ライフサイエンスコーパス: deficient cell

1 ro and in vivo and induced apoptosis in TSC2-deficient cells.

2 hibition of RAD52 leads to lethality in BRCA-deficient cells.

3 level of histone H3K27me3 increases in PRMT5 deficient cells.

4 NA methylation-competent and DNA methylation-deficient cells.

5 -nucleoporins in nuclear envelopes of Torsin-deficient cells.

6 fibers, despite the presence of HU, in BRCA1 deficient cells.

7 forks, resulting in PARPi resistance in BRCA-deficient cells.

8 e activity of NHEJ-DDR proteins in autophagy-deficient cells.

9 of the autophagy-lysosomal pathway in parkin-deficient cells.

10 lum (ER)-targeted mRNA translation in DIS3L2-deficient cells.

11 nhibition leads to robust SL induction in HR-deficient cells.

12 scues YAP1 transcriptional activity in BRCA1-deficient cells.

13 cifically confer topotecan resistance to ATM-deficient cells.

14 o8 mRNAs and Pho8 protein accumulate in zinc-deficient cells.

15 r cellular proliferation, similarly to SETD6-deficient cells.

16 fails to induce EGFR phosphorylation in GP78-deficient cells.

17 of NHEJ-DDR proteins in autophagy- and PTEN-deficient cells.

18 duced DNA virus replication observed in OASL-deficient cells.

19 d hedgehog signaling was decreased in HHIPL1-deficient cells.

20 tochondrial cholesterol accumulation in NPC1-deficient cells.

21 activation of Smad2/3 signaling in autophagy-deficient cells.

22 protein phosphorylation in ETAA1- or TOPBP1-deficient cells.

23 ase pair (bp) slippage mutagenesis in RNH201-deficient cells.

24 ses prevented multiplication of CHPV in RelA-deficient cells.

25 d selectively induce cytotoxicity within MMR-deficient cells.

26 eterminant of response to BETi in SMARCA4/A2-deficient cells.

27 higher rate of proliferation than WT or Nox2-deficient cells.

28 lly inhibiting Fen1 selectively targets BRCA-deficient cells.

29 ntation restored serine biosynthesis in GOT2-deficient cells.

30 pe, PARP-1 activation is undetectable in AAG-deficient cells.

31 ic reduction of the Mn storage capacity in P-deficient cells.

32 novel pathways of PARPi resistance in BRCA2-deficient cells.

33 xpression of IL-12 and IL-1beta in caspase-8-deficient cells.

34 and reduced delivery rate of CSCs in myosin-deficient cells.

35 on of DNA in the cytoplasm of AT and Artemis-deficient cells.

36 ed replication of C. trachomatis even in p53-deficient cells.

37 ws activation of cell signaling events of HS-deficient cells.

38 cellular mechanism, and selectivity for MMR-deficient cells.

39 to Wipi2-positive puncta are reduced in Optn-deficient cells.

40 lls, but only reduced proliferation in Nupr1-deficient cells.

41 , and Erdr1 fails to induce apoptosis in Fas-deficient cells.

42 forks are the entry point for MRE11 in BRCA-deficient cells.

43 endent degradation of stalled forks in Abro1-deficient cells.

44 ored mitochondrial membrane potential in p62-deficient cells.

45 more base substitution mutations in BRCA1/2-deficient cells.

46 bp deletion rearrangement is enhanced in ATM-deficient cells.

47 ithin the sequence context identified in RER-deficient cells.

48 DDX41 only in p53-proficient but not in p53-deficient cells.

49 to-AMPase activity were elevated in the FADD-deficient cells.

50 factor Spt4/Spt5 suppresses TC-NER in Rad26-deficient cells.

51 an overcome the H(2)O(2) sensitivity of Tsa1-deficient cells.

52 stering near the nucleus as seen in TMEM106B-deficient cells.

53 the protein transport protein Sec31A in CRT-deficient cells.

54 inactive and failed to rescue growth of ACO2-deficient cells.

55 d the response to PARP inhibition in BRCA1/2-deficient cells.

56 tegrin-mediated cell adhesion in strumpellin-deficient cells.

57 m by which RFWD3 destabilizes forks in BRCA2-deficient cells.

58 functional analysis of human primary SMARCD2-deficient cells.

59 t of the differentiated phenotype in Poldip2-deficient cells.

60 ium Red and GsMTx4, and attenuated in Piezo1-deficient cells.

61 ) did not rescue RV-A16 replication in STING-deficient cells.

