ライフサイエンスコーパス: NIH-3T3 cell

1 do not (i.e., H-Ras/NIH 3T3, MDA-MB-453, and NIH 3T3 cells).

2 ix metalloproteinase-9 in both MCF-7-Ptn and NIH 3T3 cells.

3 in primary mouse blastocysts, as well as in NIH 3T3 cells.

4 ploidy, and transformation in nontransformed NIH 3T3 cells.

5 riched membrane ruffles induced by PDGF-B in NIH 3T3 cells.

6 ation of 10T1/2 cells, and Gli activation in NIH 3T3 cells.

7 se to increased levels of activated Cdc42 in NIH 3T3 cells.

8 d by 5' RACE techniques using total RNA from NIH 3T3 cells.

9 astic growth and oncogenic transformation of NIH 3T3 cells.

10 lpha12-mediated neoplastic transformation of NIH 3T3 cells.

11 ll proliferation in rat lens explants and in NIH 3T3 cells.

12 promoted the anchorage-independent growth of NIH 3T3 cells.

13 as an oncogene, since it can transform mouse NIH 3T3 cells.

14 d activation of Notch1 signaling in 293T and NIH 3T3 cells.

15 acetylation, and increased transformation of NIH 3T3 cells.

16 s and can cooperate with RasV12 to transform NIH 3T3 cells.

17 Ras proliferative signaling in experimental NIH 3T3 cells.

18 lized human thyroid cells (Nthy-ori 3-1) and NIH 3T3 cells.

19 red to promote Ras-induced transformation of NIH 3T3 cells.

20 IE1 stimulated AP-1 activity in NIH 3T3 cells.

21 in AP-1 binding complexes in IE1 transfected NIH 3T3 cells.

22 easured in vitro), and a growth inhibitor in NIH 3T3 cells.

23 mitting reporter for imaging living HeLa and NIH 3T3 cells.

24 tive effects on the growth transformation of NIH 3T3 cells.

25 ls and was completely independent of cAMP in NIH 3T3 cells.

26 ected into nude mice, unlike LTAg-transduced NIH 3T3 cells.

27 magnetic laminin-coated microbeads bound to NIH 3T3 cells.

28 stimulates gene expression in HeLa, COS, and NIH 3T3 cells.

29 inhibited PLD activity in H-Ras-transformed NIH 3T3 cells.

30 in apoptosis of serum-starved TEL-expressing NIH 3T3 cells.

31 were measured for various forms of H-Ras in NIH 3T3 cells.

32 ression only in Rat-1 cells, not in CCl39 or NIH 3T3 cells.

33 essential for viral replication in vitro in NIH 3T3 cells.

34 ith H3me2K9 both in chicken erythrocytes and NIH 3T3 cells.

35 essed transcription in exponentially growing NIH 3T3 cells.

36 n a striking cooperative induction of MBP in NIH 3T3 cells.

37 ing led to multiple spindle abnormalities in NIH 3T3 cells.

38 Pases in vivo and to cause transformation of NIH 3T3 cells.

39 d eliminated the ability of Dbs to transform NIH 3T3 cells.

40 ladder cells, but not in nonmalignant 293 or NIH 3T3 cells.

41 retroviral vector was inoculated into XC and NIH 3T3 cells.

42 ed GTP loading when transiently expressed in NIH 3T3 cells.

43 as identified by transfection analysis using NIH 3T3 cells.

44 malignant embryonic kidney 293 or fibroblast NIH 3T3 cells.

45 nsin2 were expressed as a 170-kDa protein in NIH 3T3 cells.

46 ted forms of Clg morphologically transformed NIH 3T3 cells.

47 s in oncogenic Ras-induced transformation of NIH 3T3 cells.

48 PI3K during G(2)/M in synchronized HeLa and NIH 3T3 cells.

49 g formation of lamellipodia and filopodia in NIH 3T3 cells.

50 12 cells, and Ras-induced focus formation in NIH 3T3 cells.

51 n of the ligands with endogenous caveolin in NIH 3T3 cells.

52 activation, and decreased transformation in NIH 3T3 cells.

53 ary cultures of human trabecular meshwork or NIH 3T3 cells.

54 tivating protein, to the plasma membranes of NIH 3T3 cells.

55 ell surface markers in a large proportion of NIH 3T3 cells.

56 ely phosphorylated on Ser-271 in transfected NIH 3T3 cells.

