this study can identify clinically relevant synthetic lethal interactions and that vitamin D recepto

102 These synthetic lethal interactions are suppressed by the SSD1

103 ogram; furthermore, our outcomes uncover new synthetic lethal interactions as potential therapies for

104 tion, we have used this protocol to identify synthetic lethal interactions between genes systematical

105 riptional gene regulators, to identify novel synthetic lethal interactions between miRNA inhibition a

106 rating it in therapeutic strategies that use synthetic lethal interactions between SMARCA4-MAX and SM

107 anticancer therapies should not only exploit synthetic lethal interactions between two single genes b

108 ies for defining mammalian gene networks and synthetic lethal interactions by exploiting the natural

109 We propose that these synthetic lethal interactions can be explored for target

110 In vivo, synthetic lethal interactions have been identified betwe

111 roughput RNA interference (RNAi) to identify synthetic lethal interactions in cancer cells harboring

112 To identify synthetic lethal interactions in cancer cells harbouring

113 nal screens can offer a strategy to identify synthetic lethal interactions in cancer cells that might

114 gen sensitivity, genetic instability and the synthetic lethal interactions of a rad27 rad51 and a rad

115 netic screening efforts to gain insight into synthetic lethal interactions of CDK4/6 inhibitors in br

116 We have performed a large study of the synthetic lethal interactions of the post-Golgi sec muta

117 p-Rho3p interaction does not account for the synthetic lethal interactions or the exocyst assembly de

118 ti-species approach to develop a resource of synthetic lethal interactions relevant to cancer therapy

119 es for their aberrant growth, thus revealing synthetic lethal interactions that could be exploited fo

120 Exploiting synthetic lethal interactions to target recurrent cohesi

121 interaction networks can be used to predict synthetic lethal interactions with accuracies on par wit

122 ALL therapy and support strategies targeting synthetic lethal interactions with Akt and PIM kinases a

123 e, we report a systematic screen to identify synthetic lethal interactions with ATR pathway-targeted

124 We elected to identify synthetic lethal interactions with c-MYC overexpression

125 The toutatis gene exhibits strong synthetic lethal interactions with CtBP.

126 on Nug2-associated particles, and both show synthetic lethal interactions with nug2 mutants.

127 for growth, the grp1Delta mutation displays synthetic lethal interactions with several mutations tha

128 lular responses to these agents and identify synthetic lethal interactions with specific DNA repair f

129 ertook a genome-wide RNAi screen to identify synthetic lethal interactions with the KRAS oncogene.

130 a synthetic genetic array screen to identify synthetic lethal interactions with the yeast CL synthase

131 ction between TP53 and PLK1, other potential synthetic lethal interactions with TP53, and correlation

132 sh the role of acetyltransferase activity on synthetic lethal interactions, and (6) identify new func

133 cting nutrient rescue of essential genes and synthetic lethal interactions, and we provide detailed p

134 nd rmi1 mutants display the same spectrum of synthetic lethal interactions, including the requirement

135 ATR inhibitors exhibit synthetic lethal interactions, with deficiencies in the

136 ed to the identification of new, deleterious synthetic lethal interactions.

137 cation of genetic suppressors, enhancers and synthetic lethal interactions.

138 La cells, resulting in networks of conserved synthetic lethal interactions.

139 This model incorporates the concepts of synthetic-lethal interactions and mutation loads to expl

140 rmacological accessibility of many candidate synthetic-lethal interactions and the swift emergence of

141 Systematic analysis identifies synthetic-lethal interactions as most informative for fu

142 we explore an approach to identify potential synthetic-lethal interactions by screening mutually excl

143 ec28 Delta mutation displays allele-specific synthetic-lethal interactions with alpha-COP mutations:

144 LST1 showed synthetic-lethal interactions with the complete set of C

145 In addition to known synthetic-lethal interactions, this approach uncovered t

146 dentified a mutation in SAC3 in a screen for synthetic lethal interactors.

147 Strains with a deletion of SLK19 (synthetic lethal Kar3p gene) exhibit abnormally short mi

148 , sensitize tumors to radiation, and mediate synthetic lethal killing of BRCA2-deficient cancer cells

149 tion of the EZH2 methyltransferase acts in a synthetic lethal manner in ARID1A-mutated ovarian cancer

150 ma-mediated drug resistance and can act in a synthetic lethal manner in the context of tumor-stroma i

151 cogenic phenotypes caused by mutant p53 in a synthetic lethal manner.

