ライフサイエンスコーパス: null cell

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

2 ctivated enhancers highly transcribed in p53 null cells.

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

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

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

6 paB activation is totally diminished in cNOS null cells.

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

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

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

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

11 estabilization and enhanced fluidity in CLN3-null cells.

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

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

14 l methanesulfonate and excess Rad51 in rdh54 null cells.

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

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

17 53-dependent; this effect was ablated in p53-null cells.

18 CK showed reduced phosphorylation in DGKzeta-null cells.

19 phenocopies the cellular senescence of TAp73-null cells.

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

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

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

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

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

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

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

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

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

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

30 with significantly higher activation in Pten-null cells.

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

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

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

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

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

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

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

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

39 y, and invasion are particularly high in p53-null cells.

40 says, leading to the induction of p21 in p53-null cells.

41 n human endothelial cells and in murine CD47-null cells.

42 currents did not differ between WT and ClC-3 null cells.

43 ant pathway to selectively induce p73 in p53-null cells.

44 apical constriction and invagination in APC null cells.

45 ed SGK1 protein levels as detected in Rictor null cells.

46 ctivates AMPK and reduces p27 levels in Tsc2-null cells.

47 e-dependent inactivation in WT but not ClC-3 null cells.

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

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

50 these increases were eliminated in HIF1alpha null cells.

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

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

53 iched repressive nuclear compartments in p63-null cells.

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

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

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

57 ium membrane potentials compared with GABAAR-null cells.

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

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

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

61 centrosome, with reduced association in p53 null cells.

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

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

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

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

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

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

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

69 y smaller than currents recorded in caveolin-null cells (179.7 +/- 35.9 pA pF(1), n = 6; P < 0.05) in

70 ess-induced apoptosis compared to C/EBP beta-null cells, a finding in agreement with the decreased le

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

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

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

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

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

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

77 der resting conditions indicate that triadin-null cells also have higher Ca(2+) entry rates and lower

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

79 CD98hc-null cells also present reduced intracellular levels of

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

81 ble expression for certain genes in CBP/p300 null cells and contributed to the CBP/p300-independent e

82 tivity by high NaCl is reduced in PLC-gamma1 null cells and in HEK293 cells in which PLC-gamma1 is kn

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

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

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

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

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

88 Using cadherin and Cx-null cells, and by introducing Cx43 and Cx32, either alo

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

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

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

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

93 -wild-type HCT116 cells more than in the p53-null cells, and upregulates specific p53 targets (that i

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

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

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

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

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

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

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

101 However, BSH null cells are significantly altered in acid and salt re

102 Consistently, BMH1-null cells are SPOC deficient.

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

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

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

106 re was induction of promoter activity in the null cells as compared with the wild-type cells.

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

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

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

110 tion of wild-type TonEBP/OREBP in PLC-gamma1 null cells but not of TonEBP/OREBP-Y143A.

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

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

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

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

115 of both endogenous and exogenous p21 in p53-null cells by extending its half-life, leading to p21-de

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 In Pkd1-null cells, Casitas B-lineage lymphoma (c-Cbl), an E3-ub

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

123 Knockdown of ENTPD5 in PTEN null cells causes ER stress and loss of growth factor re

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 FN-null cells cultured on recombinant CCBD (FNIII(8-11)) wi

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

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

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

134 SENP2 null cells display biphasic NEMO SUMOylation and activat

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

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

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

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

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

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

141 In IQGAP1-null cells, EGF-stimulated tyrosine phosphorylation of E

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

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

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

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

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

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

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

149 FLCN-null cells exhibited evidence of dysregulated cofilin de

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

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

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

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

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

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

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

157 Moreover, DDK-null cells fail to activate the intra-S-phase checkpoint

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

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

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

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

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

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

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

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

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

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

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

169 tion with ryanodine, suggesting that triadin-null cells have increased basal RyR1 activity.

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

171 lso Ing4-dependent, and LPS-stimulated, Ing4-null cells have reduced levels of IkappaB alpha promoter

172 egulated following DNA damage in 14-3-3sigma null cells, implicating 14-3-3sigma as a critical regula

173 ClC-3 expression induced ICl(swell) in ClC-3 null cells in the absence of swelling or TNF-alpha, and

174 d with inhibition of tumor formation by Tsc2-null cells in vivo.

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

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

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

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

179 trate that induced expression of MTA1 in p53-null cells inhibits p21(WAF1) promoter activity and p21(

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

181 The growth of PTEN null cells is inhibited both in vitro and in mouse xenog

182 Dephosphorylated VASP in beta3-null cells is preferentially associated with Rap1-GTP-in

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

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

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

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

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

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

189 platin or telomestatin sensitivity of a FA-J null cell line as detected by cell survival or gamma-H2A

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

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

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

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

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

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

196 elta9 desaturase mRNA expression in LmNcb5or null cell line.

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

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

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

200 blotting of normal, metastatic, and vimentin-null cell lines, we show that the level of expression of

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

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

203 Rac1 null cells migrate markedly less efficiently, but surpri

204 In OXPHOS-dependent LKB1-null cells, no AMPK activation by oligomycin is detected

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

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

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

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

209 , overexpression of GCLC and GCLM in IKKbeta-null cells partially restores GSH content and prevents s

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

211 reased cell death all contribute to the PARG null cell phenotype in response to genotoxic stress.

212 In contrast, FN-null cells plated on FNIII(8-11) contiguous with FN-GFBD

213 COG null cells possess altered content and subcellular local

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

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

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

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

218 We demonstrate that in myosin II (MyoII) null cells, Ras activation is highly extended and is not

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 Importantly, the HR deficiency of PTEN-null cells renders them sensitive to the poly(ADP-ribose

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

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

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

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

230 Consequently, MTA1 expression in p53-null cells results in increased induction of gamma H2AX

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

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

233 FAT/CD36 null cells revealed similar characteristics, except that

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

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

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

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

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

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

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

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

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

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

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

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

246 In OGT null cells, stress-induced inactivation of GSK-3beta by

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 FN-null cell survival on FNIII(8-11) and noncontiguous arra

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

253 complex, since decompaction occurs in Ring1B null cells that still have PRC2-mediated H3K27 methylati

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

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

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

257 In OGT null cells the stress-induced expression of 18 molecular

258 sing and signaling by ATM were normal in Mof-null cells, the recruitment of repair mediator protein M

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

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

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

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

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

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

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

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

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

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

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 itor preadipocyte factor 1 (Pref-1) in IRS-1-null cells was markedly reduced by 3 days of BMP7 treatm

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

276 mechanism responsible for activation of NPC2-null cells was shown to be a sustained phosphorylation o

277 In OGT null cells we observed increased Ser(P)(303) HSF1; conve

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

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

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

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

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

283 Human MPS1-null cells were generated via gene targeting and reconst

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

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

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

287 1, and >18 mM, respectively), whereas GABAAR-null cells were unresponsive.

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

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

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

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

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

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

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

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

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.