ライフサイエンスコーパス: mutant cell

1 phenotypic consequences in sudemycin-treated mutant cells.

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

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

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

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

6 CK2alpha inhibition compared with NRAS(G12) mutant cells.

7 ed incidence of diastolic calcium release in mutant cells.

8 ding to specific G2/M phase blockade in KRAS-mutant cells.

9 interactions with metabolic pathways in BRCA mutant cells.

10 piratory complexes constitutively induced in mutant cells.

11 e division site are reduced in art1 and rgf3 mutant cells.

12 neutrophils and macrophages in wild type and mutant cells.

13 n consumption and ATP production observed in mutant cells.

14 sion and abrogates the proliferation of BAP1-mutant cells.

15 e RNAP II and transcription increase in Tup1 mutant cells.

16 anelle trafficking to PC dendrites in Afg3l2-mutant cells.

17 ibition leads to mitotic catastrophe in KRAS-mutant cells.

18 ppresses the temperature sensitivity of pds5 mutant cells.

19 nsmission, Syt1-R398/399Q (RQ), in syt1 null mutant cells.

20 the expression of Zeb2 and Pkd1 in HNF-1beta mutant cells.

21 recombinant LTBP4 enhanced these measures in mutant cells.

22 defects and blunted gluconeogenesis in Vps15 mutant cells.

23 ity nor cohesion defects exhibited by pds5-1 mutant cells.

24 ompounds with specific activity against tet2 mutant cells.

25 of hyperpolarized 5-(13)C-glutamate in IDH1 mutant cells.

26 sphorylation status of CtrA in wild-type and mutant cells.

27 formin FHOD1, largely rescued morphology in mutant cells.

28 duction in glucose flux to glutamate in IDH1 mutant cells.

29 ATP and membrane potential were observed in mutant cells.

30 rified from the cytoplasmic membrane of hoxR mutant cells.

31 on caused defects in respiratory capacity in mutant cells.

32 cally manifested as auxotrophy within PIK3CA mutant cells.

33 RK MAPK phosphorylation specifically in BRAF mutant cells.

34 duction in Asf1-H3 interaction in rad17Delta mutant cells.

35 iphery) moving endosomes is increased in the mutant cells.

36 reductive glutamine metabolism, but not IDH2-mutant cells.

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

38 production of reactive oxygen species in the mutant cells.

39 length aggravates missegregation in topo II mutant cells.

40 inoacylated level of tRNAHis was observed in mutant cells.

41 ailed to rescue the myosin defect in corA(-) mutant cells.

42 breast/ovarian cancer predisposition in BRCA mutant cells.

43 ial membrane potential compared with control mutant cells.

44 eroxisomal membrane structures in yeast pex3 mutant cells.

45 radation is increased in ubp8Deltaubp10Delta mutant cells.

46 in patches assembled slowly in these cofilin mutant cells.

47 ndependent of loss of primary cilia in Dzip1 mutant cells.

48 -1 and polycystin-2 is compromised in DZIP1L-mutant cells.

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

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

51 ailed to stimulate osteoclastogenesis in the mutant cells.

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

53 spindle assembly checkpoint silencing in the mutant cells.

54 lity and overall mitochondrial metabolism in mutant cells.

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

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

57 susceptibility and fitness advantage of Kras-mutant cells.

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

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

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

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

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

63 , culminating in increased PDH activation in mutant cells.

64 associate with the nuclear envelope in sap1 mutant cells.

65 e 15-times more frequent than in pilus-minus mutant cells (0.2 events/min), indicating the pili are c

66 e for wild-type cells (12 s) and pilus-minus mutant cells (13 s), suggesting the pili do not play a s

67 Chemotherapy selects for PIK3CA-mutant cells, a minor subpopulation in nearly all treatm

68 In KRAS mutant cells, a subset of proteins exhibit elevated leve

69 Because Lztfl1 mutant cells accumulate BBSome but not IFT27, it is like

70 This work reveals that nab2 mutant cells accumulate intron-containing pre-mRNA in vi

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

72 likely to account for the lethality of rad53 mutant cells after replication blocks.