152 , were well tolerated in vivo and acted in a synthetic-lethal manner to induce apoptosis in human gli

153 after CDK inhibition and contributes to this synthetic-lethal mechanism.

154 ght into the roles of Ste20p, we have used a synthetic lethal mutant screen to identify additional ge

155 mbrane-anchored Ipk1 rescued a gle1-2 ipk1-4 synthetic lethal mutant.

156 novel activators of Cdc2 kinase, we screened synthetic lethal mutants in a cdc25-22 background at the

157 le-deletion studies identified a total of 47 synthetic lethal mutants involving 67 different metaboli

158 ein function in A. nidulans, we searched for synthetic lethal mutations that significantly reduced gr

159 A screen for synthetic lethal mutations was carried out with an rtf1

160 Using a genetic approach to isolate lin-35 synthetic-lethal mutations, we have identified redundant

161 null allele yielded five recessive csl (cep1 synthetic lethal) mutations, each defining a unique comp

162 myces cerevisiae) osmosensor mutants lacking Synthetic Lethal of N-end rule1 and SH3-containing Osmos

163 The spc98-63 allele is synthetic lethal only with spc110 alleles that encode mu

164 way in p53-deficient cells can induce such a synthetic lethal outcome.

165 subtilis MurJ (murJBs; formerly ytgP) are a synthetic lethal pair.

166 ual and biological screening against several synthetic lethal pairs to explore whether two-compound f

167 hen identify over one million putative human synthetic lethal pairs to guide experimental approaches.

168 ilico methods to guide the identification of synthetic lethal pairs.

169 rns that persist across species, to identify synthetic lethal pairs.

170 The synthetic lethal paradigm has provided a framework for t

171 ukemias, and prostate cancer, as a potential synthetic lethal partner of the DNA repair protein polyn

172 To identify this factor, we screened for synthetic lethal partners of MOP family members using tr

173 e used systematic RNA interference to detect synthetic lethal partners of oncogenic KRAS and found th

174 Ras-dependent and -independent lines uncover synthetic lethal partners of oncogenic Ras.

175 This supports an alternative paradigm for synthetic lethal partnerships that could be exploited th

176 We found that both the synthetic lethal phenotype and the genetic instability p

177 This synthetic lethal phenotype can be suppressed by disrupti

178 2Deltalinker constructs exhibited a specific synthetic lethal phenotype in cells lacking CPR7.

179 skeleton architecture, induced a conditional synthetic lethal phenotype in combination with doa4-10 i

180 ATM loss of function can produce a synthetic lethal phenotype in combination with tumor-ass

181 ed specific defects in DNA replication and a synthetic lethal phenotype in the absence of DNA damagin

182 A synthetic lethal phenotype was observed when five phosph

183 he major periplasmic protease DegP confers a synthetic lethal phenotype, presumably due to the toxic

184 of a shm2Delta ade3 strain) complemented the synthetic lethal phenotype, thus revealing a novel metab

185 0/dpy-22 mutant background produced a strong synthetic lethal phenotype.

186 omosome structure and partitioning) caused a synthetic lethal phenotype.

187 gene with a mukB null mutation resulted in a synthetic lethal phenotype.

188 oss of the cold-sensitive and beta-dependent synthetic lethal phenotypes associated with increased le

189 lleles were constructed and shown to exhibit synthetic lethal phenotypes, similar to those observed i

190 to the problems of identifying essential and synthetic lethal reactions and minimal media.

191 /lox);Skp2(-/-) embryos, demonstrating their synthetic lethal relationship at a cell autonomous level

192 tifunctional mediator of HR, and establish a synthetic lethal relationship between DEK loss and NHEJ

193 d on E11.5, establishing an organismal level synthetic lethal relationship between Rb1 and Skp2 On E1

194 Our results reveal a synthetic lethal relationship between the HR pathway and

195 feration, simultaneous inhibition uncovers a synthetic lethal relationship between these two oncogeni

196 cells with either mutation alone indicates a synthetic lethal relationship between this actin allele

197 sults of this study indicate that there is a synthetic lethal relationship between UBB and UBC that h

198 It is unclear whether a similar synthetic lethal relationship exists between defects in

199 essary and sufficient for the ABT-737-shDhx9 synthetic lethal relationship.

200 severe loss of cell viability, indicating a synthetic lethal relationship.

201 tant alleles fail to grow and thus display a synthetic lethal relationship.

