ライフサイエンスコーパス: MEF

1 MEF immortalisation is thus a simple and powerful strate

2 MEF inhibits SULT1A1 turnover through an indirect (helix

3 MEFs derived from LCMT-1 knock-out mouse embryos have re

4 yte proliferation, and is increased in FTO-4 MEFs and reduced in FTO-KO MEFs.

5 m this intermediate population reverted to a MEF-like phenotype, but Ki67(high) cells advanced throug

6 interactions of SULT1A1 and mefenamic acid (MEF)-a potent, highly specific NSAID inhibitor of 1A1.

7 Although MEFs induced to express onco-Dbl generated a similar amo

8 d breaks in Mcph1(-/-)p53(-/-) lymphomas and MEFs, as determined by metaphase spread assay and spectr

9 accelerated in TIN2(+/DC) mTR(-/-) mice and MEFs compared with TIN2(+/+) mTR(-/-) controls, establis

10 oma cells but not in APP(-/-) and APLP2(-/-) MEFs.

11 ARF(-/-) MEFs exhibit mitotic defects including misaligned and la

12 ctivated DNA damage response, as p19(Arf)-/- MEFs do not senesce after serial passage.

13 ir response to acute DNA damage, p19(Arf)-/- MEFs exposed to chronic DNA damage do not senesce, revea

14 r that p53 pathway activation in p19(Arf)-/- MEFs exposed to chronic DNA damage is attenuated relativ

15 ficient to promote senescence in p19(Arf)-/- MEFs, suggesting that the role of p19(Arf) in the chroni

16 In Bmal1(-/-) MEF, CLOCK was primarily cytosolic while PML and PER2 we

17 red by incorporation of [(35)S]methionine by MEF).

18 itochondrial enzyme activities in C1qbp(-/-) MEFs.

19 ressed with wild-type (WT) CAV1 in Cav1(-/-) MEFs, CAV1-P158 functions as a dominant negative by part

20 n and accelerates CAV1 turnover in Cav1(-/-) MEFs.

21 In Cc2d2a(-/-) MEFs, subdistal appendages are lacking or abnormal by tr

22 some and decreases ciliary length in control MEFs, suggesting that centrosomal CK1delta has a role in

23 latory subunit and PP4R1 relative to control MEFs, indicating that LCMT-1 is important for maintainin

24 s still relatively low (6.34%), conventional MEFs focused on emitting sources can provide a good esti

25 Comparisons of PERK(-/-) and PERK-corrected MEF showed that HSL-C12's effects were explained in part

26 indistinguishable to those seen in Cul9(-/-) MEFs and comparable to those seen in p53(-/-) MEFs.

27 was significantly reduced in RelA-deficient MEF compared with wild type MEF cells and ectopic expres

28 rosomes were observed in the Spag6-deficient MEF cultures.

29 As a result, AMPK-deficient MEFs exhibit impaired control of vesicular stomatitis vi

30 e overcome by pretreatment of AMPK-deficient MEFs with type I IFN, illustrating that de novo producti

31 , reconstitution of FOXM1 in FOXM1-deficient MEFs alleviates the accumulation of senescence-associate

32 ssion is markedly reduced in PCBP4-deficient MEFs and mouse tissues, suggesting that PCBP4 in turn re

33 sed expression of p53 in the PCBP4-deficient MEFs and mouse tissues.

34 1, sensitized wild-type and singly deficient MEFs, but had no additional effect on doubly deficient c

35 Spag6-deficient MEFs also showed reduced adhesion associated with a non-

36 the wild-type MEFs, and some Spag6-deficient MEFs developed multiple cilia.

37 oth primary and immortalized Spag6-deficient MEFs proliferated at a much slower rate than the wild-ty

38 e-expression of SPAG6 in the Spag6-deficient MEFs rescued the abnormal cell morphology.

39 Spag6-deficient MEFs were less motile than wild-type MEFs, as shown by b

40 The Spag6-deficient MEFs were more sensitive to paclitaxel, a microtubule st

41 As a result, TCF-deficient MEFs exhibit hypercontractile and pro-invasive behavior.

42 xtent of these alterations in Cul9(Deltap53) MEFs is indistinguishable to those seen in Cul9(-/-) MEF

43 Both Cul9(-/-) and Cul9(Deltap53) MEFs proliferate faster and undergo spontaneous immortal

44 ax/Bak double knock-out mice (WT MEF and DKO MEF that were responsive to C12, DKOR MEF): nuclei fragm

45 d been isolated from a nonclonal pool of DKO MEF that were non-responsive to C12 (DKONR MEF).