73 Without agitation, mutant cells aggregate and settle out of the medium.

74 Notably, pex3 mutant cells already contain reticular and vesicular str

75 HNF-1beta mutant cells also expressed lower levels of cholesterol

76 Lastly, IDH1-mutant cells also grew poorly as subcutaneous xenografts

77 Interestingly, mutant cells also show increased transcript levels of mi

78 as Arg(82) results in reduced infectivity of mutant cells and an increase in heparin binding.

79 n and FANCC nuclear entry is defective in FA mutant cells and in cells depleted of the Fanconi A prot

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

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

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

83 signaling is increased in ciliary transport mutant cells and mTOR signaling inhibits PDGFRalpha leve

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

85 akoid membranes were still observed in vipp1 mutant cells and resembled those in a psaAB mutant that

86 hting the importance of interactions between mutant cells and the surrounding normal cells that make

87 ributes to the transformed phenotype of KRAS mutant cells and Ubc9 presents a potential target for th

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

89 ing partner of IFT27, was disrupted in Ift27 mutant cells, and Ift25-null mice displayed hair follicl

90 e synthesis of polyamines, is reduced in Mga mutant cells, and the survival of mutant ICM cells as we

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

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

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

94 Hox mutant cells are defective in osteoblastic and chondroge

95 LMNA mutant cells are known to have altered biophysical prope

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

97 Surprisingly, we found that SF3B1-mutant cells are not dependent upon the mutated allele f

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

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

100 Repeat instability in nup84, slx5, or slx8 mutant cells arises through aberrant homologous recombin

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

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

103 Thylakoid membranes in dark-maintained fdx5 mutant cells became severely disorganized concomitant wi

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

105 ially restores cohesion in eco1 wpl1 or eco1 mutant cells but robustly restores cohesion in cells blo

106 e CMG complex assembles prematurely in G1 in mutant cells, but not wild-type cells.

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

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

109 ic loss of heterozygosity, in whom biallelic mutant cells can be tracked by absent Fas expression, Fa

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

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

112 ibroblast wound-healing assay, we showed Hug mutant cells cannot establish cell polarity required for

113 In mutant cells, CDK7 inhibition decreases STAT3 chromatin

114 overexpression would similarly rescue pds5-1 mutant cell cohesion defects.

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

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

117 d cohesion defects, but do not rescue pds5-1 mutant cell condensation defects.

118 lectron microscopy, we found that PHO23 null mutant cells contain significantly more autophagosomes t

119 eltaPA1006 mutant extracts revealed that the mutant cells contain significantly reduced levels of mol

120 Moreover, mutant cells containing fluorophore-tagged receptors exh

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

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

123 ow that nascent endocytic vesicles formed in mutant cells displaying rapid, dysregulated CME are defe

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

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

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

127 han wild-type cells; expressing Flag-AbpG in mutant cells eliminates the motility defect.

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

129 specific expression of Myc oncogene, whereas mutant cells empower survival advantage upon overgrowth

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

131 Mutant cells exhibit a approximately 50% decrease in ATP

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

133 Instead, vangl2 mutant cells exhibit an anterior/animal pole bias in cel

134 VHL-mutant cells exhibit metabolic abnormalities that can ca

135 ults in altered SOD1 activity, whereas these mutant cells exhibit substantially decreased levels of C

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

137 Mutant cells exhibited decreased PDH activity and increa

138 observed that under hypoxic conditions, IDH1-mutant cells exhibited increased oxidative tricarboxylic

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

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

141 wild-type cells, these differentiating Gpc4-mutant cells expressed high levels of DOPA decarboxylase

142 Pah1p abundance was stabilized in pah1Delta mutant cells expressing catalytically inactive forms of

143 l elongation, as alpha-Spectrin and integrin mutant cells fail to columnarize.

144 vangl2 mutant cells fail to undergo this transition and to migr

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

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

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

148 prkC mutant cells glided at approximately half the frequency

149 the frequency of wild-type cells, while prpC mutant cells glided more than twice as frequently as wil

150 In addition, the quiescent pah1Delta mutant cells had 3-fold higher levels of mitochondrial s

151 Furthermore, we found that the mutant cells had a reduced P5CS enzymatic activity leadi

152 revealed that type I collagen synthesized by mutant cells had decreased electrophoretic mobility.

