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combination of mutation in RPN12 ( a lid component gene ) with mutations in RPT1 ( an ATPase genecausessynthetic lethality
the two mutationsresultedin synthetic lethality
a single mutation(passive) was caused bythe synthetic lethality
Only priC mutationscreatedsynthetic lethality
genomic mutationscausesynthetic lethality
Mutations in the RVS genesleadto synthetic lethality
the combination of mutations in the three genescausessynthetic lethality
The combination of the two viable mutations carnation and lightleadsto synthetic lethality
Mutation of conserved residuescausedsynthetic lethality
a single locus mutation(passive) was caused bythe synthetic lethality
mutation at a single locus(passive) was ... caused bythe synthetic lethality
combining a BRCA1/2 mutation and PARP inhibitioncreatessynthetic lethality
recessive lethal mutationsleadingto synthetic lethality
ste20Δ and ste7Δ mutationscausedsynthetic lethality
that genes whose mutations togetherresultin synthetic lethality
a specific interaction between PARP inhibition and BRCA1/2 mutationcan leadto synthetic lethality
mutation of any of the other factors leads to further destabilizationresultingin synthetic lethality
the additional mutation of ScSgs1 / AtRECQ4Aleadsto synthetic lethality
in women with BRCA1/2 mutationleadsto synthetic lethality
p53 mutation and Wee1 inhibition(passive) caused bythe synthetic lethality
thesld and dpb11 - 1 mutations(passive) caused bythe synthetic lethality
21 petite negative mutationsresultin synthetic lethality
20].A combination of this secY mutation and the secG deletionresultedin synthetic lethality
mutations in two genes functioning in two interacting pathways(passive) caused bysynthetic lethality
1.Loss of RKR1 and RTF1leadsto synthetic lethality
simultaneous PARP inhibition and HR deficiencycausessynthetic lethality [ 49,50
PARP inhibition in the presence of BRCA deficiencyleadsto synthetic lethality
combined Δtig::kan and ΔdnaK mutationscausesynthetic lethality
F ) Mutation of SLX1 , SLX4 , MUS81 , and MMS4causessynthetic lethality
disruption of base pairing and not an additional effect of the mutations(passive) was caused bythe synthetic lethality
however , BRCA1/2 mutations compromise HRRresultingin synthetic lethality
either mcs6ts2 or pmh1 - 26 mutations with sep10Δcausedsynthetic lethality
Mitachi T , Targeting p300 addiction in CBP - deficient cancerscausessynthetic lethality
Plasmid combinations indicated with the ' - ' symbolresultedin synthetic lethality
the co‐ablation of kri‐1 ( CCM1 ) and ccm‐3 in C. elegans(passive) caused bythe synthetic lethality
PARP1 inhibitors [ 21(passive) triggered bysynthetic lethality
The presence of a BRCA gene mutation , plus a PARP inhibitorcreatessynthetic lethality
PARP inhibitors in HR - deficient cells(passive) caused bySynthetic lethality
Similar to the loss of ATM , hypomorphic mutations of Mre11 ( Mre11ATLD1ledto synthetic lethality
and rodZ genescausedsynthetic lethality
novel therapeutic approaches to cancer | Molecular Cancer Therapeutics Abstract B24to designnovel therapeutic approaches to cancer | Molecular Cancer Therapeutics Abstract B24
from BEZ235 inhibition of ATR leading to replicative stress in TP53 deficient cellsresultingfrom BEZ235 inhibition of ATR leading to replicative stress in TP53 deficient cells
by combining Olaparib with BRCA2-Rad51 disruptors Falchi , Federico , et al 2017 ACS Chemical Biologytriggeredby combining Olaparib with BRCA2-Rad51 disruptors Falchi , Federico , et al 2017 ACS Chemical Biology
to cell death due to a synergistic effect in an already DDR - deficient background , such as PARP inhibitionleadsto cell death due to a synergistic effect in an already DDR - deficient background , such as PARP inhibition
from specific allele combinationsresultfrom specific allele combinations
by in silico removal of slc14a1 and slc14a2 genescausedby in silico removal of slc14a1 and slc14a2 genes
from an imbalance in the stoichiometry of ETC complexesresultingfrom an imbalance in the stoichiometry of ETC complexes
from inefficient or failed kinetochore assembly and consequent catastrophic increases in chromosome losswould resultfrom inefficient or failed kinetochore assembly and consequent catastrophic increases in chromosome loss
from the loss of both Mus81-Mms4 and Sgs1-Top3resultingfrom the loss of both Mus81-Mms4 and Sgs1-Top3
from multiple mutations in the sterol biosynthetic pathwayresultingfrom multiple mutations in the sterol biosynthetic pathway
in a lethal phenotypeto resultin a lethal phenotype
in part by poor complementation of the sterol intermediates with wild - type sphingolipids , suppression of lethality by mutating YND1 or GDA1is causedin part by poor complementation of the sterol intermediates with wild - type sphingolipids , suppression of lethality by mutating YND1 or GDA1