46 O MEF that were non-responsive to C12 (DKONR MEF).

47 s-mediated expression of human PON2 in DKONR MEF rendered them responsive to C12: Deltapsimito depola

48 ncluding paraoxonase 2 (PON2), whereas DKONR MEF expressed little PON2.

49 DKOR MEF had been isolated from a nonclonal pool of DKO MEF t

50 R, and Western blots showed that WT and DKOR MEF both expressed genes associated with cancer, includi

51 nd DKO MEF that were responsive to C12, DKOR MEF): nuclei fragmented; mitochondrial membrane potentia

52 study highlights the importance of expanded MEFs in regions with high and growing renewables penetra

53 The application of expanded MEFs in this case also reveals heightened emission incre

54 We discovered that CENP-F(-/-) MEFs have severely diminished MT dynamics, which underli

55 Estimates of marginal emission factors (MEFs) for the electricity sector have focused on emittin

56 n of EVs using a mouse embryonic fibroblast (MEF) cell line that can be induced to express an oncogen

57 genous Pol II in mouse embryonic fibroblast (MEF) cells using the CRISPR/Cas9 gene editing system.

58 g an established mouse embryonic fibroblast (MEF) model combining p53 inactivation with E1A or HRas-V

59 Using mouse embryonic fibroblast (MEF) models that generate inducible, low-level pathway a

60 Rictor knockout mouse embryonic fibroblast (MEF) system to further define the role of mTOR complexes

61 vated apoptosis in mouse embryo fibroblasts (MEF) from both wild type (WT) and Bax/Bak double knock-o

62 SETD2 knockout mouse embryonic fibroblasts (MEF) cells.

63 mary Rad18(-/-) mouse embryonic fibroblasts (MEF) retained robust Fancd2 mono-ubiquitination followin

64 ene-transformed mouse embryonic fibroblasts (MEF) suppressed tumor formation in immunocompromised mic

65 e-adipocyte and mouse embryonic fibroblasts (MEF) upon exposure to a mixture of hormonal mixture.

66 E359K mouse embryonic fibroblasts (MEF) were more sensitive to DNA crosslinking agents that

67 on in wild-type mouse embryonic fibroblasts (MEF).

68 ll immortalized mouse embryonic fibroblasts (MEF).

69 KSR1 disruption in mouse embryo fibroblasts (MEFs) abrogates growth factor-induced ERK activation, H-

70 Mouse embryo fibroblasts (MEFs) are convenient sources for biochemical studies whe

71 p19(Arf)-deficient mouse embryo fibroblasts (MEFs) arrest in response to acute DNA damage.

72 ul9-p53 binding in mouse embryo fibroblasts (MEFs) by a knock-in mutation in Cul9 (Deltap53) increase

73 at PCBP4-deficient mouse embryo fibroblasts (MEFs) exhibit enhanced cell proliferation but decreased

74 e demonstrate that mouse embryo fibroblasts (MEFs) lacking all three isoforms of Pim protein kinases,

75 In mouse embryo fibroblasts (MEFs) lacking CPEB, many mRNAs encoding proteins involve

76 Mouse embryo fibroblasts (MEFs) lacking Tm5NM1, which have reduced proliferative c

77 Furthermore, R137Q mouse embryo fibroblasts (MEFs) were more sensitive to DNA-damaging reagents, such

78 and in double-null mouse embryo fibroblasts (MEFs).

79 similarly treated mouse embryo fibroblasts (MEFs).

80 IFN-stimulated mouse embryonic fibroblasts (MEFs) and bone marrow-derived dendritic cells (BMDC) lac

81 and CENP-F(-/-) mouse embryonic fibroblasts (MEFs) and found drastic differences in multiple cellular

82 ve potential of mouse embryonic fibroblasts (MEFs) and is associated with a significant decrease in b

83 in interphase murine embryonic fibroblasts (MEFs) and is restricted to intragenic regions of activel

84 both Pten null mouse embryonic fibroblasts (MEFs) and Pten null mouse prostate tissues.