153 While heterozygous mutant cells had diminished signaling in response to exo

154 However, ECM over PCP mutant cells had reduced levels of laminin, Dally and Dl

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

156 The mutant cells have higher free inorganic phosphate levels

157 The pro3 mutant cells have higher intracellular reactive oxygen s

158 tation in a sample containing only 1% of the mutant cells in a mixture of wild-type cells.

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

160 TET2-first patients but by JAK2-TET2 double-mutant cells in JAK2-first patients.

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

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

163 ell compartment was dominated by TET2 single-mutant cells in TET2-first patients but by JAK2-TET2 dou

164 gent upon the presence of both wild-type and mutant cells in the same tissue.

165 In agreement with these findings, mutant cells in vivo and in vitro exhibit smaller and mo

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

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

168 omplement the Escherichia coli panD deletion mutant cells, in which panD encoding aspartate decarboxy

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

170 t the flagellar ribbons are distorted in the mutant cells, indicating that motor rotation is essentia

171 Further, these mutant cells initiate the ingression of cleavage furrows

172 otB bacteria assembled flagella, part of the mutant cell is rod shaped.

173 lack of polyP during the development of ppk1 mutant cells is partially offset by an increase of both

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

175 comQ cells is intracellular and only affects mutant cells lacking ComQ.

176 Mutant cells lacking polyP elongate during starvation an

177 In mutant cells lacking TORC2 or Gad8, the binding of the M

178 The heterologous expression of PROS in yeast mutant cells lacking Vta1p partially rescues endosomal s

179 n of GAPDH in highly glycolytic KRAS or BRAF mutant cells leads to an energetic crisis and cell death

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

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

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

183 hibitors against a gefitinib resistant T790M mutant cell line.

184 expressed at reduced levels in diverse TP53 mutant cell lines and human tumors.

185 a residual SWI/SNF complex exists in SMARCA4 mutant cell lines and plays essential roles in cellular

186 We tested crenolanib against a panel of D835 mutant cell lines and primary patient blasts and observe

187 otent across a broad panel of engineered ALK mutant cell lines and showed suitable preclinical pharma

188 ed MAPK signaling in (V600D)BRAF/(V600E)BRAF mutant cell lines and this was associated with TNF-alpha

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

190 veral MEK inhibitors specifically within Ras-mutant cell lines by antagonizing release of negative fe

191 Mutant cell lines coupled with inhibitors demonstrated t

192 Both mutant cell lines exhibited evidence of Wnt pathway dysr

193 on was also required for telomere stability; mutant cell lines had fragile telomeres, increased numbe

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

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

196 st, short-hairpin RNA depletion of GRIN2A in mutant cell lines slightly reduced proliferation.

197 ARCN1 mutant cell lines were revealed to have endoplasmic reti

198 JAK2 and MPL mutant cell lines were sensitive to CHZ868, including ty

199 nformation, it correctly predicted that BRAF mutant cell lines would be more sensitive than BRAF wild

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

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

202 tivity of QARS was significantly impaired in mutant cell lines.

203 Additionally, Moe mutant cells lost Crb from the apical membrane and accum

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

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

206 At a molecular level, in p53-competent KRAS-mutant cells, MTH1 loss provokes DNA damage and inductio

207 In p53-nonfunctional KRAS-mutant cells, MTH1 suppression does not produce DNA dama

208 ay activation by BRAF inhibitors in non-BRAF-mutant cells needs to be taken into account, which may b

209 trast, autophagosomes generated in Rab5-null mutant cells normally fuse with lysosomes during the sta

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

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

212 sms of resistance within populations of EGFR-mutant cells (PC9 and/or NCI-H1975) with acquired resist

213 The mutant cell pool rapidly generates metastases when trans

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

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

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

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

218 tions in seven mtDNA-encoded polypeptides in mutant cells, ranging from 37 to 81%, with the average o

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

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

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

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

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

224 re, we report that ELG1 deletion from pds5-1 mutant cells results in a significant rescue of cohesion

225 Transcriptional profiling of Sall1 mutant cells revealed a striking pattern, marked by the

226 Deletion of the Swe1 kinase renders mutant cells sensitive to serine palmitoyltransferase in

227 Theory predicts that the frequency of mutant cells should vary greatly between individuals.

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

229 TORC2 mutant cells show increased spontaneous nuclear Rad52 fo

230 d that EGFR-mutant NSCLC cells, but not KRAS-mutant cells, show low RBE.