57 and oncogenic when ectopically expressed in NIH 3T3 cells.

58 ictions for lentivirus replication in murine NIH 3T3 cells.

59 d the transformation of both pre-B cells and NIH 3T3 cells.

60 of Pro-LOX to the LOX-PP in Ras-transformed NIH 3T3 cells.

61 ormed NIH 3T3 cells but not in untransformed NIH 3T3 cells.

62 ls, as well as mitogenesis and chemotaxis of NIH-3T3 cells.

63 PKB) in fibrosarcoma cell line HT1080 and in NIH-3T3 cells.

64 ly and late adipogenic markers in BALB/c and NIH-3T3 cells.

65 These are highly activated and transform NIH-3T3 cells.

66 ion, we stably transfected AMF/PGI cDNA into NIH-3T3 cells.

67 F-1R) cells but not in that of untransfected NIH-3T3 cells.

68 , are targeted using RNAi in Ras-transformed NIH-3T3 cells.

69 l as well as PMA-induced Tspo mRNA levels in NIH-3T3 cells.

70 teins had slow mobility in nucleus of living NIH-3T3 cells.

71 ion of eIF3h malignantly transforms immortal NIH-3T3 cells.

72 es to the hypotonic stress-induced VSOACs in NIH/3T3 cells.

73 obes were exposed to raw nuclear lysate from NIH/3T3 cells.

74 k9(42) and Cdk9(55), are present in HeLa and NIH/3T3 cells.

75 ransactivated 20- to 30-fold in both HTB and NIH/3T3 cells.

76 XMRV in an endogenous retrovirus present in NIH/3T3 cells.

77 By this methodology, K:Molv NIH 3T3 cells, 786-O human kidney carcinoma cells, and M

78 rease in colony formation by ras-transformed NIH 3T3 cells, a finding comparable to the expression of

79 mutant also enhances Src-STAT3 signaling in NIH-3T3 cells, a pathway previously shown to be directly

80 n and tumorigenicity of Ras(V12)-transformed NIH 3T3 cells, activated SASP gene expression, and recru

81 activation of GTPases also do not transform NIH 3T3 cell and fail to activate RhoA in vivo despite p

82 e pathway in reticulocyte extracts and mouse NIH 3T3 cells and after its secretion by intracellular b

83 of PRMT7, we knocked down its expression in NIH 3T3 cells and analyzed global gene expression.

84 osine phosphorylation of endogenous TRIP6 in NIH 3T3 cells and c-Src-expressing fibroblasts, which is

85 of mPcl1, the mouse counterpart of hPHF1, in NIH 3T3 cells and cells of the mouse male germ cell line

86 orted Sec insertion in mammalian HEK 293 and NIH 3T3 cells and did so more efficiently than the natur

87 inhibits colony formation by Ras-transformed NIH 3T3 cells and hinders proliferation of a variety of

88 f phosphotyrosine STAT3 in v-Src-transformed NIH 3T3 cells and human cancer cells potently (IC(50) va

89 EGF binding to Flk-1 in Flk-1-overexpressing NIH 3T3 cells and human prostate tumor cells with an IC(

90 ened a yeast two-hybrid library derived from NIH 3T3 cells and identified ERK as a Us2-interacting pr

91 erference (RNAi) screen in K-ras-transformed NIH 3T3 cells and identify 28 genes required for Ras-med

92 is protein, relative to that of F43, both in NIH 3T3 cells and in the brains of infected mice.

93 In NIH 3T3 cells and in the human retinal pigment epitheliu

94 uses distinct effector pathways to transform NIH 3T3 cells and induce pheochromocytoma cell (PC6) dif

95 f RhoA and p160ROCK activity in fibroblastic NIH 3T3 cells and its presence in epithelial NMuMG cells

96 These mutants also transformed NIH 3T3 cells and led to an enhanced metastatic phenotyp

97 overexpression of Xenopus Aur-A transformed NIH 3T3 cells and led to tumors in nude mice.

98 since it can morphologically transform mouse NIH 3T3 cells and other fibroblast lines.

99 amma2-mediated adipogenic gene expression in NIH 3T3 cells and promoted preadipocyte differentiation

100 uction of AP-1 and relB promoter activity in NIH 3T3 cells and SMCs.

