ライフサイエンスコーパス: mutant cell

1 ty with DNA repair defects (e.g., in BRCA1/2 mutant cells).

2 racellular cysteine, particularly NRF2/KEAP1 mutant cells.

3 d E2F targets upon loss of E2F4 in RB family-mutant cells.

4 ion, inhibited osteoclastogenesis of caAcvr1-mutant cells.

5 ated, cancers already contain drug-resistant mutant cells.

6 ing to the nuclear envelope were impaired in mutant cells.

7 of changes in the spectral properties of the mutant cells.

8 e cell function was also observed in Snrnp40-mutant cells.

9 isruption of the mitochondrial shape in H2AX mutant cells.

10 ors of PHLPP2 can suppress MYC and kill PTEN mutant cells.

11 into deregulated pathways of mutant and non-mutant cells.

12 tein, were significantly decreased in POLR3A-mutant cells.

13 d definitive hematopoietic potential in DKC1 mutant cells.

14 e effect in the low micromolar range in KRAS mutant cells.

15 degraded, and this process is attenuated in mutant cells.

16 with other PI3K-pathway inhibitors in PIK3CA mutant cells.

17 phenotypic consequences in sudemycin-treated mutant cells.

18 ype cells have lower MET expression than CBL mutant cells.

19 ctivator (GliA) in wild-type but not in Sufu mutant cells.

20 associate with the nuclear envelope in sap1 mutant cells.

21 ically normal, despite the presence of these mutant cells.

22 formin FHOD1, largely rescued morphology in mutant cells.

23 cally manifested as auxotrophy within PIK3CA mutant cells.

24 p53-pathway in p53-wild-type as well as p53-mutant cells.

25 -1 and polycystin-2 is compromised in DZIP1L-mutant cells.

26 f restore growth to conditional-lethal MCM10 mutant cells.

27 d abnormally accumulate in the cilia of both mutant cells.

28 ailed to stimulate osteoclastogenesis in the mutant cells.

29 r correction during anaphase in wild-type or mutant cells.

30 ameliorated cholesterol accumulation in Npc1 mutant cells.

31 spindle assembly checkpoint silencing in the mutant cells.

32 lity and overall mitochondrial metabolism in mutant cells.

33 ts of Atm mutant cells, in contrast to Brca1 mutant cells.

34 susceptibility and fitness advantage of Kras-mutant cells.

35 vated response to stressors is noted in T150 mutant cells.

36 minal phosphorylation state in wild-type and mutant cells.

37 d in vivo drug-resistance phenotypes of FBW7-mutant cells.

38 signaling network and inhibits growth of p53-mutant cells.

39 , culminating in increased PDH activation in mutant cells.

40 etabolism that is severely compromised in CI mutant cells.

41 the benomyl resistance of both set1 and H3K4 mutant cells.

42 tely 200 proteins with reduced levels in the mutant cells.

43 ation reduced the YARS2 protein level in the mutant cells.

44 compromised DNA repair machinery of BRCA1/2-mutant cells.

45 cells from 70% in wild-type cells to 20% in mutant cells.

46 gnaling and reducing drug sensitivity of RAS-mutant cells.

47 sphingolipid storage and trafficking in NPC1 mutant cells.

48 erapy drugs stimulated A3B expression in p53 mutant cells.

49 oughly 1,000 acceptor sites in wild type and mutant cells.

50 Loss of poly(A)polymerase PAPD5 in PARN-mutant cells accelerates hTR maturation and restores hTR

51 liferation under low oxygen levels (2%), the mutant cells accumulated oxidative DNA damage, activated

52 Mutant cells also had decreased WNT10A protein expressio

53 NPM1 impairs the viability of the U2AF1-S34F mutant cells and causes ribosomal RNA (rRNA) processing

54 tem with Cre or Tomato (MASCOT) for tracking mutant cells and demonstrate its utility for modeling cl

55 stic moduli (Y) in large populations of live mutant cells and in conditions affecting cell diameter i

56 The effect is specific for FLT3-mutant cells and is ascribed to the transcriptional acti

57 Fur protein is ~31% in the E. coli iscA/sufA mutant cells and is decreased to ~4% in WT E. coli cells

58 We have characterized the physiology of mutant cells and isolated PSII protein complex and concl

59 a 60% reduction in the presence of cilia on mutant cells and loss of cilia length regulation for the

60 ves the best therapeutic window between KRAS mutant cells and normal, untransformed cells.