62 thway that is important for survival of BRCA-deficient cells.

63 itro, leading to selective cell death in ATM-deficient cells.

64 tion exacerbates genome instability in BRCA2 deficient cells.

65 s able to rescue MBC differentiation in Hhex-deficient cells.

66 ctivities fail to maintain viability of BRCA-deficient cells.

67 d release of cathepsins B and L in autophagy-deficient cells.

68 endent transcription were decreased in PACRG-deficient cells.

69 RNA in zinc-replete cells to LLT HNT1 RNA in deficient cells.

70 s, though by far not as significant as RAD50-deficient cells.

71 cued cell cycle abnormalities in progranulin-deficient cells.

72 e and Fe-containing metabolic proteins in Fe-deficient cells.

73 hology to naive cells was greater from GCase deficient cells.

74 DNA-PKcs and XLF was diminished in autophagy-deficient cells.

75 ide CRISPR knockout genetic screen in PARP14-deficient cells.

76 successful screens in both wild-type and p53-deficient cells.

77 In cNHEJ-deficient cells, a remarkable ~25% of CSR can be achieve

78 Using LITAF-deficient cells, a second, subsequent whole-genome CRISP

79 -catenin-binding domain of LEF1 in HNF-1beta-deficient cells abolishes the increase in Lef1 transcrip

80 BLM deficient cells accumulate extensive chromosomal aberrat

81 Stalled forks in BRCA2-deficient cells accumulate phosphorylated and ubiquitina

82 TOE1-deficient cells accumulated hTR precursors, including ol

83 ly, elevated intracellular calcium in DIS3L2-deficient cells activates calcium signaling response gen

84 Nherf1-deficient cells also exhibit an altered transcription pa

85 Importantly, HLTF-deficient cells also exhibit reduced double-strand break

86 XRN2-deficient cells also showed enhanced PARP1 activity.

87 alpha induction was attenuated in AMPKalpha2-deficient cells and accompanied by its enhanced hydroxyl

88 , such as diminished PARPi efficacy in BRCA1-deficient cells and altered repair of damaged telomeres,

89 We studied ATP7B-deficient cells and animals to identify strategies to de

90 tolerance, which sustains survival of BRCA2-deficient cells and can be exploited therapeutically thr

91 Phosphorylated TFEB accumulated in STUB1-deficient cells and in tissues of STUB1-deficient mice r

92 nform on mechanism of PARPi resistance in HR-deficient cells and present Dictyostelium as a convenien

93 is abolished in C18orf8-, Ccz1- and Mon1A/B-deficient cells and restored by a constitutively active

94 on of RIPK1 is defective in TAK1- or SHARPIN-deficient cells and restoring phosphorylation protects t

95 s3 encoding galectin-3 was increased in Tsc2-deficient cells and serum of Tsc2cKO(Prrx1)-cre mice.

96 modulator of stalled fork stability in BRCA2-deficient cells and show that codepletion of RFWD3 rescu

97 ER) as a backup pathway for RER in RNase HII-deficient cells and the known mutagenic profile of DnaE,

98 Moreover, Atm-deficient cells and tumors were sensitive to the PARP in

99 TOR signaling pathway is deregulated in CDK8-deficient cells and, accordingly, these cells are highly

100 tors was not observed in G(2)-M arrested p53-deficient cells and, therefore, it seems to represent a

101 pathway as essential for viability of PARP14-deficient cells, and identified regulation of DNA replic

102 uch ubq-pRPA intermediate is formed in BRCA1-deficient cells, and our results suggest that BRCA1 may

103 n maintaining survival of cytidine deaminase-deficient cells, and ribosomal DNA transcription and sta

104 hat regulates tumorigenic properties of Tsc2-deficient cells, and that may serve as a potential thera

105 pite amino acid sufficiency, tRNA-thiolation deficient cells appear amino acid starved.

106 ds into activated CD8(+) T cells, and MFSD2A-deficient cells are at a competitive disadvantage result

107 Here we show that autophagy-deficient cells are defective in NHEJ, as indicated by d

108 Notably, wall-deficient cells are flexible and are able to maneuver th

109 o show that although the mitochondria of SDH-deficient cells are less active per se, their higher mas

110 or efficient stalling of translation because deficient cells are refractory to the inhibition of mTOR

111 We found that BRCA2-deficient cells are selectively dependent on multiple pa

112 In this system, IL-21R-deficient cells are unable to compete with wild-type pop

113 RIPK1-deficient cells are unable to cope with energetic stress

114 t when their mitochondria are uncoupled, SDH-deficient cells are unable to preserve their viability,

115 itor-induced loss of stemness than the BRCA1-deficient cells are.

