ライフサイエンスコーパス: MEF

1 MEF inhibits SULT1A1 turnover through an indirect (helix

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

3 MEFs help quantify the health, environmental, and climat

4 thylation in mouse embryonic fibroblasts (2i-MEFs) derived from DNA-hypomethylated 2i/L ES cells with

5 gions that are hypomethylated in Dnmt3 KO 2i-MEFs.

6 genes in Dnmt3a and Dnmt3b knockout (KO) 2i-MEFs, respectively.

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

8 hibitor GSK2606414, while the Foxo(1/3/4-/-) MEFs expressing lower levels of PERK are more sensitive

9 rexpression assays as well as Foxo(1/3/4-/-) MEFs, we establish the endoplasmic reticulum (ER)-stress

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

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

12 The chromosomal fragmentation in Cdk1(AF) MEFs does not rely on CDK2 and is partly caused by prema

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

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

15 e mechanism by which Hipk2 (-/-) neurons and MEFs are more resistant to mitochondrial toxins is in pa

16 In addition, Hipk2 (-/-) neurons and MEFs show increased expression of PGC-1alpha (peroxisome

17 Pafah1b1-deficient neocortical NPCs and MEFs similarly exhibited cleavage plane displacement wit

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

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

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

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

22 hing charging time with the lowest available MEF.

23 Though historically derived regression-based MEFs are generally more accurate, our simulated MEFs pro

24 gainst historically derived regression-based MEFs.

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

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

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

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

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

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

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

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

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

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

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

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

37 Finally, PGAM5 deficient MEFs, upon infection with vesicular stomatitis virus (VS

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

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

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

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

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

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

44 h is still expressed in Arpp19 (Delta/Delta) MEFs, suggesting that ARPP19 is essential for mitotic di

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

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

47 c fibroblasts (MEFs), 182 miRNAs in dividing MEFs, and 127 miRNAs in mouse embryonic stem cells (mESC

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

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

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

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

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

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

54 Policymakers could use these dynamic MEFs to target demand-reduction strategies at high-emiss

55 inhibition promoted apoptosis of eEF2K(-/-) MEFs under proteostatic stress induced by the proteasome

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

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

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

59 ach associated with myocyte enhancer factor (MEF) 2 and estrogen-related receptor (ERR) signaling and

60 es the concept of marginal emission factors (MEFs) and uses person-level travel activity data to simu

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

62 s it to simulate marginal emissions factors (MEFs) for the 2014-2017 United States (U.S.) electric gr

63 n referred to as mechanoelectrical feedback (MEF), via stretch-activated channels.

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

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

66 In mouse embryonic fibroblast (MEF) cells we show that Prom1 is required for chloride i

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

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

69 cell cycles from Mouse Embryonic Fibroblast (MEF) primary cells.

70 ically decreased mouse embryonic fibroblast (MEF) viability by perturbing the temporal pattern of pro

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

72 SETD2 knockout mouse embryonic fibroblasts (MEF) cells.

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

74 d in ATG16L1 KO mouse embryonic fibroblasts (MEF) upon proteasome inhibition.

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

76 Here using mouse embryonic fibroblasts (MEF), we investigate the ciliary roles of two mammalian

77 ll immortalized mouse embryonic fibroblasts (MEF).

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

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

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

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

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

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

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

85 s in K41 wild-type mouse embryo fibroblasts (MEFs), CRT null MEFs were unresponsive.

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

87 similarly treated mouse embryo fibroblasts (MEFs).

88 -actin knockout mouse embryonic fibroblasts (MEFs) after reprograming to adipocytes.

