ライフサイエンスコーパス: null cell

1 used in sarcoma (FUS) is higher in Itgalpha1-null cells.

2 and normal cell cycle progression of TCF7L1-Null cells.

3 mutants to rescue filopod formation in myo7-null cells.

4 ) mediates increased AURKA expression in VHL-null cells.

5 d Ar-mediated transcription in purified Pten-null cells.

6 JBP2 is needed, as it does not occur in JBP2-null cells.

7 f further increasing mTORC1 activity in TSC2-null cells.

8 driven by beta-catenin transcription in VHL-null cells.

9 centrosome, with reduced association in p53 null cells.

10 orated by CDK5-dependent proliferation of AR null cells.

11 mice, which are a mosaic of normal and Mecp2-null cells.

12 ate mechanism for AURKA dysregulation in VHL-null cells.

13 lorectal carcinoma HCT-116 cells but not p53 null cells.

14 the cytoplasm in both wild type and isoform-null cells.

15 n of AhR and induction of CYP1A1 in MEF RelA null cells.

16 sponse that was completely ablated in Ptp4a3-null cells.

17 ctivated enhancers highly transcribed in p53 null cells.

18 osis, as all are enhanced in cortexillin III-null cells.

19 ion of Pla2g16 increased the invasion of p53-null cells.

20 s, but cargo export completely fails in vps1-null cells.

21 paB activation is totally diminished in cNOS null cells.

22 ulator KEAP1 permitted the survival of BRCA1-null cells.

23 estore cellular senescence in Pparbeta/delta-null cells.

24 log zDHHC9 rescues the phenotypes of sp-erf2 null cells.

25 m starvation (SS), was reduced in the Has1/3 null cells.

26 estabilization and enhanced fluidity in CLN3-null cells.

27 ion rescues survival and ROS levels in BRCA1-null cells.

28 rol efflux and LDL receptor activity in ORP1-null cells.

29 egulator of the inflammatory program in NPC2-null cells.

30 G1 and LARP1 are upregulated in Arf- and p53-null cells.

31 l methanesulfonate and excess Rad51 in rdh54 null cells.

32 e expression and cell cycle arrest in Merlin-null cells.

33 53-dependent; this effect was ablated in p53-null cells.

34 CK showed reduced phosphorylation in DGKzeta-null cells.

35 phenocopies the cellular senescence of TAp73-null cells.

36 and the Ca(2+) transients were longer in the null cells.

37 are protected to the same extent as Bax/Bak-null cells.

38 PTx-induced signaling events lacking in TCR null cells.

39 ted cells, a variety of cancer cells and Rho-null cells.

40 y and stalling at the G2/M checkpoint in Mrp null cells.

41 regulates cell polarity and invasion in LKB1-null cells.

42 was tested by expression of TgPhyA in DdphyA-null cells.

43 circuitry is significantly altered in H3VCTG null cells.

44 etic signature similar to that seen in HDAC3-null cells.

45 with significantly higher activation in Pten-null cells.

46 PUMA promoter after genotoxic stress in TP53-null cells.

47 in the induction of VEGF expression in SMAD4 null cells.

48 d to increase SDC4 promoter activity in RelA-null cells.

49 f each OSN revealed altered activity in Bbs8-null cells.

50 on of dynamin 2 by oxLDL was impaired in vav null cells.

51 accumulation in uracil DNA glycosylase (UNG) null cells.

52 he level of Gli2 at the tips of cilia of PKA-null cells.

53 ndependent of MKK6 because it occurs in MKK6-null cells.

54 for the recombination defect in UBE2T/FANCT null cells.

55 ampers the microbes from spreading from CypA null cells.

56 entered alpha-DG-expressing but not alpha-DG-null cells.

57 ide Pol II promoter-proximal pausing in PTEN null cells.

58 lin in initial adhesion patches of kindlin-3-null cells.

59 the decreased transformation potential in IR-null cells.

60 enic FANCI-, FANCD2- and FANCI:FANCD2 double-null cells.

61 iched repressive nuclear compartments in p63-null cells.

62 ariant, also restored PM cholesterol in ORP1-null cells.

63 ium membrane potentials compared with GABAAR-null cells.

64 rmalized in PLCgamma1/DAG kinase zeta double null cells.

65 e restores autophagic cell death in Bax/Bak1 null cells.

66 -dependent repression, as confirmed in Dicer-null cells.