116 illin, and securin was decreased in DNA-PKcs-deficient cells, as were phosphorylation of Aurora A on

117 TFEB-deficient cells attempt to compensate for this limitatio

118 aperone GRP94 was hyperglycosylated in STT3A-deficient cells, bearing glycans on five silent sites in

119 expression was drastically reduced, but MK2-deficient cells became highly sensitive to necroptosis e

120 dispensable, with all stress defects of Sty1-deficient cells being suppressed by expression of the At

121 MRE11 is highly unstable in PTEN-deficient cells but stability can be significantly resto

122 ARID1B preserves SWI/SNF function in ARID1A-deficient cells, but defects in SWI/SNF targeting and co

123 generation of Ly6G(+) eosinophils from Trib1-deficient cells, but is not sufficient to restore normal

124 otein that promotes fork degradation in BRCA-deficient cells by acetylating H4K8 at stalled replicati

125 Loss of 53BP1 rescues the HR defect in BRCA1-deficient cells by increasing resection, suggesting that

126 iling of MHC-I peptides in wild-type and RQC-deficient cells by mass spectrometry showed that RQC sub

127 iquitinating H2A, promoted apoptosis in BAP1-deficient cells by suppressing expression of the prosurv

128 Adipogenesis defects in PAGR1-deficient cells can be rescued by the ectopic expression

129 Re-expression of PAR-1 in PAR-1-deficient cells combined with a limiting-dilution transp

130 effect toward breast cancer gene 1 ( BRCA1)-deficient cells compared to isogenic BRCA1-proficient ce

131 s severe resection defects of MRE11 nuclease-deficient cells compared to those lacking CtIP.

132 Homologous repair-deficient cells compared with homologous repair-proficie

133 d in human renal angiomyolipoma-derived TSC2-deficient cells compared with TSC2 add-back cells.

134 c stimuli are significantly reduced in GSDME-deficient cells comparing with wild type cells.

135 show here that the depletion of Mdm4 in p53-deficient cells compromises DNA replication fork progres

136 s 5 infection in IFN-alpha-pretreated, ISG15-deficient cells, confirming that resistance was due to t

137 esterol accumulation that characterises NPC1-deficient cells, consistent with direct lysosome to ER c

138 Telomerase activity in TOE1-deficient cells could be rescued by wild-type TOE1 but n

139 Mechanistically, NS-deficient cells demonstrate a significantly reduced HR r

140 effect of HDAC inhibition in DNA methylation-deficient cells demonstrates that DNA methylation and hi

141 We uncovered key deficits in FMRP-deficient cells demonstrating abnormal neural rosette fo

142 internalization of EMCV was observed in TNK2 deficient cells demonstrating that TNK2 functions in EMC

143 usion protein dispersed melanosomes in MyoVa-deficient cells, dendrites were significantly less elong

144 Moreover, Gnaq/Gna11-deficient cells did not respond to purinergic receptor P

145 Strikingly, HIR1-deficient cells display altered transcriptional amplitud

146 Consistently, NEK10-deficient cells display heightened sensitivity to DNA-da

147 These alignment-deficient cells display normal chromosome copy numbers i

148 Notably, N-linked glycans produced by GNE-deficient cells displayed enhanced binding to galectin-1

149 Moreover, FAM173A-deficient cells displayed increased mitochondrial respir

150 SMCHD1-deficient cells displayed reduced ATM S1981 phosphorylat

151 Depleting MRE11 in BRCA2-deficient cells does block fork degradation, but it does

152 The pattern of NF-kappaB dynamics in TRIF-deficient cells does not, however, directly reflect the

153 Induced-expression of SETDB1 in CSB-deficient cells downregulated PAR and normalized mitocho

154 it fails to localize to the midbody in SCCRO-deficient cells during abscission, and its inactivation

155 monstrate that LBPA enrichment in human NPC2-deficient cells, either directly or via its biosynthetic

156 RNase L activity promotes survival of ADAR1 deficient cells even in the presence of MDA5 and MAVS, s

157 TRMT1-deficient cells exhibit decreased proliferation rates, a

158 ent survival differences, we found that Wwox-deficient cells exhibit enhanced homology directed repai