61 pronounced PI3K/AKT signaling in NRAS(G12V) mutant cells and pronounced mitogen-activated protein ki

62 wn tooth development genes) was perturbed in mutant cells and quite significantly for PAX9 and RUNX2.

63 cued secretion and bud growth defects in boi mutant cells, and abrogated NoCut checkpoint function.

64 to stabilization of beta-catenin in cohesin-mutant cells, and that Wnt-responsive gene expression is

65 directed PSM extension fails in many septin-mutant cells, and, for those that do succeed, walls are

66 ome-editing enzymes and identify the desired mutant cells/animals.

67 Double mutant cells are able to grow under excess illumination,

68 Hox mutant cells are defective in osteoblastic and chondroge

69 p53 mutant cells are insensitive to LDIR and outcompete wild

70 the endogenous EGFP-tagged protein, whereas mutant cells are marked with mCherry upon inversion.

71 Somatic scribble mutant cells are selectively eliminated from the growing

72 Notably, PPM1D mutant cells are shown to be sensitive to NAMPT inhibito

73 nstrates that cilia in both Dnchc2 and Wdr34 mutant cells are stumpy.

74 Tandem duplications in BRCA1 mutant cells arise by a replication restart-bypass mecha

75 tch to a more invasive phenotype in the BRAF-mutant cells as a potential therapy escape mechanism.

76 Our data suggest that mutant cells attempt to maintain global O-GlcNAcylation

77 Follicular Hras mutant cells autonomously and nonautonomously enhance re

78 eactive oxygen species were also observed in mutant cells bearing both m.14502T > C and m.11778G > A

79 rental cells, tumor growth was enhanced with mutant cells becoming the predominant population in dist

80 transporter, results in hem1Delta abc3Delta mutant cells being unable to grow in the presence of hem

81 ly restores TERC levels in immortalized DKC1 mutant cells, but it remains unknown if modulation of po

82 anscripts and proteins are upregulated in Rp mutant cells by auto-regulatory expression that depends

83 the effects including the elimination of Rp mutant cells by competition with wild type cells.

84 combinase approach that creates mosaic Pdgfr mutant cells by Cre/lox recombination with a linked Flp/

85 CK1alpha similarly destabilizes FOXO4 in RAS-mutant cells by phosphorylation at serines 265/268.

86 to aneuploidy tolerance in both TP53-WT and mutant cells by reducing basal caspase-2 levels and prev

87 Thus, p53-mutant cells can be depleted from the normal esophagus b

88 ps observed in a population of wild-type and mutant cells can be explained by this mechanism, coupled

89 y in DCMU-treated algae or in PSII-deficient mutant cells can be partly compensated for by the indire

90 ines coupled with phenotypic analysis of the mutant cells can yield mechanistic insights into driver

91 SOX2 ablation attenuates proliferation, and mutant cells cannot be expanded in vitro.

92 In mutant cells, CDK7 inhibition decreases STAT3 chromatin

93 s forced targeting of PALB2 to DNA breaks in mutant cells circumvents BRCA1 haploinsufficiency.

94 at are occupied by beta-catenin in HNF-1beta mutant cells colocalize with HNF-1beta-occupied sites in

95 olism pathways that lack in near homoplasmic mutant cells compared to wild type cells.

96 is hypermethylated and downregulated in CMD1 mutant cells compared to wild-type cells, causing a redu

97 quitination of MET was also decreased in CBL mutant cells compared to wildtype cells.

98 rrangements were also more common in BRCA1/2 mutant cells compared with the wild-type control.

99 IGF1R inhibition was effective in KEAP1-mutant cells compared with WT, especially under conditio

100 sistant membrane fractions from wildtype and mutant cells, consistent with the prediction that carote

101 Mutant cells contained high copper concentrations and hi

102 a bright red color when expressed in E. coli mutant cells containing an elevated intracellular free i

103 Moreover, mutant cells containing fluorophore-tagged receptors exh

104 ifficile DdlR is essential, as the ddlR null mutant cells could not grow even in complex laboratory m

105 In both mutants, cell cycle progression is remarkably delayed an

106 asmic chaperone Skp contributes to yciB dcrB mutant cell death by possibly mistargeting stalled porin

107 Cep57 mutant cells defective in Cep63 binding exhibited improp

108 xamining the lineage from the Hox-expressing mutant cells demonstrates no loss of stem cell populatio

109 pe, Dnchc2 (dynein 2 heavy chain), and Wdr34 mutant cells demonstrates that cilia in both Dnchc2 and

110 tion, and Yki-mediated hyperplasia, spectrin mutant cells, despite showing myosin II activation and Y

111 In vitro, VE-cadDEE mutant cells displayed defects in polarization and cell

112 stically, BITC induces p73 expression in p53-mutant cells, disrupts the interaction of p73 and mutant

113 Mutant cells dominated the blood system, but not other t

114 ietic stem cells, which give an advantage to mutant cells, driving their clonal expansion and potenti

115 epair pathway was extensively compromised in mutant cells due to decreased NAD(+) availability.