85 ry AL cells and mouse embryonic fibroblasts (MEFs) and rescues their proliferation defects, at least

86 Mouse embryonic fibroblasts (MEFs) and retinal cells from Csnk1d (CK1delta)-null mice

87 ice and primary mouse embryonic fibroblasts (MEFs) and showed that loss of PCBP2 leads to decreased p

88 id oxidation in mouse embryonic fibroblasts (MEFs) by targeting the AMP-activated protein kinase (AMP

89 Trim13(-/-) murine embryonic fibroblasts (MEFs) challenged with EMCV or poly(I .

90 s attenuated in mouse embryonic fibroblasts (MEFs) compared with an isogenic virus encoding mitochond

91 Murine embryonic fibroblasts (MEFs) deficient in PTPN12 underwent increased ROS-induce

92 Here, we derive mouse embryonic fibroblasts (MEFs) deleted in all three Tet genes and examine their c

93 EGR1(-/-) mouse embryonic fibroblasts (MEFs) demonstrated lower susceptibility to VEEV-induced

94 tioned media of mouse embryonic fibroblasts (MEFs) derived from Fam20a knock-out (KO) mouse, while it

95 adipocytes and mouse embryonic fibroblasts (MEFs) derived from FTO overexpression (FTO-4) mice exhib

96 emonstrate that mouse embryonic fibroblasts (MEFs) derived from Hace1(-/-) mice are highly sensitive

97 nt, as shown in mouse embryonic fibroblasts (MEFs) derived from Rel null mice.

98 mitochondria in mouse embryonic fibroblasts (MEFs) determines the shape of intracellular energy gradi

99 Tmem30a-mutant mouse embryonic fibroblasts (MEFs) exhibited diminished PS flippase activity and incr

100 d from primary murine embryonic fibroblasts (MEFs) exposed in vitro to carcinogens recapitulate key f

101 e show that, in mouse embryonic fibroblasts (MEFs) from Fut8(-/-) mice, another N-glycan branching st

102 in immortalized mouse embryonic fibroblasts (MEFs) from PINK1(-/-) mice, and in BE(2)-M17 cells stabl

103 Using mouse embryonic fibroblasts (MEFs) from Tpcn1(-/-) and Tpcn2(-/-) animals, we show th

104 Lin28 (SNEL) in mouse embryonic fibroblasts (MEFs) generated high-quality iPSCs more efficiently than

105 ults, Atf3(-/-) mouse embryonic fibroblasts (MEFs) had more aberrant chromosomes and micronuclei, and

106 1 knockout (KO) mouse embryonic fibroblasts (MEFs) have significantly diminished E3 ligase activity t

107 cell lines and mouse embryonic fibroblasts (MEFs) induces oversized cells containing either a single

108 ancer cells and mouse embryonic fibroblasts (MEFs) into entering epirubicin-induced senescence, with

109 PTB to convert mouse embryonic fibroblasts (MEFs) into functional neurons.

110 eprogramming of mouse embryonic fibroblasts (MEFs) into induced pluripotent stem cells (iPSCs).

111 imary Ola1(-/-) mouse embryonic fibroblasts (MEFs) is impaired due to defective cell cycle progressio

112 ed by growth on mouse embryonic fibroblasts (MEFs) isolated from IFN-alpha/betaR-/- mice, while growt

113 e metabolism in mouse embryonic fibroblasts (MEFs) isolated from mice that have triple knock-outs (TK

114 Murine embryonic fibroblasts (MEFs) lacking Fyn and cells in which Fyn expression was

115 Primary mouse embryonic fibroblasts (MEFs) lacking the ARF tumor suppressor contain abnormal

116 However, murine embryonic fibroblasts (MEFs) lacking TSC2 were highly resistant to ceramide-ind

117 Mouse embryonic fibroblasts (MEFs) or primary adult cardiac fibroblasts isolated from

118 Cebpg(-/-) mouse embryonic fibroblasts (MEFs) proliferate poorly and exhibit oxidative stress du

119 Cdk10-knockout mouse embryonic fibroblasts (MEFs) proliferated normally; however, Cdk10-knockout MEF

120 in late-passage mouse embryonic fibroblasts (MEFs) recruited cytoplasmically localized HDAC1 to the n

121 C1qbp(-/-) mouse embryonic fibroblasts (MEFs) resembled the human disease phenotype by showing m

122 d SerpinB2(-/-) mouse embryonic fibroblasts (MEFs) resulted in increased tumour growth, aberrant remo

123 t (Cdc14B(-/-)) mouse embryonic fibroblasts (MEFs) showed defects in repairing ionizing radiation (IR

124 ized TIN2(+/DC) mouse embryonic fibroblasts (MEFs) showed telomere shortening with proliferation.