159 MCM8IP-deficient cells exhibit HR defects, especially in long-t

160 SENP3-deficient cells exhibit hypersumoylation of E2F1 and are

161 expression of Il1b and Il12b, but caspase-8 deficient cells exhibited a further decrease in expressi

162 CL-deficient cells exhibited decreased GFP-tagged mitochond

163 RNASEH2-deficient cells exhibited elevated levels of DNA damage

164 These IRF5-deficient cells exhibited impaired influenza virus-induc

165 Using a heterologous NHE6-deficient cell expression system, we show that the bioch

166 Here, we demonstrate that HLTF-deficient cells fail to undergo fork reversal in vivo an

167 However, the primed Helios-deficient cells failed to expand upon secondary challeng

168 highlighting critical roles for ATX in TSC2-deficient cell fitness and in TSC tumorigenesis.

169 In JNK3-deficient cells, Foxo3a is suppressed which leads to Egr

170 In contrast, smArf-deficient cells from mice of the Arf(M45A) strain are as

171 inhibition of mTORC1 signalling rescues ATF4-deficient cells from MYC-induced endoplasmic reticulum s

172 MTCH2 read-through-deficient cells, generated using CRISPR-Cas9, showed inc

173 We found that RAD51D-deficient cells had a reduced capacity for HR-mediated g

174 TSPYL1-deficient cells had prolonged S and G2 phases with reduc

175 cluding human disease, and conclude that PC2-deficient cells have increased susceptibility to cell de

176 We showed previously that Trex1-deficient cells have reduced mammalian target of rapamyc

177 ring mitochondrial replication, with PrimPol-deficient cells having increased mtDNA copy number but d

178 In BRCA1-deficient cells Hippo pathway is "turned On." Phosphoryl

179 les the aberrant proliferation of diverse RB-deficient cells in part by opposing the down-regulation

180 human oncogene-expressing wild-type and p53-deficient cells in physiological oxygen conditions revea

181 alleviates cholesterol accumulation in NPC1-deficient cells in spite of its low binding affinity for

182 as an acquired vulnerability of 53BP1;BRCA1-deficient cells in vitro and in vivo.

183 ively reduces the growth and survival of VHL-deficient cells in vitro and in vivo.

184 the observed hematopoietic defects in METTL3-deficient cells in vitro and in vivo.

185 s, the increase in the mutation frequency in deficient cells included a remarkable contribution of C>

186 Multiple proteins were oxidized in FH-deficient cells, including many metabolic proteins such

187 bal methylation levels was observed in DNMT3-deficient cells, including reproducible focal demethylat

188 e dramatic increase of CC formation in FANCM deficient cells, including the dissolvase complex (BLM-T

189 yrosine kinase (RTK) signaling in SMARCA4/A2-deficient cells, including the oncogenic RTK HER3.

190 Genetic analyses using ATG7-deficient cells indicate that neutrophils secrete IL-1be

191 calized to the vicinity of lysosomes in CLN5 deficient cells, indicating it may have a lysosome-relat

192 Upon RA-mediated differentiation, Oct1-deficient cells induce lineage-appropriate developmental

193 nversely, the high MYC levels present in APC-deficient cells induce phosphorylation of eIF2alpha via

194 t miR-29b acts as an oncogenic miRNA in Tsc2-deficient cells: inhibition of miR-29b suppressed cell p

195 analogous to CFSs, fragile telomeres in BLM-deficient cells involved double-strand break (DSB) forma

196 The secretome of ERK3-deficient cells is defective in chemotaxis of neutrophil

197 te that PALB2 DSB recruitment in BRCA1/53BP1-deficient cells is mediated by an interaction between PA

198 ization of mitochondrial homeostasis in APTX-deficient cells is not available.

199 C18orf8-deficient cells lack Rab7 activation and show severe def

200 21, and a reduction of mature NPCs in Torsin-deficient cells lead us to conclude that the hallmark ph

201 lso showed that IFN-alpha treatment of ISG15-deficient cells led to significant inhibition of global

202 nced GR turnover observed in beta-arrestin-1-deficient cells limits the duration of the glucocorticoi

203 Here, using four different TRAF2-deficient cell lines (A20.2J, CH12.LX, HAP1, and mouse e

204 P. aeruginosa and with CRISPR-generated CD18-deficient cell lines in human monocytes and murine neutr

205 to cause in vitro transformation of Cdkn2ab-deficient cell lines primarily through CDK6 activation.