67 lc1a5 and increased glutamine uptake in Tsc2-null cells.

68 estore Kif7 levels at the ciliary tip of RP2 null cells.

69 chondrial damage and promoted growth of Tsc2-null cells.

70 these increases were eliminated in HIF1alpha null cells.

71 hat they become functionally similar to Tsc1-null cells.

72 d these results were confirmed using miR-451(null) cells.

73 ion, forced expression of tuberin in tuberin-null cells abolished the expression of fibronectin prote

74 his mechanism, beta-catenin deletion in Foxo null cells abrogated both the increased cyclin D1 expres

75 Conversely, LKB1-overexpression in LKB1-null cells abrogated invasion, migration and mammosphere

76 ORP1-null cells accumulated cholesterol in LEL and had reduce

77 Here we show that in myosin V (myo52 myo51) null cells, actin cables are curled, bundled, and fail t

78 eted phosphorylation sites and, in Itgalpha1-null cells, activated EGFR promotes FUS phosphorylation

79 K13 failed to protect NEMO-null cells against TNF-alpha-induced cell death but prot

80 Emerin-null cells also had significantly less HDAC3 at the nucl

81 Importantly, ASAH1-null cells also lose the ability to form cancer-initiati

82 CD98hc-null cells also present reduced intracellular levels of

83 ul attempts of generating Dictyostelium lkb1-null cells, an RNAi-based knockdown approach proved effe

84 observed mitochondrial fragmentation in CCP1 null cells and in neurons from pcd mice, and we document

85 ally decreases tumour formation, even in p53-null cells and inactivation of Bcl11a in established tum

86 er acute LPS treatment were reduced in EBP50-null cells and mice as compared with WT.

87 the cell surface of both wild type and gp96-null cells and thereby abrogated the cellular response t

88 We have used TRAP1-null cells and transient TRAP1 silencing/overexpression

89 terestingly, H-RAS-expressing Pparbeta/delta null cells and tumors having increased cell proliferatio

90 LOX activity was decreased in Efemp2-null cells, and collagen cross-linking was diminished in

91 wn restored IFN-gamma responsiveness in BRG1-null cells, and it mimicked the ability of BRG1 to induc

92 nes, whose expression is compromised in Nfe2-null cells, and many other genes that become active late

93 ongation and fusion were grossly impaired in null cells, and myogenic gene expression was not coordin

94 expression was most prominent in mouse PTEN-null cells, and phosphatidylinositol 3-kinase/Akt activi

95 mycin inhibited cell growth and induced TSC2-null cell apoptosis, abrogated TSC2-null tumor growth, i

96 wnregulation of RhoA markedly increased TSC2-null cell apoptosis.

97 lation of global Wnt signaling because PORCN null cells are completely incapable of autocrine Wnt sig

98 hpm1 null cells are defective in early rRNA processing, resul

99 maH2AX foci formation assays show that Foxm1-null cells are hypersensitive to DNA damage, epirubicin

100 y is a direct result of Ku inhibition, as Ku-null cells are insensitive to Ku-DBi's.

101 Lig3-null cells are not sensitive to several DNA-damaging age

102 for proliferation and invasion, whereas MUC1-null cells are not.

103 rnatively, when challenged with rapalogs TSC-null cells are reprogrammed to express mesenchymal-like

104 Consistently, BMH1-null cells are SPOC deficient.

105 These studies indicate that TSC2-null cells are the inciting cells for TSC skin hamartoma

106 We show that Aid-null cells are transiently hyper-responsive to the repro

107 ChIP-seq using CBP-null cells as a control revealed nearby CBP recruitment

108 -mesenchymal transition (EMT) in BVE(Cyp24a1-null) cells, associated with downregulation of genes inv

109 In 29 Casq1-null cells, B was 40 (3.6).

110 ed that in contrast with parental cells, BSG-null cells became highly sensitive to phenformin, an inh

111 phosphorylation sites in PKA-intact and PKA-null cells both revealed a preference for basic amino ac

112 in adult mice behaves largely similar to Atm-null cells but shows greater deficiency in homologous re

113 t endpoints; cargo export is delayed in mvp1-null cells, but cargo export completely fails in vps1-nu

114 cargo export is deficient in mvp1- and vps1-null cells, but with distinct endpoints; cargo export is

115 adhesion phenotypes can be restored in PKP2-null cells by dampening the RhoA pathway or silencing be

116 rectly evaluate the efficacy of rescuing K14-null cells by supplementation with wild-type K14 complem

117 These defects in Mule-null cells can be partially reversed by HDACis and fully

118 Stalled replication forks in Pten-null cells can be reactivated by ectopic Rad51 or PTEN,

119 phological and functional impairments in p73 null cells can be rescued by p75(NTR) re-expression.