125 n in STAT3-null mouse embryonic fibroblasts (MEFs) stably expressing wild-type STAT3 or STAT3 from wh

126 macrophages or mouse embryonic fibroblasts (MEFs) suppressed IFN-beta and TNF-alpha induction follow

127 HS landscape of mouse embryonic fibroblasts (MEFs) synergistically.

128 embryos and in mouse embryonic fibroblasts (MEFs) through the modulation of p300-dependent acetylati

129 r complex, from mouse embryonic fibroblasts (MEFs) to examine the role of Gabp in mitochondrial bioge

130 as and derived murine embryonic fibroblasts (MEFs) were both more sensitive to irradiation.

131 Mouse embryonic fibroblasts (MEFs) were isolated from Spag6-deficient and wild-type e

132 SOCS3 knockout mouse embryonic fibroblasts (MEFs) were significantly reduced compared to those from

133 Hsp70(-/-) murine embryonic fibroblasts (MEFs) were transformed by E1A/Ras and generated tumors i

134 ing of primary murine embryonic fibroblasts (MEFs) with cre/loxP-mediated vinculin gene disruption in

135 g p19(Arf) null mouse embryonic fibroblasts (MEFs), and overall Egr DNA-binding activity was suppress

136 on occupancy in mouse embryonic fibroblasts (MEFs), induced pluripotent stem cells (iPSCs) and pre-iP

137 ic knockout in murine embryonic fibroblasts (MEFs), led to significant reductions in VACV growth foll

138 In mouse embryonic fibroblasts (MEFs), Sirt6 knockout (KO) increased R-Ras2 lysine fatty

139 Using knockout mouse embryonic fibroblasts (MEFs), we demonstrate that cyclin C directs the extensiv

140 gg extracts and mouse embryonic fibroblasts (MEFs), we show here that NCOA4 is a minichromosome maint

141 t (KO) model of mouse embryonic fibroblasts (MEFs).

142 n Ada3-deleted murine embryonic fibroblasts (MEFs).

143 caveolin-1 null mouse embryonic fibroblasts (MEFs).

144 es, B cells and mouse embryonic fibroblasts (MEFs).

145 ols H4R3me2s in mouse embryonic fibroblasts (MEFs).

146 PDGF-stimulated mouse embryonic fibroblasts (MEFs).

147 PP4, and PP6 in mouse embryonic fibroblasts (MEFs).

148 mor tissue, and mouse embryonic fibroblasts (MEFs).

149 pha (eIF2alpha) mouse embryonic fibroblasts (MEFs); moreover, ECD mRNA levels were increased, suggest

150 acrophages, and mouse embryonic fibroblasts [MEFs]) apoptosis induced by a wide spectrum of proapopto

151 ing the interfacial magnetic exchange field (MEF) from a ferromagnetic EuS substrate.

152 The magnetic exchange field (MEF) induced by an adjacent magnetic insulator enables e

153 d surface-bound metal-enhanced fluorescence (MEF) substrates (silver island films, SIFs) as signal en

154 The addition of MVs isolated from MEFs expressing onco-Dbl to cultures of fibroblasts stro

155 rlying mechanism, we found that in Fut8(-/-) MEFs Wnt/beta-catenin signaling is up-regulated, and an

156 lated genes were also increased in Fut8(-/-) MEFs.

157 in and N-cadherin was increased in Fut8(-/-) MEFs.

158 Hace1(-/-) MEFs exhibit increased Gln uptake and ammonia secretion,

159 cks soft agar colony formation by Hace1(-/-) MEFs.

160 on increases superoxide levels in Hace1(-/-) MEFs, and NADPH oxidase inhibitors block the induction o

161 d ROS elevation and cell death in Hace1(-/-) MEFs.

162 However, MEFs lacking both p53 and 4E-BPs show greatly enhanced r

163 revious observations in the exogenous Pol II MEF cell line.

164 r protein to the perinucleus in immortalized MEF cells is correlated with the translocation of p53-st

165 expression of AhR and induction of CYP1A1 in MEF RelA null cells.