206 and lack of TCR signaling restoration in LAT-deficient cell lines reconstituted with a synthetic LAT

207 PPM1F-deficient cell lines show constitutive integrin phosphor

208 Here, we demonstrate in several ATM-deficient cell lines that the olaparib and AZD6738 combi

209 itulating previously published data in LEMD2-deficient cell lines, and additional experiments suggest

210 LC3/GABARAP isoforms were expressed in ATG4-deficient cell lines, suggesting that LC3/GABARAP can at

211 nNAc at increasing sialic acid levels in GNE-deficient cell lines.

212 Similar to BRCA1-deficient cells, LMO2-positive DLBCLs and T cell acute l

213 e studies increase our understanding of TSC2-deficient cell metabolism, leading to novel potential th

214 We show that in MAX-deficient cells, MNT binds to MLX, but also forms homodi

215 In MAX-deficient cells, MNT was overexpressed and redistributed

216 Using an IP3R-deficient cell model rescued with each of the three IP3R

217 p53-deficient cells, not expressing p21, failed to induce se

218 IL-1beta/TNF depleted autophagy-deficient cells of ATP, and ATP depletion and cell death

219 wever, such effects were abolished in TRPML1-deficient cells or by TRPML1 inhibitors.

220 essential for maintaining viability of BRCA-deficient cells owing to its ability to promote DNA/RNA

221 In SHARPIN-deficient cells, PACRG prevented LUBAC destabilization,

222 Employing the WASp-sufficient and WASp-deficient cell-pair model of human T and B lymphocytes,

223 Notably, in WRN exonuclease-deficient cells, persistence of RAD51 correlates with el

224 In CSB-deficient cells, poly (ADP ribose) polymerase (PARP) is

225 onfirmed diminished neurogenesis in the MCT8-deficient cell population as well as aberrant migration

226 ISG15-deficient cells pretreated with IFN-alpha were resistant

227 viral glycoproteins fail to mature in SPCA1-deficient cells preventing viral spread, which is eviden

228 TET2 knockdown in BRCA2-deficient cells protected stalled replication forks (RFs

229 urvival and sensitivity to ER stress in USF3-deficient cells provide avenues for therapeutic and adju

230 ission/fusion ratio and proliferation in MCU-deficient cells recovered after MCU restoration or inhib

231 ecrosis factor (TNF)-induced cell death, Rel-deficient cells remained resistant, calling into questio

232 f how RAD52 contributes to viability of BRCA-deficient cells remains unknown.

233 ugs that selectively affect viability of TSC-deficient cells, representing promising candidates for r

234 is poorly understood, it is unclear why BRCA-deficient cells require APE2 for viability.

235 Furthermore, BRCA2-deficient cells require the 5' flap endonuclease but not

236 BRCA2-deficient cells require the apurinic endonuclease activi

237 Furthermore, TBC1D5 depletion in autophagy-deficient cells rescues retromer recruitment to endosoma

238 We show that in BRCA2-deficient cells, rescuing fork degradation might not be

239 However, ULK1-deficient cells responded normally to DMXAA, indicating

240 ST-DNA polymerase alpha (Pol-alpha) in BRCA1-deficient cells restores HDR and PARPi resistance.

241 essment of replication fork dynamics in BRG1-deficient cells revealed increased origin firing mediate

242 by the tmeA strain of Chlamydia, since AHNAK-deficient cells revealed no invasion phenotype.

243 Transcriptomics of PSEN1-deficient cells reveals strongly downregulated ER-to-lys

244 the PFN2-dynamin interaction domain in miRNA-deficient cells reverses the endocytosis defect.

245 In zinc-deficient cells, RTC4 RNA with longer transcript leaders

246 Autophagy-deficient cells secreted increased amounts of type I int

247 Tet1-deficient cells showed decreased localization of DNMT3A

248 In addition, PGAM5 deficient cells showed diminished expression of IFNbeta

249 Transcriptome analysis of NLUCAT1-deficient cells showed repressed genes within the antiox

250 In BRCA-deficient cells, ssDNA gaps developed because replicatio

251 therapeutic approach to selectively kill HR-deficient cells submitted to replication stress.

252 stored normal replication fork rates in PDS5-deficient cells, suggesting that chromatin-bound cohesin

253 ding Cul3(KLHL9/KLHL13), was intact in SCCRO-deficient cells, suggesting that SCCRO selectively, rath

254 ts with reduced total K(V) 2.1 expression or deficient cell-surface expression.