120 icate that: (a) apoptotic cell death in FLCN-null cells can be triggered by SSH2 knockdown through ce

121 A3B expression in UNG-null cells causes a buildup of genomic uracil, and the e

122 Depletion of JAK2 or use of JAK2-null cells causes defects in MT anchoring and increased

123 ed delivery of cholesterol to the PM in ORP1-null cells, cholesterol was diverted to the ER resulting

124 r)UCA-C47:6U levels in sla1-rrm but not sla1-null cells, consistent with non-specific low-affinity in

125 SIRT3 null cells contain high levels of iron and lose iron-dep

126 alyses of BITC-treated xenografts using LKB1-null cells corroborate in vitro mechanistic findings and

127 transplantation demonstrated that Gabpalpha null cells could not contribute to the myeloid compartme

128 ds also reduced in vitro cyst growth of Pkd1-null cells cultured in a 3D matrix.

129 When overexpressed in PakB-null cells, dAbp1 completely blocks early development at

130 iling revealed that depletion of p62 in Tsc2-null cells decreased intracellular glutamine, glutamate,

131 Analysis of Ku-null cells demonstrates that Ku-DBi's cellular activity

132 aberrant mTORC1 activation might confer TSC-null cell dependence on transcriptional regulation.

133 In LKB1-null cells derived from an autochthonous murine model of

134 TAp63/p53-null cells derived from these mice also showed an enhanc

135 Casp1(Null) cells did not release IL-1beta and IL-18 in respon

136 Conversely, we find that E2A null cells display a defect in their neural differentiat

137 SENP2 null cells display biphasic NEMO SUMOylation and activat

138 however, upon transplantation in vivo, FOXG1-null cells display increased astrocyte differentiation a

139 were isolated and cultured in vitro, Ptp4a3-null cells displayed greatly reduced migration compared

140 Non-adherent myosin II null cells do not exhibit these curvature waves.

141 Overexpression of HSP70 in WASF3 null cells does not enhance invasion.

142 Deletion of CUL9 in p53 null cells does not lead to further increase of DNA dama

143 eomics in fibroblasts reveals that mitofusin-null cells downregulate respiratory chain complexes and

144 he UPR could be targeted to eradicate TSC1/2-null cells during patient therapy.

145 n alters PARP inhibitor sensitivity of BRCA1-null cells, end-joining activity, and immunoglobulin cla

146 Yet, Greatwall-null cells enter into mitosis with normal kinetics.

147 astasis model, the HCT116 parental and H2A.X-null cells exhibit a similar metastatic behaviour, but t

148 lement-binding protein (SREBP) pathway, Idol-null cells exhibit an altered response to multiple regul

149 Emerin-null cells exhibit an epigenetic signature similar to th

150 the catalytic activity of HDAC3, and emerin-null cells exhibit increased H4K5 acetylation, which is

151 Unexpectedly, Jurkat CD47 null cells exhibited a striking defect in beta1 and beta

152 to ICL lesions prior to FANCD2, and Merit40-null cells exhibited delayed ICL unhooking coupled with

153 FLCN-null cells exhibited evidence of dysregulated cofilin de

154 eas heparin lyase-treated and beta1 integrin-null cells exhibited more selective decreases.

155 Moreover, V-1-null cells exhibited pronounced defects in macropinocyto

156 Interestingly, however, trex2(null) cells exhibited reduced spontaneous sister chromat

157 ted spontaneous broken chromosomes and trex2(null) cells exhibited spontaneous chromosomal rearrangem

158 s was recapitulated in cultured beta-catenin-null cells exposed to externally applied forces.