101 bolished the ability of v-H-Ras to transform NIH 3T3 cells and to induce germinal vesicle breakdown i

102 v-ErbB:ER conditionally transformed NIH-3T3 cells and abrogated cytokine dependence of hemat

103 to stimulate anchorage-independent growth in NIH-3T3 cells and in SKBR3 cells and also inhibits cell

104 B:ER, on the morphological transformation of NIH-3T3 cells and the abrogation of hematopoietic cell c

105 lf-life of RhoB mRNA from 63 min to 3.3 h in NIH/3T3 cells and from 87 min to 2.7 h in normal human k

106 creased ethanol inhibition of L1 adhesion in NIH/3T3 cells and NG108-15 cells.

107 his, activated Rac1 co-localizes with Dbs in NIH 3T3 cells, and natively expressed Rac1 relocalizes i

108 N4) lens epithelial cells and in mouse lung, NIH-3T3 cells, and HeLa cells, which served as positive

109 lls, and alphaTN4 cells and from HeLa cells, NIH-3T3 cells, and partially purified GR, which served a

110 er from either species were transfected into NIH-3T3 cells, and reporter activity was highly represse

111 utively activated FGFR3 (K/E-FR3) transforms NIH-3T3 cells, and that SHP2 is a critical mediator of t

112 nucleotides) on genome editing capability in NIH/3T3 cells, and its efficiencies on generating Factor

113 nal repression mediated by the RE element in NIH 3T3 cells appears to differ significantly from the m

114 ies of TGFBR1*6A, we assessed its effects on NIH-3T3 cells as well as its effect on the migration and

115 d cellular uptake of NPs in SVCT2 expressing NIH/3T3 cells as compared to plain PLGA and PLGA-b-mPEG

116 nted signaling by the Tgfbr1/Smad2/3 axis in NIH/3T3 cells, as well as primary lung fibroblasts, smoo

117 ecreased Gli-luciferase reporter activity in NIH/3T3 cells, as well as the endogenous hedgehog-respon

118 expressing rAdpC (V2846) invaded fibroblast NIH 3T3 cells at a 40-fold-higher frequency than control

119 ly reconstruct the lineage of cultured mouse NIH 3T3 cells based on mutations affecting the length of

120 For NIH 3T3 cells bearing wild-type CD151, adhesion strength

121 (referred to as "fast-cycling"), transformed NIH 3T3 cells because of its ability to interfere with e

122 When expressed in NIH/3T3 cells, both K(v)4.2 and K(v)4.3 channels were al

123 nd endogenous UBF from exponentially growing NIH 3T3 cells but not by hypophosphorylated UBF from cel

124 le to affect splicing of the E1A reporter in NIH 3T3 cells but not in L-G cells.

125 ons of the Fas promoter in K-ras-transformed NIH 3T3 cells but not in untransformed NIH 3T3 cells.

126 erminus retain high transforming capacity in NIH 3T3 cells but transform lymphocytes poorly.

127 eLa and ME-180 cervical carcinoma cells, and NIH 3T3 cells but was without significant effect in H129

128 migration in HMECs and in CXCR2-transfected NIH 3T3 cells, but not in RBL2H3 cells, which do not exp

129 n which apoptosis resistance is conferred on NIH 3T3 cells by ectopic expression of eIF4E.

130 FRAP also suppressed transformation of NIH 3T3 cells by ras, with DBA/2 FRAP being more efficie

131 EGFRvIII and inhibits the transformation of NIH 3T3 cells by the EGFRvIII.

132 t that the suppression of Notch signaling in NIH 3T3 cells by the expression of either the extracellu

133 However, when introduced into NIH 3T3 cells by using a protein delivery reagent, it ef

134 Sixteen genes induced in NIH 3T3 cells by wild type EVI1-VP16 but not by mutant f

135 Further, while overexpression of CRY2 in NIH 3T3 cells caused a dose-dependent decrease in rhythm

136 Ectopic MENT expression in NIH 3T3 cells caused a large-scale and specific remodeli

137 Ectopic expression of MetAP2 in NIH-3T3 cells caused transformation, evidenced by the fo

138 indicates that expression of the receptor in NIH 3T3 cells causes an increased secretion of vascular

139 en transcripts were found in both IMR-90 and NIH 3T3 cells (CHIC2, GADD45B, HO-1, PTGS2, RGS2, TIEG,

140 MCF-7-Ptn cell xenografts and MCF-7-Ptn cell/NIH 3T3 cell cocultures closely resembled breast cancers

141 pressing 290-base sense and antisense RNA in NIH 3T3 cells controlled by tetracycline or doxycycline.