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

90 Mouse embryonic fibroblasts (MEFs) and hepatocytes from Ccne1(T) and control mice wer

91 a population of mouse embryonic fibroblasts (MEFs) and identify topographical nonuniformity in this s

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

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

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

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

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

97 ia in Drp1-null mouse embryonic fibroblasts (MEFs) compared to wild-type (wt) MEFs, indicating that t

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

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

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

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

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

103 PGAM5 deficient mouse embryonic fibroblasts (MEFs) exhibited decreased phosphorylation levels of IRF3

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

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

106 Mouse embryonic fibroblasts (MEFs) from the double knockout embryos display an absenc

107 we established mouse embryonic fibroblasts (MEFs) from wild type, zQ175, and zQ175::Srsf6(+/-) mice

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

109 in neurons and mouse embryonic fibroblasts (MEFs) has a broad protective effect from cell death indu

110 1 knockout (KO) mouse embryonic fibroblasts (MEFs) have significantly diminished E3 ligase activity t

111 PCs in vivo and mouse embryonic fibroblasts (MEFs) in vitro from Pafah1b1-deficient mutants.

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

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

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

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

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

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

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

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

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

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

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

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

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

125 ere, we show in mouse embryonic fibroblasts (MEFs) that this MNNG-dependent phenotype does not involv

126 D) immortalized mouse embryonic fibroblasts (MEFs) to search for genes that when mutated cooperate wi

127 murine NADs in mouse embryonic fibroblasts (MEFs) via deep sequencing of chromatin associated with p

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

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

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

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

132 6l1 (ATG16L1 KO mouse embryonic fibroblasts (MEFs)), an essential autophagy gene, and observed defici

133 ntact-inhibited mouse embryonic fibroblasts (MEFs), 182 miRNAs in dividing MEFs, and 127 miRNAs in mo

134 ed macrophages, mouse embryonic fibroblasts (MEFs), and human HeLa cells upon IFN stimulation.

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 In eEF2K(-/-) mouse embryonic fibroblasts (MEFs), inhibition of HSP90 by its specific inhibitor AUY

138 In mouse embryonic fibroblasts (MEFs), inhibition of mitochondrial metabolism does not m

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

140 , in Kif3a null mouse embryonic fibroblasts (MEFs), the overall TonEBP-dependent hyperosmotic respons

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

142 d senescence of mouse embryonic fibroblasts (MEFs), whereas overexpression of Pak2 accelerated senesc

143 (-/-)/Arf (-/-) mouse embryonic fibroblasts (MEFs), which failed to inhibit cell proliferation, despi

144 elial cells and mouse embryonic fibroblasts (MEFs)-using four different probe technologies: 1) atomic

145 comparison with 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 t (KO) model of mouse embryonic fibroblasts (MEFs).

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

151 s (MCF10A), and mouse embryonic fibroblasts (MEFs).

152 t activation in mouse embryonic fibroblasts (MEFs).

153 WT or PERK -/- Mouse Embryonic Fibroblasts (MEFs).

154 ut (eEF2K(-/-)) mouse embryonic fibroblasts (MEFs).

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

156 2.LX, HAP1, and mouse embryonic fibroblasts [MEFs]) reconstituted with wild-type or phosphorylation m

157 primary cells (mouse embryonic fibroblasts, MEFs), to assess different behaviors between cell types.

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

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

160 fection in the Junbo mouse middle ear fluid (MEF).

161 n of cells with metal-enhanced fluorescence (MEF) and subsequent precise and direct ionization of the

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

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

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

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

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

167 After generating hourly MEFs using a multiple linear regression model, we estima

168 Littermate-derived WT and ICF1 MEFs demonstrated no significant differences in subtelom

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

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

171 and Thm2 have unique and redundant roles in MEF.

172 ants reduced mitochondrial calcium uptake in MEF cells.

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

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

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

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

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

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

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

180 is developmentally regulated, and present in MEFs but not in undifferentiated embryonic stem (ES) cel

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

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

183 milar production cost create large swings in MEFs throughout the day.

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

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

186 Knockout (KO) of vimentin in MEFs caused a diminution of traction reported by TM, as

187 om 11 to 34 h in mESCs and contact-inhibited MEFs, respectively.

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

189 ATAC-Seq in knockout MEFs revealed that actin-dependent reduction of Cebpa ex

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

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

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

193 Klhl9 and Klhl13 was elevated in ATG16L1 KO MEFs and siRNA-mediated knockdown of Klhl9, Klhl13, or C

194 ATG16L1 KO MEFs displayed reduced protein content of insulin recept

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

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

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

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

199 this paradoxical OMTC result in vimentin-KO MEFs could be attributed to reduced cell thickness.