116 The fitness of CMD1 mutant cells during exposure to high light levels is red

117 sed production of reactive oxygen species in mutant cells, emphasizing PDH as an interesting therapeu

118 e cell imaging of mechano-insensitive formin mutant cells established that mechanoregulation of formi

119 rther demonstrate that the low heteroplasmic mutant cells exhibit a coordinate induction of transcrip

120 Consequently, because PIK3CA mutant cells exhibit a profound reliance on glucose meta

121 xenografted into immunocompromised mice, RB1 mutant cells exhibit an elevated propensity to seed new

122 These mutant cells exhibit delayed recruitment of putative CAR

123 c profiling reveals that REDD1-deficient/RAS mutant cells exhibit enhanced uptake of lysophospholipid

124 VHL-mutant cells exhibit metabolic abnormalities that can ca

125 IDH2 and SRSF2 double-mutant cells exhibited aberrant splicing and reduced exp

126 Plated on muscle-like stiffness matrix, mutant cells exhibited contractile stress fibre accumula

127 Mutant cells exhibited decreased PDH activity and increa

128 aching (FRAP) results indicated that NKKY101 mutant cells exhibited increased plasma membrane rigidit

129 However, the mutant cells exhibited increased turnover as well as fun

130 Mutant cells exhibited Mpk1-dependent Sir3 hyperphosphor

131 nge (MADR), which permits stable labeling of mutant cells expressing transgenic elements from precise

132 While RB1-mutant cells fail to arrest at G(1)-S in response to cel

133 However, double-mutant cells fail to complete HR, as excessive shieldin

134 y, C/EBPalpha or c-Fos overexpression in the mutant cells failed to control the up-regulated RBP-J ex

135 es with similar competitive fitness collide, mutant cell fate reverts towards homeostasis, a constrai

136 n-matrix based model we show that TIE2-L914F mutant cells form enlarged lumens mimicking vascular les

137 Furthermore, proteomic analyses of WT and mutant cell fractions revealed that, in addition to comp

138 n-depth analyses of nucleic acids, including mutant cell-free (cf) DNA in the plasma.

139 pids, repair cellular organelles and protect mutant cells from acute iron overload.

140 ent depletion, PIKfyve activity protects Ras-mutant cells from starvation-induced cell death and supp

141 s are required for the active elimination of mutant cells from the tissue, while utilizing both endog

142 Mutant cells further underwent changes in structure and

143 rocess affects the fixation probability of a mutant cell generating such a signal, and find that this

144 t, thus prompting the question of how single mutant cells give rise to neoplasia.

145 in suppressed the growth of subcutaneous MET-mutant cell grafts in mice, including that of MET inhibi

146 Yet the double mutant cells grow, recruit MCM2-7 normally to chromatin,

147 ished, and actual cilia defects in the WDR34 mutant cells have also not been completely characterized

148 Here we show that ugtP mutant cells have increased levels of cell wall precurso

149 In mutant cells, higher IP(6) level is expected to be assoc

150 Metabolomics profiling of mutant cells highlighted purine, arginine/urea cycle and

151 es from extended precursors but that in PARN-mutant cells hTR maturation kinetically stalls and unpro

152 ranscriptome analysis of wild-type and T357I-mutant cells identified 36 differentially expressed gene

153 rom intracellular DSM20231 and isogenic clpC mutant cells identified alterations in transcription of

154 Lack of cpUPR induction in MARS1 mutant cells impaired their ability to cope with chlorop

155 Maize tan1 mutant cells improperly position the preprophase band (P

156 Increasing PNKP activity in mutant cells improves genome integrity and cell survival

157 studied the effects of the expansion of Tet2-mutant cells in atherosclerosis-prone, low-density lipop

158 ene set is differentially regulated in GATA3 mutant cells in culture and in tumors bearing similar mu

159 ve roles in the organism: it selects against mutant cells in developing tissues, prevents the propaga

160 egy in differential tagging of wild-type and mutant cells in mosaics.