142 ce of overexpressed eIF3h in rapidly induced NIH-3T3 cells correlates tightly with the stimulation of

143 of transformation, LANA- and kCYC-transduced NIH 3T3 cells demonstrated minimal or no anchorage-indep

144 Immunoblot analysis of infected NIH 3T3 cells demonstrated the accumulation of uncleaved

145 Mouse NIH 3T3 cells depleted of Ctip were arrested at G(1) wit

146 In an Arf-null NIH 3T3 cell derivative (MT-Arf cells) engineered to ree

147 pressed in XC cells was smaller than that in NIH 3T3 cells due to altered N glycosylation in XC cells

148 genous and transfected thrombin receptors in NIH 3T3 cells, ectopic expression of muscarinic receptor

149 NIH 3T3 cells ectopically expressing C/EBP alpha (NIH-C/

150 t insulin-stimulated glucose uptake, whereas NIH 3T3 cells ectopically expressing PPAR gamma (NIH-PPA

151 Similar to EGFR Mut R1-6/L393H in NIH 3T3 cells, EGFR variant type III, a highly oncogenic

152 cutaneous xenografts of Src Y527F expressing NIH 3T3 cells elicited dose-dependent tumor shrinkage wi

153 hese data suggested that during infection of NIH 3T3 cells, endocytosis brings Moloney MLV to early l

154 ants grew in soft agar, and PPFP-transfected NIH 3T3 cells exhibited efficient focus formation, sugge

155 ent with 700 pM ET-743 of stably transfected NIH 3T3 cells expressing a human type II procollagen gen

156 ne alone allowed efficient foci formation of NIH 3T3 cells expressing BCR-ABL (triple positive cells)

157 Our previous work demonstrated NIH 3T3 cells expressing different FGF-2 forms, displaye

158 In addition, XMRV poorly infects NIH 3T3 cells expressing human Xpr1 but relatively effic

159 athways in the absence of added ligands, and NIH 3T3 cells expressing ORF74 are tumorigenic in nude m

160 NIH 3T3 cells expressing Shp2E76K produce higher levels

161 noprecipitations of the EGFR in HMECs and in NIH 3T3 cells expressing the CXCR2 confirmed that the EG

162 he results of these studies demonstrate that NIH 3T3 cells expressing the EIAV receptor ELR1 and equi

163 stance to latrunculin A was also observed in NIH 3T3 cells expressing the mutant actin.

164 of tumors formed by s.c. injection of mouse NIH-3T3 cells expressing oncogenic c-Met mutants.

165 iscovered using high-throughput screening in NIH-3T3 cells expressing the F508del-CFTR mutation.

166 on of AUG-alpha stimulates transformation of NIH/3T3 cells expressing ALK, induces IL-3 independent g

167 In NIH/3T3 cells expressing either wild-type or mutant EGFR

168 In NIH-3T3 cells, expression of an inhibitor of all three g

169 pression of both PPARgamma and C/EBPalpha in NIH 3T3 cells facilitates production of abundant quantit

170 dition, acetylation of SP1 was detectable in NIH/3T3 cells following exposure to SCFAs.

171 IRF-7-expressing NIH 3T3 cells formed tumors in athymic mice.

172 When expressed in NIH/3T3 cells, full-length rClC-2 yielded inwardly recti

173 NIH 3T3 cells grown in conventional Dulbecco's modificat

174 hibits the oncogenic Src tyrosine kinase and NIH 3T3 cell growth.

175 d by hydrogen peroxide is greatly reduced in NIH 3T3 cells harboring antisense caveolin-1.

176 ly advanced bladder carcinoma with UMUC3 and NIH 3T3 cells have high levels of fibroblasts and an acc

177 re not sufficient to elevate PLD activity in NIH 3T3 cells; however, expression of both activated Ral

178 expressed alone could only weakly transform NIH 3T3 cells; however, when constitutively active Cdc42

179 excess of the respective noncancerous cells [NIH 3T3 cells, human embryonic kidney (HEK) 293 cells, o

180 me frequencies of transformation as parental NIH 3T3 cells, (iii) fibroblasts established from double

181 EGFR Mut R1-6) that spontaneously transforms NIH 3T3 cells in a ligand-independent manner.

182 city of ovarian surface epithelial cells and NIH 3T3 cells in athymic nu/nu mice.