from such a drastic perturbation of SecY complex structure that suppressors would cause a significant but compensatory alterationcould resultfrom such a drastic perturbation of SecY complex structure that suppressors would cause a significant but compensatory alteration
to our understanding of SecYE structurehad contributedto our understanding of SecYE structure
from the failure to express the essential gene(swould resultfrom the failure to express the essential gene(s
from an inability to repair SSBs by either PARP1-dependent SSB repair or BRCA1/2-dependent HRRresultingfrom an inability to repair SSBs by either PARP1-dependent SSB repair or BRCA1/2-dependent HRR
from simultaneous deletion of PRS1 and PRS5 or PRS3 and PRS5 [ 7,9resultingfrom simultaneous deletion of PRS1 and PRS5 or PRS3 and PRS5 [ 7,9
from the combination of two temperature - sensitive mutations affecting the same essential process , such as DNA replicationresultsfrom the combination of two temperature - sensitive mutations affecting the same essential process , such as DNA replication
from the overexpression of Nop17l[Scer\UAS.Tresultingfrom the overexpression of Nop17l[Scer\UAS.T
from loss of SETD2 and WEE1resultingfrom loss of SETD2 and WEE1
from the combination of the ΔltaS mutation with the ΔtagO mutation , which eliminates WTA ... suggesting that LTA and WTA have complementing essential functionsresultsfrom the combination of the ΔltaS mutation with the ΔtagO mutation , which eliminates WTA ... suggesting that LTA and WTA have complementing essential functions
from an accumulation of DNA lesions in the double mutant cells that might be detectable as genome instability in the viable double mutants , pol3 - 5DE or -5DV with rad27-pcould resultfrom an accumulation of DNA lesions in the double mutant cells that might be detectable as genome instability in the viable double mutants , pol3 - 5DE or -5DV with rad27-p
from combination of a tsa1Δ mutation with defects in postreplication repair or recombinationresultingfrom combination of a tsa1Δ mutation with defects in postreplication repair or recombination
from inhibition of DNA replicationresultedfrom inhibition of DNA replication
from the concomitant inhibition of two independent pathways that are nonessential per seresultingfrom the concomitant inhibition of two independent pathways that are nonessential per se
cell viability that can point to potential cancer treatment targets ( McLornan et al .preventscell viability that can point to potential cancer treatment targets ( McLornan et al .
from the combined effects of tubulin misfolding and defects in microtubule assembly caused by the stu1 - 5 mutationmay resultfrom the combined effects of tubulin misfolding and defects in microtubule assembly caused by the stu1 - 5 mutation
from the driverresultingfrom the driver
DNA damage or prevent DNA repaircauseDNA damage or prevent DNA repair
from PARP1 inhibition and BRCA1 or BRCA2 lossresultingfrom PARP1 inhibition and BRCA1 or BRCA2 loss
in profound tumor cell cytotoxicityresultingin profound tumor cell cytotoxicity
from ELP3 and H4 tail mutationresultingfrom ELP3 and H4 tail mutation
to phase - specific cytotoxic drugscould be createdto phase - specific cytotoxic drugs
in the disintegration of the tumor cell ( Figure 1resultingin the disintegration of the tumor cell ( Figure 1
in its ability to promote cytotoxicity and death of refractory cancers that have mutations in tumor suppressor functionsresultsin its ability to promote cytotoxicity and death of refractory cancers that have mutations in tumor suppressor functions
when mutant KRAS and mutant EGFR are co - expressed in human lung adenocarcinoma ( LUAD ) cells ... revealing the biological basis for the mutual exclusivity of KRAS and EGFR mutations in lung cancersresultswhen mutant KRAS and mutant EGFR are co - expressed in human lung adenocarcinoma ( LUAD ) cells ... revealing the biological basis for the mutual exclusivity of KRAS and EGFR mutations in lung cancers
to functional HRR - mediated DNA repairleadsto functional HRR - mediated DNA repair
from deletion of both regulatory genesresultingfrom deletion of both regulatory genes
from a genomic rather than a plasmid - borne mutationresultedfrom a genomic rather than a plasmid - borne mutation
when mutant KRAS and mutant EGFR are coexpressed in human lung adenocarcinoma ( LUAD ) cells , revealing the biological basis for the mutual exclusivity of KRAS and EGFR mutations in lung cancersresultswhen mutant KRAS and mutant EGFR are coexpressed in human lung adenocarcinoma ( LUAD ) cells , revealing the biological basis for the mutual exclusivity of KRAS and EGFR mutations in lung cancers