159 We found that Twist1-null cells expressed high levels of the T cell chemoattr

160 Using vinculin-null cells expressing vinculin mutants, we demonstrate t

161 gic low-proliferating conditions, human TP53 null cells fail to increase expression of NDRG1 compared

162 ued to generate BCR-ABL-expressing Gabpalpha-null cells for months that were serially transplantable

163 sitivity was seen among PALB2-null and BRCA2-null cells for the ethanol metabolite, acetaldehyde, ass

164 Increased CD4(+) CD28(null) cell frequencies were associated with delayed graf

165 Furthermore, Dicer1 null cells from a sarcoma cell line, though depleted of

166 In a genetic complementation assay in GATA-1-null cells, GATA-1 expels FOG-1-dependent target genes f

167 criptomics analysis revealed that, in POU5F1-null cells, gene expression was downregulated not only f

168 HspB1-null cells, generated by CRISPR/Cas9 nuclease genome edi

169 dent activation of RhoA is required for TSC2-null cell growth and survival and suggest that targeting

170 in inhibiting the survival of tuberin (TSC2)-null cells, growth of TSC2-null xenograft tumors, and de

171 acity to bind LDL and when expressed in LDLR null cells had compromised LDL uptake as compared to the

172 by treatment with AZA demonstrated that Tet2-null cells have an engraftment advantage over Tet2-WT ce

173 Correspondingly, CLN3-null cells have reduced caveolae, and impaired caveolae-

174 orylation and directed cell migration in Rho-null cells in a manner dependent on phosphorylation of S

175 We demonstrate that TSC1- or TSC2-null cells, in contrast to their wild-type counterparts,

176 ely, PKA-dependent. Upregulated sites in PKA-null cells include Ser256 of AQP2, which is critical to

177 es was analyzed using a combination of CIITA-null cells, including a novel cell line created using CR

178 ysis of the phosphopeptides increased in PKA-null cells indicates that vasopressin activates one or m

179 duced fluorescence near the levels in GABAAR-null cells indicating that FMR-Red-Dye, a barbiturate de

180 igands have no effect on LDLR levels in Idol-null cells, indicating that Idol is required for LXR-dep

181 presence of beta3-integrin in beta1-integrin-null cells, indicating that integrins containing differe

182 chanism by which secretin multimers kill psp null cells is by causing a profound defect in the cytopl

183 nterestingly, alternative exon usage by PTEN null cells is increased under metabolic stress in contra

184 yocytes treated with Plk1 inhibitors or Plk1-null cells is triggered by the spindle assembly checkpoi

185 ells lacking costimulatory CD28 (CD4(+) CD28(null) cells) is associated with latent cytomegalovirus (

186 Coronin 1C-null cells isolated from this model are more invasive in

187 t decrease cell proliferation in BVE(Cyp24a1-null) cells, it strengthened antitumor responses to the

188 the basic actin machinery was intact, Cdc42 null cells lacked the ability to polarize their Golgi an

189 The latter was used to generate a Cul3-null cell line (HEK293T(Cul3KO)).

190 latin or telomestatin sensitivity of a fancj null cell line and exerted a dominant negative effect.

191 d to rescue cisplatin sensitivity of a FANCJ null cell line as detected by cell survival or gamma-H2A

192 se cell aggregation experiments using a rumi null cell line indicate that a complete lack of Rumi doe

193 The resulting LIGIV-null cell line was viable, verifying that the gene and C

194 METHODS AND We compared a VEC-null cell line with the same line reconstituted with VEC

195 tion assay, (2) expression levels in a Dicer null cell line, and (3) Ago2 pulldown.

196 We generated a PDE12-null cell line, HeLaDeltaPDE12, using transcription acti

197 ly, when we expressed this variant in a TP53-null cell line, it induced cell motility, proliferation,

198 ts were expressed in DT40-3KO cells, an IP3R null cell line.

199 elta9 desaturase mRNA expression in LmNcb5or null cell line.

200 w that STRADalpha protein is reduced in LKB1-null cell lines (mutation or homozygous deletion) and th

201 These K14-null cell lines provide a disease model for studying the

202 Flp recombinase to restore expression in two null cell lines to demonstrate how our system confirms c

203 rescued by re-expression of IQGAP1 in IQGAP1-null cell lines.

204 DNA damage, we stimulated TP53 wild-type and null cell-lines with doxorubicin and performed RNA seque

205 stores ionizing radiation sensitivity to p53 null cells, making LRF an attractive biomarker to direct

206 ErkB null cells migrate slowly and orientate poorly over broa

207 and that reintroduction of SNF5 into SMARCB1-null cells mimics the primary transcriptional effects of

208 SPRTN null cells or cells derived from patients with Ruijs-Aal

209 ath by chemotherapeutic drugs but E-cadherin null cells or those expressing E-cadherin only in the cy

210 All N-glycans in the TbRft1-null cells originate from mDLO indicating that the M5-DL

211 nificantly decreased this advantage for Tet2-null cells (P = .002) but not Tet2-WT cells (P = .212).