183 ble to degrade IRF3 when expressed in murine NIH 3T3 cells in contrast to the EW and RRV NSP1 protein

184 Serum-induced circadian rhythms in NIH 3T3 cells in culture were disrupted by transfection

185 sustain cellular proliferation, to transform NIH 3T3 cells in culture, and to elicit apoptosis on ser

186 inhibit poly(I:C)-directed IRF3 activity in NIH 3T3 cells in the absence of detectable IRF3 degradat

187 enpols that can effectively deliver siRNA to NIH 3T3 cells in vitro and exhibit minimal toxicity.

188 nhibits Dlk1 expression in preadipocytes and NIH 3T3 cells in vivo, whereas down-regulation of KLF6 i

189 ivated Ran mutant is sufficient to transform NIH-3T3 cells in an mTOR- and epidermal growth factor re

190 NF-alpha-induced activation of NF-kappa B in NIH 3T3 cells, including degradation of I kappa B-alpha,

191 Anisomycin treatment of NIH 3T3 cells increased phosphorylation of Ser(52) and S

192 activity and elevated levels of GTP.RhoA in NIH 3T3 cells, indicating that Dbs is activated by the i

193 orced expression of full-length AQP1 cDNA in NIH-3T3 cells induced many phenotypic changes characteri

194 A model system in culture of NIH 3T3 cells induces the collective effects of serum gr

195 dition, TNF-alpha activation of NF-kappaB in NIH 3T3 cells is dependent on Rac activation, as evidenc

196 Rit was unable to stimulate ERK activity in NIH 3T3 cells, it potently activated ERK in PC6 cells.

197 s unable to stimulate MAP kinase activity in NIH 3T3 cells, it potently activated isoform-specific p3

198 pha-S51A variant has been shown to transform NIH 3T3 cells, it was unable to transform the murine fib

199 rmed colonies in soft agar, whereas BCR-ABL+ NIH 3T3 cells lacking IL-3 receptor expression did not.

200 ated separately by Bcr-Abl, whereas BCR-ABL+ NIH 3T3 cells lacking the IL-3 receptor do not utilize t

201 Here we report that NS4B can transform NIH-3T3 cells, leading to tumor formation in vivo.

202 Expression of LO in ras-transformed NIH 3T3 cells led to decreased NF-kappa B binding and ac

203 of both activated RalA and activated ARF6 in NIH 3T3 cells led to increased PLD activity.

204 holipid hydroperoxide-specific GPx (GPx4) in NIH/3T3 cells led to increases in cellular peroxidation

205 ed transcriptional profiling using inducible NIH 3T3 cell lines expressing 1 of 4 members of the C/EB

206 ression in the COS-7, HEK 293T/17, HeLa, and NIH 3T3 cell lines.

207 Engineered NIH-3T3 cell lines that overexpress a dominant negative

208 ependent growth exhibited by Notch-repressed NIH 3T3 cells may result from prolonged FGFR stimulation

209 receptor-mediated [35S]GTPgammaS binding to NIH-3T3 cell membranes, supporting a possible role for C

210 pe and extensive remodeling of the MCF-7-Ptn/NIH 3T3 cell microenvironment; it up-regulated expressio

211 cells harvesting efficiency from a live/dead NIH-3T3 cells mixture, and separation of MG-63 cells fro

212 C/EBPbeta, which enhances transformation of NIH 3T3 cells, mutants bearing alanine substitutions at

213 protein-tagged PKCalpha-C2 was expressed in NIH-3T3 cells, mutations of phosphoinositide-binding res

214 Activation of the HIV-1 LTR by HIC in NIH 3T3 cells occurs at the RNA level and is mediated by

215 s, transient cotransfections in nonerythroid NIH/3T3 cells of SP1, SP3, BKLF, or EKLF and HS2 epsilon

216 Dialysis into NIH/3T3 cells of these two peptides (but not of syntheti

217 We used this platform to track NIH 3T3 cells on polyacrylamide gels over 20 hrs.

218 mulated wild-type CFTR currents expressed in NIH 3T3 cells or Chinese hamster ovary cells in a dose-d