255 cells are hyporesponsive against MHC class I-deficient cell targets in vitro and in vivo, despite hig

256 bitors, however, resensitizes VHL- and EglN3-deficient cells that are otherwise cisplatin-resistant.

257 ologous expression of this protein in PIEZO1-deficient cells, that exhibit no baseline mechanosensiti

258 In contrast, in GPRC6A-deficient cells, the effect of testosterone to activate

259 and cadC are substantially increased in Tdg-deficient cells, those of both AP- and betaE-sites are u

260 xis partially restore the ability of a BRCA1-deficient cell to form RAD51 filaments at resected DSBs

261 The exquisite sensitivity of BRCA-deficient cells to 3' blocks indicates that they represe

262 DNA replication initiation and enables BRCA1-deficient cells to avoid further genomic instability.

263 in starved cancer cells and causes autophagy-deficient cells to be more dependent on fatty acid oxida

264 n, a ChK1 inhibitor further sensitized RECQ1-deficient cells to gemcitabine and increased cell death.

265 Hypersensitivity of autophagy gene-deficient cells to IFNgamma was mediated by tumor necros

266 ntegrity and promotes the resistance of BRCA-deficient cells to PARP-inhibitors.

267 This is not due to reduced homing of Grasp55-deficient cells to these organs but to increased spontan

268 ling BLM-deficient and/or cytidine deaminase-deficient cells to tolerate constitutive DNA damage and

269 ort chain reduced neurite outgrowth in ZIP12 deficient cells. Transcriptional coactivator PGC-1alpha,

270 Mice receiving 5-LO-deficient cell transplant or zileuton treatment had prol

271 ls were not protective, EVs secreted by CysC-deficient cells treated with exogenous human CysC signif

272 t, and AKT or ERK1/2 signaling in human TSC2-deficient cells treated with GLPG1690.

273 telomeric 8-oxoG in chronically exposed OGG1-deficient cells triggers replication stress, as evidence

274 gets that restrict the proliferation of Tsc1-deficient cells under nutrient restriction (NR).

275 ensation and cell cycle progression in MCPH1 deficient cells under undamaging conditions.

276 oly (ADP ribose) (PAR) was determined in CSB-deficient cells using ADPr-ChAP (ADP ribose-chromatin af

277 In turn, BRCA-deficient cells utilize error-prone DNA-repair pathways,

278 ammaCD restores cellular homeostasis in NPC1-deficient cells via enhancing lysosomal dynamics and fun

279 the release of alpha-syn fibrils from GCase deficient cells was significantly increased.

280 essing cells and ectopic AR expression in AR-deficient cells, we demonstrate an inverse relationship

281 Using ATM-deficient cells, we demonstrate that AZD7648, in combina

282 not significantly affected in TLS polymerase-deficient cells, we examined a possible role of replicat

283 differential survival of HR-proficient vs HR-deficient cells, we found that the combination of UV irr

284 gonally, by serial passaging of virus on EMC-deficient cells, we identified two non-synonymous point

285 tochondrial cell priming, we found that CD27-deficient cells were equally as sensitive as CD27-suffic

286 Moreover, while EVs secreted by CysC-deficient cells were not protective, EVs secreted by Cys

287 SETD6-deficient cells were observed to progress faster through

288 mouse models of gastric cancer, whereby Fzd7-deficient cells were retained in gastric adenomas but we

289 ative potential or rate of apoptosis, ARID1A-deficient cells were sensitized to HSP90 inhibition, pot

290 In PTDSS1-deficient cells where PS is low, LDL cholesterol leaves

291 ecreased WNT activity phenotype seen in FLCN-deficient cells, whereas silencing the transcription fac

292 f fork stability and PARPi responses in BRCA-deficient cells, which provides key insights into target

293 inhibited the migration and invasion of Tsc2-deficient cells while silencing of ING4 reversed the RAR

294 ng why R-tracts do not accumulate in RNase H-deficient cells, while double-strand breaks do.

295 Restoring beta1-integrin activation in talin-deficient cells with a beta1-integrin activating antibod

296 ovel approach for selectively targeting MGMT-deficient cells with ATR inhibitors and temozolomide.

297 een previously shown that enrichment of NPC1-deficient cells with LBPA results in cholesterol clearan

298 Treatment of MGMT-deficient cells with temozolomide increased sensitivity

299 vated type I IFNs were detected in caspase-3-deficient cells without any infection.

300 In zinc-deficient cells, Zap1 binds to zinc responsive elements