166 hermore, H3 acetylation levels were lower in MEF-KO than MEF-WT.

167 small amount of association was observed in MEF-WT after 5 days of treatment during adipogenesis.

168 The model predictions on PGE2 in MEF and 4T1 cells at 48 hours after 10-Gray radiation we

169 DAC3 are stably associated with PPARgamma in MEF-KO, whereas only a small amount of association was o

170 the methodology to incorporate renewables in MEF estimates and demonstrate a case study for the Midco

171 ants reduced mitochondrial calcium uptake in MEF cells.

172 In MEFs, activation of ERK by TPA stimulation induced a com

173 Lysosomal clearance is also compromised in MEFs harboring a p97 mutation that causes inclusion body

174 pendently, however, since PRMT5-depletion in MEFs resulted in loss of H4R3me2s, without affecting H3K

175 pts are up-regulated on deletion of DUSP5 in MEFs and mouse skin.

176 FAK, Src, and PI3K and rescue experiments in MEFs, we found that the FAK/Src/PI3K/Akt signaling pathw

177 Reducing Evi5l expression in MEFs lacking Tgifs resulted in a partial restoration of

178 S) are required to rescue cilia formation in MEFs(Csnk1d null).

179 ced expression of stress-responsive genes in MEFs, the transcription profiles of several mouse tissue

180 Specific inhibition by chemical genetics in MEFs confirmed the involvement of JNK2 in cyclin D1-CDK4

181 Fibulin 3 inhibits migration and invasion in MEFs by mechanisms involving p38alpha/beta inhibition.

182 of a CDK4 inhibitor, increased FAO rates in MEFs and myotubes.

183 rt, mediated by fibulin 3 down-regulation in MEFs.

184 /beta production, and antiviral responses in MEFs in response to RNA virus infection.

185 We show that, in MEFs, TCF inactivation significantly inhibits over 60% o

186 pre-iPSCs are much more phased than those in MEFs and iPSCs.

187 rect parental allele-specific transcripts in MEFs.

188 Correlated with this aberrant translation in MEFs, a macrophage cell line depleted of CPEB and treate

189 is in human lymphomas, and translocations in MEFs reveals that AID damages different genes in differe

190 oliferated normally; however, Cdk10-knockout MEFs developed longer cilia.

191 scence in p53 wild-type but not p53 knockout MEFs.

192 Nedd4-1 KO MEFs manifest increased p53 levels and activity, a more

193 l in the late endosomes/lysosomes of Arf6 KO MEFs results from mistrafficking of Niemann-Pick type C

194 ncreased in FTO-4 MEFs and reduced in FTO-KO MEFs.

195 Finally, reducing PI4P levels in KO MEFs through independent mechanisms rescues aberrant ret

196 , but those with the conditioned media of KO MEFs failed to mineralize in vitro.

197 In contrast, Tm5NM1 KO MEFs, which show reduced nuclear translocation of pERK,

198 rimed hESCs on mouse embryonic feeder layer (MEF) to a naive state within 5-6 days in naive conversio

199 Reprogramming of Lsh(-/-) MEFs into induced pluripotent stem (iPS) cells leads to

200 -independent and occurs in Lxralphabeta(-/-) MEFs.

201 DNA-damaging agent treatment by maintaining MEFs in low oxygen and administering 0.5 G y gamma-irrad

202 in Miro1(-/-) MEFs compared with Miro1(+/+) MEFs.

203 Consequently Miro1(-/-) MEFs migrated slower than control cells during both coll

204 ly and stability was decreased in Miro1(-/-) MEFs compared with Miro1(+/+) MEFs.

205 The mitochondrial network in Miro1(-/-) MEFs was restricted to the perinuclear area, with few mi

206 ce of genotoxic stress, wild-type and mutant MEFs showed similar growth rates and cell cycle distribu

207 s, is absent and ninein is reduced in mutant MEFs.

208 3) and Akt(T308) in ciliary transport mutant MEFs.