219 Furthermore, IL-6 treatment of NIH 3T3 cells or expression of a constitutively active f

220 ion with MYC, RAS, or E1A fails to transform NIH/3T3 cells or primary mouse embryonic fibroblasts, re

221 se IGF-I did not induce TDAG51 expression in NIH-3T3 cells overexpressing a dominant-negative IGF-I r

222 1 suppressed anchorage-independent growth of NIH-3T3 cells overexpressing CrkI, whereas knockdown of

223 factor-1 (IGF-1) receptors in PC12 cells and NIH-3T3 cells overexpressing insulin (NIH-3T3(IR)) or IG

224 gent 4-nitroquinoline 1-oxide was applied to NIH-3T3 cells overexpressing normal IGF-IRs (NWTb3 cells

225 In NIH-3T3 cells, PKCepsilon overexpression induced Tspo pr

226 ARgamma in C/EBPalpha-deficient fibroblasts (NIH 3T3 cells) produces a modest amount of adiponectin,

227 combinant Alix on the culture substratum for NIH/3T3 cells promotes alpha5beta1-integrin-mediated cel

228 In normal NIH 3T3 cells, (Raf-1[51-220]GFP) showed minimal membran

229 In cotransfection analysis of SMCs and NIH 3T3 cells, RelB and p50 proteins failed to induce Bc

230 ive oxygen-generating enzyme Nox1 transforms NIH 3T3 cells, rendering them highly tumorigenic and, as

231 NIH 3T3 cells responded to the micropatterned rigidity b

232 trated that the overexpression of PD2 in the NIH 3T3 cells result in enhanced growth rates in vitro a

233 me cancer tissues, and its overexpression in NIH 3T3 cells resulted in cellular transformation, thus

234 Ectopic expression of Neuritin in NIH 3T3 cells resulted in changes in cell morphology and

235 Immunofluorescence analysis of NIH 3T3 cells revealed that the two tyrosine-phosphoryla

236 In vitro studies with NIH 3T3 cells revealed up-regulation of CHOP as well as

237 In NIH 3T3 cells, RhoA or RhoB overexpression causes transf

238 Among the known Rho GTPases expressed in NIH 3T3 cells, RhoA was predominantly activated by oncog

239 nd CasE#1 but are resistant to PMVs, whereas NIH 3T3 cells show the reciprocal pattern, susceptibilit

240 ared to that of nonfluorinated apg PNA, with NIH 3T3 cells showing better permeability compared to He

241 ly glycosylated form of CFTR in IB3 cells or NIH 3T3 cells stably expressing Delta F508 CFTR.

242 Using NIH-3T3 cells stably expressing EGFR, we observe concent

243 mM), like ethanol, inhibited L1 adhesion in NIH/3T3 cells stably transfected with hL1, whereas suban

244 s of PIs were observed at plasma membrane of NIH 3T3 cells, stimulated by various growth factors.

245 the cytoplasmic accumulation of hnRNP A1 in NIH 3T3 cells subjected to OSM.

246 nhibited Ras(V12)-mediated transformation of NIH 3T3 cells, suppressed their tumorigenicity in nude m

247 study, we demonstrated in stably transfected NIH-3T3 cells that activation of Stat3 by EGFR was elimi

248 boRFP-based DNA damage reporter cell line in NIH-3T3 cells that fluoresce to report genotoxic stress

249 roviral system to introduce CXCR1 into mouse NIH 3T3 cells (that lack endogenous CXCR1) and monitored

250 Here we have examined in NIH 3T3 cells the cause of this cellular stress response

251 Here we show that in NIH 3T3 cells the expression of CtIP is regulated by the

252 required for JSRV-induced transformation of NIH 3T3 cells, the downstream target Akt kinase was foun

253 oprotein IX promoter in L-G cells but not in NIH 3T3 cells, the fusion protein was able to affect spl

254 owth and tumorigenicity of K-ras-transformed NIH 3T3 cells; these nine genes have not previously been

255 Dl1 and J1 act as N signaling antagonists in NIH 3T3 cells, they do display disparate functions.

256 molecular beacons (MBs) are introduced into NIH/3T3 cells, they elicit a nonspecific signal in the n

257 downregulated by H-Ras(V12) in immortalized NIH 3T3 cells through a mechanism involving p19(Arf) los

258 utants were stably expressed in both L-G and NIH 3T3 cells through retroviral transduction.