212 Exocytosis is impaired in vti1a null cells, partly due to fewer Ca(2+)-channels at the p

213 COG null cells possess altered content and subcellular local

214 Furthermore, KLF4 null cells proliferate rapidly, forming large, invasive,

215 Isolated CD4(+) CD27(-) CD28(null) cells proliferated in response to peripheral blood

216 data demonstrate that mTORC2 modulates TSC2-null cell proliferation and survival through RhoA GTPase

217 ruption of alphaB-crystallin suppressed Tsc2-null cell proliferation and tumorigenesis.

218 TSC2-null cell proliferation was inhibited not only by reexpr

219 Zyxin-null cells reconstituted with zyxin variants that lack e

220 in vivo and in vitro proliferation of CD98hc-null cells, reconstitution of the integrin signaling fun

221 Inhibition of uPA expression in Tsc2-null cells reduced the growth and invasiveness and incre

222 ty acid binding mutant R126Q) into FABP4/aP2 null cells reduced UCP2 expression, suggesting that the

223 ile reintroducing PC1-CTT into cultured Pkd1 null cells reestablishes normal growth rate, suppresses

224 The genome of Aid-null cells remains hypermethylated in reprogramming cell

225 ress, and restoring Plk3 expression in Lrh-1-null cells rescues ER stress resolution.

226 t changes in abundance in PKA-intact and PKA-null cells, respectively.

227 nation lethality; expression of PTEN in PTEN-null cells restored drug sensitivity, and knockdown of P

228 sion of Cmas and Slc35a1 into the respective null cells restored sialic acid expression and T3SA(+) b

229 Here we show that depleting 53BP1 in BRCA1-null cells restores PALB2 accrual at resected DSBs.

230 absence of Ews and depletion of Fbxw7 in Ews-null cells restores PGC-1alpha expression and mitochondr

231 y, reintroduction of SOX10 into human Merlin-null cells restores the ability of these cells to induce

232 hdrawal, whereas expression of mutp53 in p53 null cells results in resistance to glutamine deprivatio

233 To test whether UBE2T null cells retain HR activity, the UBE2T genes were knoc

234 Pharmacologic ATM inhibition and use of ATM-null cells revealed a critical role for ATM in this proc

235 RNA-seq data from p21-null cells revealed that gene downregulation by TP53 gen

236 Reconstitution of NEMO-null cells revealed that the N-terminal 251 amino acid r

237 ng of MTs in P1c(-/-), as well as in plectin-null, cells revealed decreased MT dynamics.

238 The K14-null cells show elevated levels of stress correlating wi

239 ot exacerbate the vti1a phenotype, and vti1b null cells show no secretion defects, indicating that vt

240 Under such conditions null cells show oxidative stress and intracellular AA im

241 ated with AT-SCT presented on MHC class I/II-null cells show reduced cytokine production, slower kine

242 Analysis of GANAB-null cells showed an absolute requirement of GIIalpha fo

243 mutant p.Arg412( *) PIGA construct into PIGA-null cells showed partial restoration of GPI-anchored pr

244 rocess invasion, and cultured laminin alpha2-null cells showed reduced migratory potential, indicatin

245 diac fibroblasts, and lineage tracing of the null cells showed their inability to undergo EMT.

246 yellow fluorescent protein in the ctxI/ctxII-null cells significantly rescues the wild-type phenotype

247 role for this atypical cytotoxic CD4(+) CD28(null) cell subset in kidney transplantation and points t

248 deficient cells to a similar degree as FANCE null cells, suggesting the significance of the FANCE-FAN

249 g murine fibroblasts but not isogenic IGF-1R-null cells, supporting specificity for IGF-1R.

250 TSC2-null cells surrounding the hair bulb expressed markers o

251 Egr1 mRNA is much more effective in 4E-BP1/2-null cells than in control.

252 ines that represent ideal models to study AR-null cells that have upregulated GR to sustain growth.