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

232 as in vitro ciliogenesis experiments in CCNO-mutant cells showed defective mother centriole generatio

233 DMRT1 protein only remains in non-mutant cells, showing that SOX9/8 maintain Dmrt1 express

234 king defect observed previously in syt1 null mutant cells, similar to wild type Syt1 (Syt1-wt).

235 le to (i) the high X-ray sensitivity of EGFR-mutant cells, since EGFR mutation is associated with a d

236 However, these mutant cells subsequently fail to mature and die after a

237 rations in the mechanical properties seen in mutant cells, suggesting a defect in the connection betw

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

239 ssenger RNAs were strongly down-regulated in mutant cells, suggesting a potential activating role for

240 ition caused accumulation of miR-100 only in mutant cells, suggesting KRAS-dependent miRNA export.

241 The IFT52 mutant cells synthesized a significantly reduced amount

242 ment have been discovered, the initial steps mutant cells take to escape tissue integrity and trigger

243 In mutant cells TGFBR1 was co-localized with lysosomes.

244 ty, neurodegeneration and cancer) typical of mutant cells that cannot make it strongly suggests that

245 uppressor mutations were identified in spxA1 mutant cells that conferred resistance to hydrogen perox

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

247 electively required for the survival of KRAS-mutant cells that harbour a broad spectrum of phenotypic

248 by uncontrolled proliferation of transformed mutant cells that have lost the ability to maintain tiss

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

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

251 Importantly, in slx4Delta sae2Delta double mutant cells these phenotypes are exacerbated, causing a

252 f inhibitors block the MAPK pathway in B-Raf mutant cells, they induce conformational changes to wild

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

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

255 BCL-XL knockdown sensitized KRAS mutant cells to GDC-0623-mediated apoptosis, as did the

256 that JNK pathway inhibition sensitized BRAF mutant cells to GLV-1h68-mediated cell death, mimicking

257 rogramming increased the sensitivity of IDH1-mutant cells to hypoxia or electron transport chain inhi

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

259 ute to the deregulation of mitosis, allowing mutant cells to progress through mitosis at the expense

260 rotein levels and sensitized NFE2L2 or KEAP1-mutant cells to radiation.

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

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

263 itness defect that is particularly severe in mutant cells treated with the alkylating agent methyl me

264 ion and c-Fos expression are altered in both mutant cell types, but the motor neurons exhibit a strik

265 rate of cellular proliferation was higher in mutant cells under low serum conditions, but median cell

266 Unlike the wild type, cki3 mutant cells undergo bipolar growth when S phase is bloc

267 and DNA content analysis indicate that uhrf1 mutant cells undergo DNA re-replication and that apoptos

268 Mutant cells undergo neoplastic transformation, and mice

269 er through a more direct path whereby a TP53-mutant cell undergoes genome doubling, followed by the a

270 rmediate in preparatory scale from coa1Delta mutant cells, using Mss51 as bait.

271 nt of ferulic acid units ester linked to the mutant cell walls is increased by 40% when compared with

272 DH activity in U87 glioblastoma and NHA IDH1 mutant cells was associated with relative increases in P

273 of rGCase on restoring lysosomal numbers in mutant cells was enhanced in the presence of overexpress

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

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

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

277 Mutant cells were also more sensitive to MET inhibitor S

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

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

280 Colonies formed by mutant cells were larger and contained more Ki-67 positi

281 on electron microscopy showed that DeltagacA mutant cells were longer and more flagellated than wildt

282 m and on plant surfaces, while most ppGpp(0) mutant cells were not viable on plant surfaces 24 h afte

283 On fermentable growth medium, the mutant cells were prone to acquire respiratory deficits

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

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

286 denced by enhanced virus growth in NOD1 E56K mutant cells (which failed to interact with RIPK2).

287 -opted into new hair growths by beta-catenin mutant cells, which non-cell autonomously activate Wnt s

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

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

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

291 Mutant cells with decreased Rap1 activation at the poles

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

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

294 ically inactive forms of Pah1p and dgk1Delta mutant cells with induced expression of DGK1-encoded dia

295 While mutant cells with only polar flagella navigate by a "run

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

297 Treatment of mutant cells with the Hh agonist purmorphamine restored

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 ty and failure to restore growth to profilin mutant cells, without exhibiting gain-of-function toxici