259 However, sJ1, like sDl1, induces a NIH 3T3 cell tranformed phenotype mediated by FGF signal

260 NIH 3T3 cells transduced with the human IL-3 receptor al

261 NIH 3T3 cells transfected with a mutant Lrp6 plasmid res

262 Similarly, NIH 3T3 cells transfected with the CXCR2 migrated toward

263 scopy and an in vitro functional assay using NIH-3T3 cells transfected with a beta-klotho reporter ge

264 f poly(ADP-ribose) polymerase was reduced in NIH 3T3 cells treated with ATM small interfering RNA, su

265 mTOR, we compared the expression profiles of NIH 3T3 cells treated with rapamycin versus PP242.

266 ies indicate that the BCR-ABL/IL-3 receptor+ NIH 3T3 cells utilize the Gab2/PI-3 kinase pathway activ

267 When expressed in 293T or NIH-3T3 cells, VHY was concentrated at the plasma membra

268 promoter, the expression of the PU.1 gene in NIH 3T3 cells was found to enhance the luciferase activi

269 the ras recision activity of the LOX gene in NIH 3T3 cells was mapped to its propeptide region.

270 C/EBPbeta down-regulation in NIH 3T3 cells was reversed by expression of p19(Arf), bu

271 ing activity of RET(Y791F) and RET(S891A) in NIH-3T3 cells was also inhibited by U0126, indicating a

272 Using NIH 3T3 cells, we show that phorbol esters, acting throu

273 In NIH 3T3 cells, we show that recombinant rootletin filame

274 alysis, hydrolysis rates, and experiments in NIH-3T3 cells, we link the allosteric switch to the cont

275 porter gene assay in PC12, HEK293, HeLa, and NIH-3T3 cells, we show that the anti-apoptotic protein B

276 ferase-reporter vector transfected into live NIH/3T3 cells, we measured a significant difference in t

277 NIH 3T3 cells were cultured on circular or linear ECM is

278 al vein endothelial cells (HUVEC) and murine NIH 3T3 cells were stably transduced by using recombinan

279 When NIH 3T3 cells were stimulated with platelet-derived grow

280 HepG2, CHO, and NIH 3T3 cells were transfected with polyethylenimine (PE

281 ration and transformation, N-Ras-transformed NIH-3T3 cells were employed.

282 When NIH-3T3 cells were treated with agents to induce ER stre

283 Transfection efficiency in HeLa and NIH/3T3 cells were comparable between the copolymers but

284 eta-galactosidase fusion expressed in living NIH 3T3 cells, where beta-galactosidase activity was red

285 FR) and induces phenotypic transformation in NIH 3T3 cells, whereas PDGF AA activates alpha-PDGFR onl

286 thesis genes in a 4E-BP1-dependent manner in NIH 3T3 cells, whereas S6 kinase 1 is the dominant regul

287 ll as the wild-type Smith strain in vitro in NIH 3T3 cells, whereas the transposon insertion preclude

288 42 mutant to induce microspikes/filopodia in NIH 3T3 cells, whereas they eliminated its ability to tr

289 c Ras down-regulates C/EBPbeta expression in NIH 3T3 cells, which are immortalized by a deletion of t

290 ha induced an increase in Per1 expression in NIH 3T3 cells, which was blocked by TNF-alpha antagonism

291 ta-mediated synergy were further explored in NIH-3T3 cells, which express little if any PLCbeta2.

292 le overexpression of Kos1 inhibits growth of NIH 3T3 cells, while the kinase-dead Kos1(CN) promotes c

293 us Dab2-Dvl-3 and Dvl-3-axin interactions in NIH-3T3 cells, while Dab2 overexpression leads to mainte

294 rexpression induced STAT3 phosphorylation in NIH-3T3 cells, while PKCepsilon knockdown reduced STAT3

295 n transiently transfected HeLa, HEK 293, and NIH 3T3 cells with farnesyltransferase inhibitors (FTIs)

296 Treatment of NIH 3T3 cells with myocilin and its fragments induced in

297 Treatment of NIH 3T3 cells with myofiber-derived exosomes downregulat

298 urthermore, treatment of K/E-FR3-transformed NIH-3T3 cells with PD98059 or LY294002, specific inhibit

299 Stable transfection of NIH/3T3 cells with human L1 resulted in clonal cell line

300 Using transient transfection of NIH/3T3 cells with wild type (WT-L1) and mutated L1, we