209 mgn1(-/-), Hmgn2(-/-), and Hmgn1(-/-)n2(-/-) MEFs reveals that loss of both, but not a single HMGN va

210 on potential of naive hESCs converted in NCM-MEF, however, all naive hESCs fail to differentiate towa

211 thin 5-6 days in naive conversion media (NCM-MEF), 6-10 days in naive human stem cell media (NHSM-MEF

212 NCOA4(-/-) MEFs display unscheduled origin activation and reduced i

213 10 days in naive human stem cell media (NHSM-MEF) and 14-20 days using the reverse-toggle protocol (R

214 -expression of caveolin-1 in caveolin-1 null MEFs restores reactive oxygen species-induced acetylatio

215 on of this model, we show that 4E-BP1/2-null MEFs express less ATGL and accumulate more fat than cont

216 s, while knock down of Egr1 in 4E-BP1/2-null MEFs increases ATGL expression and decreases fat storage

217 ase of Ezh2 levels in Pten/Trp53 double-null MEFs and in prostate tumors of Pten/Trp53 double-null mu

218 G0s2-null MEFs were readily transformed with HRAS or EGFR treatmen

219 proliferation, and MYC targets in G0s2-null MEFs.

220 oncogene-induced transformation of G0s2-null MEFs.

221 tion, was markedly reduced in Gabpalpha-null MEFs.

222 Detailed cell cycle analyses of MEF cell lines from several PINK1(-/-) mice demonstrate

223 Reprogramming of MEFs deficient in TDG is similarly impaired.

224 To derive the imprinting signature of MEFs and potentially detect novel imprinted genes we per

225 Based on the imprinting signature of MEFs, these cells provide valid models for understanding

226 d phased chromatin architecture than that of MEFs and iPSCs.

227 also illustrate spatiotemporal variations of MEFs and explore implications for energy storage technol

228 (Cip1/Waf1) Accumulation of p21 in Ola1(-/-) MEFs is due to enhanced mRNA translation and can be prev

229 Finally, LCMT-1 homozygous knock-out MEFs exhibited hyperphosphorylation of HDAC3, a reported

230 lecting nonemitting sources can overestimate MEFs for CO2, SO2, and NOx by about 30%.

231 EFs and comparable to those seen in p53(-/-) MEFs.

232 Compared with Mcph1(+/+)p53(-/-) MEFs, homologous recombination and non-homologous end-jo

233 and break (DSB) repair in Mcph1(-/-)p53(-/-) MEFs as demonstrated by neutral Comet assay.

234 hromosomal aberrations in Mcph1(-/-)p53(-/-) MEFs.

235 ignificantly decreased in Mcph1(-/-)p53(-/-) MEFs.

236 Patz1(+/-) MEFs can surpass the senescence barrier of Ink4a/Arf loc

237 iPS colonies can be induced from Patz1(+/-) MEFs than wild type MEFs; while the addition of Patz1 si

238 However, Patz1(-/-) MEFs gave the lowest reprogramming efficiency which may

239 Restoration of PDCD5(WT) in PDCD5(-/-) MEFs restores ET-induced HDAC3 cleavage.

240 es in PERK(-/-) and PERK-corrected PERK(-/-) MEF.

241 urified cyclin C to unstressed permeabilized MEF cultures induced complete mitochondrial fragmentatio

242 tion is significantly reduced in PI3KgammaKO MEF, suggesting accelerated dephosphorylation.

243 and associated PP2A activity in PI3KgammaKO MEFs, resulting in decreased ERK activation.

244 In Pml(-/-) MEF transfected with mutant K487R PML, we observed that

245 cytosolic distribution of CLOCK in Pml(-/-) MEF.

246 In primary MEFs lacking both Tgifs, the number of cells with primar

247 ce transcription factor C/EBPbeta in primary MEFs undergoing senescence.

248 Deletion of Tudor-SN protein (MEF-KO) affects but does not completely abolish the asso

249 However, Hsp70(-/-) E1A/Ras MEFs generated significantly larger tumors than their WT

250 0 days using the reverse-toggle protocol (RT-MEF).

251 d for adipogenesis, as deletion of Tudor-SN (MEF-KO) impairs dexamethasone, 3-isobutyl-1-methylxanthi

252 of Dirac electrons resulting from the strong MEF may give rise to quantized spin-polarized edge trans

253 netic insulator (EuS) produces a substantial MEF (>14 T) with the potential to reach hundreds of tesl

254 In Tg2576 MEFs, the beta-inhibitor blocked transport, but the gamm

255 ouse embryonic fibroblasts (WT MEFs), Tg2576 MEFs, and N2a neuroblastoma cells but not in APP(-/-) an

256 acetylation levels were lower in MEF-KO than MEF-WT.