200 r, stiffness reported by OMTC in vimentin-KO MEFs was greater than in wild type.

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

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

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

204 This method that combines microarrays, MEF, and MALDI-MS presents an effective platform for lip

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

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

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

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

209 Further, Thm1;Thm2 double-mutant MEF show enhanced cilia disassembly, and increased impai

210 We examined the ciliary phenotypes of mutant MEF.

211 Thm1-mutant MEF show decreased cilia assembly, increased cilia disas

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

213 H, enhances MNNG cytotoxicity in Mutyh (-/-) MEFs and that MUTYH expression enhances MNNG-induced gen

214 er survival of Mutyh-deficient (Mutyh (-/-)) MEFs, but this blockade had no additive cytotoxicity in

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

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

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

218 10 days in naive human stem cell media (NHSM-MEF) and 14-20 days using the reverse-toggle protocol (R

219 ated by T-helper (Th) cells in noninoculated MEF, and the effector Th (CD44(+)) cell population incre

220 Thm2-null MEF show normal ciliary dynamics and Hedgehog signaling,

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

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

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

224 pe mouse embryo fibroblasts (MEFs), CRT null MEFs were unresponsive.

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

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

227 oncogene-induced transformation of G0s2-null MEFs.

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

229 hese responses remained intact in Kif3a null MEFs.

230 iency in lamin A/C-depleted cells (Lmna null MEFs and lamin A/C-knockdown U2OS).

231 Also, Lmna null MEFs displayed reduced expression of several core BER en

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

233 In this work, we investigate the effects of MEF on cardiac alternans, which is an alternation in the

234 The effects of MEF on the electrophysiology at high pacing rates are sh

235 dant alternans, may occur in the presence of MEF and when its strength is sufficiently large.

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

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

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

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

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

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

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

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

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

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

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

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

248 Expression of Akt3 in p47 (phox-/-) MEFs failed to induce ROS and to inhibit cell proliferat

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

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

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

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

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

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

255 with altered iron metabolism in p53(R270H/-) MEFs and cancer cells carrying mutant p53.

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

257 eraction between STAT2 and IFNAR2 in resting MEFs, an interaction that is dependent on the associatio

258 IFNAR1 and IFNAR2, respectively, in resting MEFs.

259 0 days using the reverse-toggle protocol (RT-MEF).

260 historical data, and compares its simulated MEFs against historically derived regression-based MEFs.

261 s are generally more accurate, our simulated MEFs provide a more nuanced picture of how clusters of l

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

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

264 Ccne1(T) MEFs had defects that promoted chromosome missegregation

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

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

267 e the dominant immune cell population in the MEF and that NTHi infection significantly increased thei

268 ecreased the proportion of live cells in the MEF at day 1, and this further decreased gradually on ea

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

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

271 In addition, our results also show that the MEF effects, depending on the stretch-activated channels

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

273 ete splicing of Htt was recapitulated in the MEFs and we demonstrated that ablation of SRSF6 did not

274 TKO MEFs exhibit reduced levels of superoxide dismutase (Sod

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

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

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

278 re responsive to hypoosmolarity in wild-type MEFs, and these responses remained intact in Kif3a null

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 ive to PERK inhibition compared to wild-type MEFs.

285 Like most cell types, MEFs have the capacity to uncouple the glycolytic utiliz

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

287 ially reduces GHG emissions, even when using MEFs that are up to seven times higher than average elec

288 It is only when MEFs are forced to use mitochondrial oxidative metabolis

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

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

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

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

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

294 blockade had no additive cytotoxicity in WT MEFs, suggesting the cytotoxicity is due to MUTYH intera

295 tors suppresses the cell proliferation of WT MEFs, suggesting a synergistic effect between CARM1 and

296 nse and increased G1 arrest compared with WT MEFs.

297 tially expressed in STINGko compared with WT MEFs.

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

299 ibroblasts (MEFs) compared to wild-type (wt) MEFs, indicating that the drastically reduced GTP turnov

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

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