202 Our screen was designed to identify synthetic lethal relationships between translation facto

203 mRNA export defect of the Deltap15 rae1-167 synthetic lethal S. pombe strain, suggesting that the NE

204 We performed a small synthetic lethal screen and identified a compound (macbe

205 Here, we use a genome-wide RNAi-synthetic lethal screen and transcriptomic profiling to

206 By uncovering genetic interactions, the synthetic lethal screen described here provides an attra

207 line, was employed in a paclitaxel-dependent synthetic lethal screen designed to identify gene target

208 e of these drugs, we conducted a genome-wide synthetic lethal screen for candidate olaparib sensitivi

209 A mad1Delta synthetic lethal screen identified 16 genes whose deleti

210 An arf1 synthetic lethal screen identified DRS2/SWA3 along with

211 An arf1Delta synthetic lethal screen identified SWA3/DRS2, which enco

212 Using a synthetic lethal screen in human PDAC cells, we identifi

213 tial U1 snRNP protein Prp40p, we performed a synthetic lethal screen in Saccharomyces cerevisiae.

214 Using a synthetic lethal screen of a RNAi library of nuclear enz

215 cohesion components, we analyzed a ctf4Delta synthetic lethal screen performed on microarrays.

216 A synthetic lethal screen resulted in the isolation of siw

217 9p, a novel mRNA export factor from the same synthetic lethal screen that led to the identification o

218 tial nature of TFIIS encouraged the use of a synthetic lethal screen to elucidate the in vivo roles o

219 We have undertaken a synthetic lethal screen to identify mutations that enhan

220 e we report the results of a small molecule, synthetic lethal screen using mouse embryonic fibroblast

221 Here, we report a synthetic lethal screen with a library of deubiquitinase

222 visiae SWA2 gene, previously identified in a synthetic lethal screen with arf1, was cloned and found

223 hese three components, we have carried out a synthetic lethal screen with cdc9-p, a DNA ligase mutati

224 In a synthetic lethal screen with the mitochondrial heat shoc

225 Using a synthetic lethal screen with the nucleoporin NUP1, we ha

226 er understand dim1p function, we undertook a synthetic lethal screen with the temperature-sensitive d

227 or Pol30p in yeast) activity, we performed a synthetic lethal screen with the yeast pol30-104 mutatio

228 lin 1, we performed an unbiased, genome-wide synthetic lethal screen with yeast cells lacking profili

229 In a synthetic lethal screen, pan-PI3K inhibition synergized

230 From a high throughput synthetic lethal screen, we identified a small molecule,

231 Using a synthetic lethal screen, we identified residues of YidC

232 Using data from a genome-wide shRNA synthetic lethal screen, we show that BRCA1 and members

233 ore about Mot3 function, we have performed a synthetic lethal screen.

234 n redundantly in cytokinesis, we conducted a synthetic-lethal screen in a septin-deficient strain and

235 We report here a synthetic-lethal screen in Caenorhabditis elegans that o

236 A synthetic-lethal screen uncovered genetic interactions b

237 eins that function in the absence of Sgs1, a synthetic-lethal screen was performed.

238 T301) by using a small interfering RNA-based synthetic lethal screening method.

239 er of correlative studies, here we develop a synthetic lethal screening methodology for the mammalian

240 We demonstrate the usefulness of synthetic lethal screening of a conditionally BCL6-defic

241 ced 14-3-3 protein levels were identified by synthetic lethal screening.

242 We used synthetic lethal screens in budding yeast to identify mu

243 to whole-genome forward-genetic analysis and synthetic-lethal screens.

244 o these drugs, we performed a PARP-inhibitor synthetic lethal short interfering RNA (siRNA) screen.

245 ete set of haploid deletion mutants revealed synthetic lethal/sick phenotypes with genes involved in

246 Similarly, a synthetic lethal siRNA screen conducted in a broad panel

247 A PARP1/2 inhibitor-synthetic lethal siRNA screen revealed that ERCC1 defici

248 elop novel drug combinations, we conducted a synthetic lethal siRNA screen using a library that targe

249 Using a genome-wide synthetic lethal siRNA screen, we identified the folate

250 These results highlight the potential of synthetic lethal siRNA screens with chemical inhibitors

251 genes in a given cancer and targeting their synthetic lethal (SL) partners.

252 ild-type or mutant PIK3CA to search for PI3K synthetic-lethal (SL) genes.