161 m tracking of Tet2 mutant or Tet2/Id3 double-mutant cells in our MASCOT model revealed a dynamic shif

162 es the proliferative capacity of MYC- or p53-mutant cells in spite of higher genetic damage and a lar

163 rift and can also cause downward invasion of mutant cells in the crypt.

164 nizing radiation (LDIR) on wild-type and p53 mutant cells in the transgenic mouse esophagus.

165 ork increased sensitivities to TKIs in K-Ras mutant cells in which EGFR knockdown inhibited growth.

166 eased phosphorylation of S269, even in S256A mutant cells in which S256 phosphorylation cannot occur.

167 etion does not rescue the HDR defects of Atm mutant cells, in contrast to Brca1 mutant cells.

168 zed to the ER in p24delta3delta4delta5delta6 mutant cells, in contrast to plasma membrane proteins wi

169 ibition of TWIST1 in EGFR TKI-resistant EGFR-mutant cells increased sensitivity to EGFR TKIs.

170 g assays further demonstrated that DeltagacA mutant cells indeed predominate on the edge and that ini

171 that Xrp1/Irbp18 is the complex active in Rp mutant cells, independently of other complexes that shar

172 nomously enhance regeneration, which directs mutant cells into continuous tissue cycling to promote i

173 oposed how cell level properties can lead to mutant cell invasion, but has not incorporated detailed

174 e that mutations in APC can lead directly to mutant cell invasion.

175 distribution of ER-alpha and FOXA1 in GATA3-mutant cells is associated with altered chromatin archit

176 y, unfaithful chromosome replication in Dna2-mutant cells is exacerbated by Pif1, which triggers the

177 elopment of wild-type (WT) Dictyostelium and mutant cells lacking ChdC, a Type III CHD protein orthol

178 ntrast, cryo-EM structures of ribosomes from mutant cells lacking K63 ubiquitin resolved at 4.4-2.7 a

179 Mutant cells lacking polyP elongate during starvation an

180 Mutant cells lacking three TFs (Sok2/Phd1/Yap6) displaye

181 ell phenotype, which increases the risk that mutant cells lead to long lasting clones in the tissue.

182 When CBL was knocked down in the mutant cell line H1975 (erlotinib-resistant), it became

183 wild-type Aalpha in a patient-derived P179R-mutant cell line restored enzyme function and significan

184 In each mutant cell line, gene reactivation occurs to 6% genes a

185 hibitors against a gefitinib resistant T790M mutant cell line.

186 soil genotoxicity, as evaluated with either mutant cell line.

187 hagy-independent cell death synergy in FGFR3-mutant cell lines between mTOR (mammalian target of rapa

188 mutant ER, we developed multiple isogenic ER-mutant cell lines for the most common LBD mutations, Y53

189 Analysis of 5'-capped RNA transcripts in mutant cell lines identified the usage of an intermediat

190 rest, and terminal differentiation in DNMT3A-mutant cell lines in vitro.

191 Knockdown of TET1 in p53-mutant cell lines induced senescence through a program i

192 LMTK3 silencing reduced viability of all KIT-mutant cell lines tested, even those with drug-resistant

193 as taken up at higher rates in KRAS and BRAF mutant cell lines than in wild-type KRAS cancer cell lin

194 his protocol allows generation of homozygous mutant cell lines using an insertion cassette which auto

195 ARCN1 mutant cell lines were revealed to have endoplasmic reti

196 Cas9 was less active in TP53-WT than in TP53-mutant cell lines, and Cas9-induced p53 pathway activati

197 critical for Nrf2-dependent growth in KEAP1-mutant cell lines, including the redox proteins thioredo

198 ffector dependency were observed across KRAS mutant cell lines, indicative of heterogeneous utilizati

199 Chinese hamster lung V79 cells and its mutant cell lines, V-C8 (BRCA2 deficient) and V-C8 with

200 e-resistant, palbociclib-resistant, and ESR1 mutant cell lines.

201 horylation, and STAT3 activity in KRAS(G12D)-mutant cell lines.

202 es consistently deregulated across all UPF3B mutant cell lines.

203 on the unstable genomic phenotype of BRCA1/2 mutant cells manifest mainly as large-scale rearrangemen

204 In contrast, mutant cells manipulated with a lentiviral vector expres

205 ion of compensatory pathways active in NT5C2 mutant cells may antagonize the emergence of NT5C2 mutan

206 xt nominates a DNA repair dependency in KRAS-mutant cells, mediated by a network containing BRCA1.