253 rcinoma HepG2 (p53 wild type) and Hep3B (p53 null) cells that was accompanied with decreased expressi

254 Moreover, in CD98hc-null cells the deficiency of CD98hc/xCT cannot be compen

255 heparin-induced cell cycle arrest and in PKR null cells the STAT1 phosphorylation in response to hepa

256 rection of the high O(2) requirement of P4H1-null cells, therefore revealing both glycosylation-indep

257 ecovered the mitochondrial functions of OPA1-null cells, thus demonstrating the functional significan

258 le Rac1 rescues the migration defect of Rac1-null cells to a greater extent than wild-type Rac1.

259 ion (EMT) program that commits embryonic FAK-null cells to an epithelial status highlighted by the ex

260 nal shift from an osteolytic program in KLF4 null cells to an osteogenic program.

261 Finally, p62 depletion sensitized Tsc2-null cells to both oxidative stress and direct inhibitio

262 in levels enhanced by mTORC1 sensitized TSC2-null cells to iron deprivation due to constitutive ISC b

263 unction appeared rooted in a failure of Sun2-null cells to reorganize their microtubule network to su

264 scued by lowering the elevated HDAC2 in Mule-null cells to the normal levels as in wild-type cells.

265 whose loss selectively resensitized the p53-null cells to this chemotherapeutic agent.

266 mma-secretase complex presenilin 1 from Tsc1-null cells to wild-type cells leading to the activation

267 mes derived from tuberous sclerosis 1 (Tsc1)-null cells transform phenotypes of neighboring wild-type

268 NF2-null cells treated with an ERBB3-neutralizing antibody p

269 nd cleaved protein was up-regulated in Wfdc1-null cells treated with lipopolysaccharide or polyinosin

270 does not inhibit TonEBP/OREBP in PLC-gamma1-null cells unless PLC-gamma1 is reconstituted.

271 Knockdown of SSH2 in FLCN-null cells was associated with an alteration in cell cyc

272 rt that faster cell cycle entry of p27(kip1)-null cells was impaired by the concomitant deletion of s

273 reover, rapamycin-enhanced migration of TSC2-null cells was inhibited by the uPA inhibitor UK122, dex

274 Growth of gmps null cells was only rescued by supraphysiological guanin

275 ntation assay and RNA interference in GATA-1-null cells, we demonstrate a vital link between GATA-1 a

276 Using Fis1-null, Mff-null, and Fis1/Mff-null cells, we show that both Fis1 and Mff have roles in

277 ssing structure-based talin mutants in talin null cells, we show that while the C-terminal actin-bind

278 Global transcript profiles in Dot1l-null cells were barely altered.

279 However, p120 null cells were essentially nonadherent, excluded from t

280 The glucose-deprived PTEN null cells were found to continue global gene transcript

281 First, we found that beta-catenin null cells were incapable of undergoing acinar to ductal

282 Two days after virus injection, Panx1-null cells were less abundant than Panx1-expressing cell

283 ration was significantly greater when IQGAP1-null cells were reconstituted with IQGAP1 Y1510A than wh

284 p53/Rb-null cells were sensitive to p53-induced translation str

285 1, and >18 mM, respectively), whereas GABAAR-null cells were unresponsive.

286 C-NAP1-null cells were viable and had an increased frequency of

287 CD4(+) CD28(null) cells were found predominantly in CMV-seropositive

288 ion, and impaired tumorigenesis of Ink4a/Arf-null cells, whereas expression of an activated PI3K muta

289 vere block in differentiation than in Dnmt3a-null cells, whereas loss of Dnmt3b resulted in a mild ph

290 Bax restore mitochondrial fusion in Bax/Bak-null cells, which otherwise exhibit fragmented mitochond

291 in both differentiating wild-type and Ppard null cells, while macrophage/DC marker genes were up-reg

292 We compared KLF4 null cells with cells transduced with a DOX-inducible KL

293 Reconstitution of PTEN-null cells with either wild-type PTEN or a catalytically

294 en associated with the metastasis of tuberin-null cells with hyperactive mammalian target of rapamyci

295 h this observation, reconstitution of IQGAP1-null cells with IQGAP1 GRD-2K significantly increased th

296 Reconstitution of Rictor-null cells with myristoylated AKT (Myr-AKT) rescued vasc

297 pools of p21 (p53 independent) provided p53 null cells with protection from the combination therapy.

298 Reconstitution of RelA null cells with the RelA(T305A) mutant illustrates the i

299 Transfection of Prx6 null cells with wild-type and C47S mutant Prdx6, but not

300 d with BRCA1 loss, rescues survival of BRCA1-null cells without restoring ROS levels.