253 Here, we show that dut recA mutants are synthetic-lethal; specifically, dut mutants depend on th

254 Synthetic sick or synthetic lethal (SS/L) screens are a powerful way to id

255 RNAs after genetic depletion of SRP40 in the synthetic lethal strain indicating that it is indeed the

256 irect targeting of MYC has remained elusive, synthetic lethal strategies are attractive.

257 We found that the synthetic lethal strategy employing dinaciclib and nirap

258 x vivo and in vivo, representing a promising synthetic lethal strategy for treating the disease.

259 cell cytotoxicity can be achieved through a synthetic lethal strategy using poly(ADP)-ribose polymer

260 otoxic agents or PARP inhibitors following a synthetic lethal strategy.

261 Our data therefore identify a new synthetic-lethal strategy to selectively target cancer c

262 results identify viral transformation-driven synthetic lethal targets for therapeutic intervention.

263 In a search for potential synthetic-lethal targets for FLCN using a phosphatase si

264 pient miRNA technology to the aforementioned synthetic lethal therapeutic strategies.

265 te that cellular context will be critical to synthetic-lethal therapies.

266 s olaparib, have been proposed to serve as a synthetic lethal therapy for cancers that harbor BRCA1 o

267 ifying small molecule compounds that (1) are synthetic lethal to mutant KRAS, (2) block KRAS/GEF inte

268 nce (RNAi) screen to identify genes that are synthetic lethal to the IDH1(R132H) mutation in AML and

269 stance and myelosuppression attributed to a 'synthetic lethal toxicity' arising from simultaneous inh

270 represents a promising approach for inducing synthetic lethal vulnerability in cells harboring otherw

271 Using a random screen for synthetic lethals we found a ppGpp-dependent functional

272 In Escherichia coli, the synthetic lethal with a defective Min system (SlmA) prot

273 addressing the molecular mechanism of SlmA (synthetic lethal with a defective Min system)-mediated N

274 e-specific endonuclease ERCC1-XPF (ERCC4) is synthetic lethal with ATR pathway inhibitors.

275 utation rate at the yeast CAN1 locus, and is synthetic lethal with both proofreading deficiency and m

276 rd with these data, 1 and 3 were found to be synthetic lethal with certain mutations in DNA DSB repai

277 Each synthetic lethal with clf1Delta2 (slc) mutant is splicin

278 We also show that loss of DBP2 is synthetic lethal with deletion of the nuclear RNA decay

279 Deltasrs2 is also synthetic lethal with Deltarhp54, another homologous rec

280 Synthetic lethal with Dpb11-1 (Sld2) is required for the

281 Here we report that ATM loss-of-function is synthetic lethal with drugs inhibiting the central growt

282 ile removal of uracil catabolism alleles was synthetic lethal with eogt knock-down.

283 ATM (ataxia telangiectasia mutated) as being synthetic lethal with FLT3 inhibitor therapy.

284 gues report that oncogenic MYC activation is synthetic lethal with inhibition of the core spliceosome

285 sistent with this observation, ldb18Delta is synthetic lethal with mutations affecting the Kar9 spind

286 o mediate single-stranded DNA (ssDNA) and is synthetic lethal with mutations in other key recombinati

287 e F-BAR protein Cdc15, and for3 deletion was synthetic lethal with mutations that cause defects in co

288 e temperature-sensitive mutation cdc25-22 is synthetic lethal with nim1/cdr1 mutations, suggesting th

289 athway reduction to 16% of normal levels was synthetic lethal with oncogenic Ras expression in cultur

290 Defining processes that are synthetic lethal with p53 mutations in cancer cells may

291 genes, including pbp1Delta, were found to be synthetic lethal with pfy1Delta.

292 two snr7 alleles, U5A and U6A, are dominant synthetic lethal with prp18 alleles.

293 els of Ras signaling, like RAS2(val19), were synthetic lethal with sin4.

294 In contrast, the spc97 alleles are synthetic lethal with spc110 alleles that encode mutatio

295 targeting the Na(+)/K(+)-ATPase (ATP1A1) is synthetic lethal with STK11 mutations in lung cancer.

296 lymerase and aurora kinase inhibitors may be synthetic lethal with the common aberrations in DNA dama

297 A screen for mutations synthetic lethal with xrn1Delta identified a mutation in

298 g the nuclear guanylyltransferase, were also synthetic lethal with xrn1Delta, whereas mutations in PR

299 In BY4741, rrp44-exo was synthetic-lethal with loss of the cytoplasmic 5'-exonucl

300 s, in which DNA nicks become detectable, are synthetic-lethal with recA inactivation, substantiating