207 Tre1 mutant cells migrate randomly with transient enrichment

208 s their neighbors, whereas adjacent beta-Pix mutant cells move in random directions.

209 Despite not entering the cilium in mutant cells, mutant PC2 accumulates at the ciliary base

210 aneous disorders, as phenotypically distinct mutant cells often give rise to lesions in patterns dete

211 follicle stem cells and discovered that Hras mutant cells outcompete wild-type neighbors yet are inte

212 acking methodology to follow individual CCR5 mutant cells over time in vivo, reinforcing that CCR5 ge

213 sort desired (e.g., experimentally evolved, mutant) cell phenotypes based on their electrical impeda

214 ated that altering the selective pressure on mutant cell populations may cause them to expand or cont

215 C2 dispensable for proliferation in 2D, KRAS mutant cells preferentially rely on SHOC2 for ERK signal

216 the mutations led to low levels of IFT81 and mutant cells produced elongated cilia, had altered hedge

217 The DeltaflcA mutant cells produced fewer, abnormally tilted and short

218 ged with an isogenic SpA-deficient S. aureus mutant, cells proliferated in the BM survival niches and

219 has been shown to inhibit both RAS and BRAF mutant cell proliferation in vitro and xenograft tumor g

220 ance on glucose metabolism to sustain PIK3CA mutant cell proliferation.

221 Loss of this function in Apc mutant cells reduces directed cell migration, potentiall

222 oduced a second mutation in ORC2 in the ORC5 mutant cells, rendering both ORC5 and ORC2 proteins unde

223 at the altered lipid metabolism found in NF2-mutant cells renders them sensitive to elevated levels o

224 s and suggest that metabolic dependencies of mutant cells represent vulnerabilities that can be targe

225 Accordingly, RBP-J silencing in the mutant cells rescued osteoclastogenesis with C/EBPalpha

226 ated by p53 and p73 in p53-wild-type and p53-mutant cells respectively; and in a feed-forward mechani

227 of wild-type levels of mcm10-4A in mcm5-bob1 mutant cells resulted in severe growth and DNA replicati

228 ed in both bleached mutants, indicating that mutant cells retain some plastid remnants.

229 of the transcriptome and epigenome in SmcHD1 mutant cells reveals the appearance of sub-megabase doma

230 Furthermore, spectrin mutant cells show differentiation and polarity defects o

231 The pkd2 mutant cells show signs of osmotic stress, including tem

232 nd lung cell lines we demonstrated that KRAS mutant cells showed a dependency on PDHK4 whereas KRAS w

233 Mutant cells showed consistent and severe mitotic failur

234 In addition, the mutant cells showed elevated levels of reactive oxygen s

235 Consistently, the mutant cells showed significantly reduced DNA strand bre

236 ation sequencing (ChIP-seq) in wild-type and mutant cells showed that ablation of HNF-1beta increases

237 ctional rescue experiment using Jpx-deletion mutant cells shows that human JPX can functionally compl

238 me, also exhibits abnormal morphology in the mutant cells, similar to our 3D results on the Smoothene

239 On long-term passage, the mutant cells stably produced proteinase K (PK)-resistant

240 activator of transcription 3 (STAT3) in APC-mutant cells, STAT3 target genes were not induced.

241 rmal yeast strain and two condensin-modified mutant cell strains.

242 IDH2(R140Q), with only recipients of double mutant cells succumbing to leukemia.

243 s, preferentially impairs the growth of KRAS-mutant cells, suggesting a druggable synthetic lethal in

244 carrying wild type (wt) TP53 but not in p53-mutant cells, suggesting involvement of ribosomal stress

245 Upon verifying mutant cell surface expression and proteolytic cleavage,

246 pkd2 mutant cilia lack mastigonemes, and mutant cells swim with reduced velocity, indicating a mo

247 WNT10A-mutant cells (T357I, R360C, and R379C mutants) showed re

248 Deletion of fliD leads to non-motile mutant cells that are unable to assemble flagellar filam

249 lain how organisms are able to eliminate the mutant cells that arise occasionally during development.

250 ut the genome, providing a vast reservoir of mutant cells that can expand, repopulate the tumor, and

251 apidly lost and repopulation occurred by non-mutant cells that had escaped recombination, suggesting

252 dies reveal that deletion of BB0270 leads to mutant cells that have less PF (4 +/- 2 PF per cell tip)

253 stabilization, in Arabidopsis lnp1-1 lnp2-1 mutant cells, the ER becomes a dense tubular network.