257 l findings were corroborated by showing that MEFs lacking AMPK activity also failed to up-regulate IF

258 The MEF effect shown in our graphene/EuS devices therefore p

259 the magnetization of EuS, a hallmark of the MEF.

260 st structure of an NSAID allosteric site-the MEF-binding site of SULT1A1-is determined using spin-lab

261 Utilizing the MEF of a magnetic insulator can induce magnetic order an

262 TKO MEFs exhibit reduced levels of superoxide dismutase (Sod

263 In addition, TKO MEFs exhibited elevated production of glutathione from e

264 ly decreased ATP concentration in the Rb TKO MEFs but not the wild-type (WT) MEFs.

265 termediate alpha-ketoglutarate to the Rb TKO MEFs reversed the inhibitory effects of glutamine depriv

266 cytotoxic effects of K-Ras(G12V) in the TKO MEFs.

267 lls regulate cyclin C in a manner similar to MEF cells, U2OS osteosarcoma cultures display constituti

268 or Tpcn2 expression; thus, while Tpcn1(-/-) MEFs have impaired trafficking of cholera toxin from the

269 membrane to the Golgi apparatus, Tpcn2(-/-) MEFs show slower kinetics of ligand-induced platelet-der

270 ng were apparent in VACV-infected TRAF2(-/-) MEFs, treatment of wild-type cells with a JNK inhibitor

271 In oncogene-transformed MEFs lacking both genes, tumor formation was strongly su

272 s to both amino acids and glucose, TSC2(-/-) MEFs also had a survival advantage when extracellular am

273 brogated the survival advantage of TSC2(-/-) MEFs upon ceramide treatment most likely by increasing n

274 n RelA-deficient MEF compared with wild type MEF cells and ectopic expression of RelA restored the ex

275 During 4-h treatments of wild-type MEF, HSL-C12 potentially activated NF-kappaB p65 by prev

276 induced from Patz1(+/-) MEFs than wild type MEFs; while the addition of Patz1 significantly represse

277 Treatment of wild-type MEFs with a CK2 inhibitor to block phosphorylation of th

278 nificantly reduced compared to the wild-type MEFs, and some Spag6-deficient MEFs developed multiple c

279 ted at a much slower rate than the wild-type MEFs, and they had a larger surface area.

280 ficient MEFs were less motile than wild-type MEFs, as shown by both chemotactic analysis and wound-he

281 V-induced cell death than isogenic wild-type MEFs, indicating that EGR1 modulates proapoptotic pathwa

282 A damage is attenuated relative to wild-type MEFs, suggesting a role for p19(Arf) in fine-tuning p53

283 AS or EGFR treatment compared with wild-type MEFs.

284 To explore endogenous mutagenesis, we used MEFs ectopically expressing activation-induced cytidine

285 Importantly, using MEFs, we demonstrate that the established downstream med

286 ential for adipogenic differentiation, while MEFs derived from FTO knockout (FTO-KO) mice show reduce

287 e (WT) and Bax/Bak double knock-out mice (WT MEF and DKO MEF that were responsive to C12, DKOR MEF):

288 ells with the conditioned media of Fam20a WT MEFs mineralized, but those with the conditioned media o

289 in wild-type mouse embryonic fibroblasts (WT MEFs), Tg2576 MEFs, and N2a neuroblastoma cells but not

290 , while it was detected in the media from WT MEFs.

291 In WT MEFs and N2a neuroblastoma cells exposed to beta- or gam

292 eases ROS levels in Hace1(-/-) but not in wt MEFs, and treatment with the antioxidant N-acetyl cystei

293 taining HS disappeared from the nuclei of WT MEFs.

294 gamma-glutamylcysteine ligase relative to WT MEFs.

295 nse and increased G1 arrest compared with WT MEFs.

296 educed compared to those from wild-type (WT) MEFs at 24 and 48 h postinfection.

297 nced cell death compared with wild-type (wt) MEFs, and Gln depletion or chemical inhibition of Gln up

298 ssed in Arf-deficient but not wild-type (WT) MEFs, leading to Cebpb downregulation.

299 m2 compared with lysates from wild-type (WT) MEFs.

300 n the Rb TKO MEFs but not the wild-type (WT) MEFs.