254 Interestingly, in lnp1-1 lnp2-1 mutant cells, the expression level of RHD3 is higher tha

255 ynthesis is selectively blocked in hem1Delta mutant cells, the heme analog zinc mesoporphyrin IX (ZnM

256 ctive rDNA repeats remains unaffected in the mutant cells, the overall rDNA copy number increases ~2-

257 For MAP kinase pathway activation in KRAS-mutant cells, the requirement for coincident growth fact

258 in high CO2 was due to the inability of the mutant cells to adjust photosynthesis to high CO2 The li

259 We then expressed the mcm10-4A in mcm5-bob1 mutant cells to bypass the defects mediated by diminishe

260 alternative prenylation, and sensitized RAS-mutant cells to growth inhibition by FTI.

261 g human mitochondrial disease complex I (CI) mutant cells to identify genes whose increased function

262 w wild-type cells limit the proliferation of mutant cells to maintain proper tissue homeostasis.

263 Failure of Deltaami1 mutant cells to separate also led to dysregulation of Ft

264 ibutions of TSC2 heterozygous and homozygous mutant cells to the pathogenesis of TSC and the importan

265 omic states with linked epitopes(1), aligned mutant cells to their wild-type equivalents and identifi

266 We show that hypersensitivity of ATM-mutant cells to topotecan or the poly-(ADP-ribose) polym

267 re-like cardiomyocytes in control cells but, mutant cells transition to a pathological state with red

268 t to enable survival and proliferation of CI mutant cells under nutrient stress conditions.

269 hat correcting mis-splicing of BRD9 in SF3B1-mutant cells using antisense oligonucleotides or CRISPR-

270 ong the factors promoting cell separation in mutant cells was a protein of previously unknown functio

271 The amount of IFT injection in dynein mutant cells was higher than that in control cells.

272 Although the motility of the cheD mutant cells was indistinguishable from that of the wild

273 In Trp53(-/-);Brca2(-/-) mutant cells, we documented a relative increase in sensi

274 e IL-22 signalling in wild-type (WT) and APC-mutant cells, we performed RNA sequencing (RNAseq) of IL

275 Mutant cells were also more sensitive to MET inhibitor S

276 owever, the mRNA levels of the wild-type and mutant cells were comparable.

277 n example dataset in which wild-type and anr mutant cells were grown as biofilms on the Cystic Fibros

278 When small subpopulations of Y537S ESR1 mutant cells were injected along with WT parental cells,

279 tate protein synthesis was unaffected, SF3B1 mutant cells were more sensitive to the clinically-relev

280 Mutant cells were some 50% longer than parental strain c

281 mma radiation, such as Nrf2 gain-of-function mutant cells, were sensitive to alpha-particles.

282 ated with a decrease in the PSI titer of the mutant cells, whereas the PSII content was unaffected.

283 e phenotypes with those of TPP1(L104A/L104A) mutant cells, which have short and stable telomeres simi

284 ivates robust responses to eliminate somatic mutant cells, which if left unpurged, can impact brain a

285 e-of-flight model using Chlamydomonas dynein mutant cells, which show slower retrograde transport spe

286 dscape to support tumorigenic growth of LKB1-mutant cells, while resulting in potential therapeutic v

287 ate age-dependent mutations that provide the mutant cells with a selective advantage, leading to the

288 Quadruple mutant cells with additional P53 loss displayed the high

289 Treatment of NF2-mutant cells with agents that inhibit the production of

290 ormally decorates the apical surface of Tsc1-mutant cells with E-cadherin and alpha-catenin.

291 ene expression profiles of wild-type and SP5 mutant cells with genome-wide SP5 binding events reveals

292 By comparing wild-type and mutant cells with impaired aggregation, we found the lon

293 , we determined that compared with WT cells, mutant cells with long microtubules exhibit fewer mitoch

294 However, upon chronic treatment of BRCA1-mutant cells with PARP inhibitors, resistant clones can

295 microtubules exhibit fewer mitochondria, and mutant cells with short microtubules have an increased n

296 etion, is severely compromised in telomerase mutant cells with short telomeres.

297 Treatment of FLT3-ITD- and JAK2V617F-mutant cells with the antioxidant N-acetylcysteine dimin

298 enes, whereas P53 inactivation allowed Caph2 mutant cells with whole-chromosome gains and structural

299 Ciliogenesis was also disrupted in the mutant cells, with a 60% reduction in the presence of ci

300 anced capacity to integrate and contain Hras mutant cells within both homeostatic and perturbed tissu