ライフサイエンスコーパス: mouse embryonic fibroblast

1 phagic cell death in Bax/Bak1 double-deleted mouse embryonic fibroblasts.

2 e that PGC-1alpha modulates the secretome of mouse embryonic fibroblasts.

3 n both gene- and transcript-targeted primary mouse embryonic fibroblasts.

4 e that adipogenesis is enhanced in Rnf146-/- mouse embryonic fibroblasts.

5 yl-dG with wild-type and pol kappa deficient mouse embryonic fibroblasts.

6 V) but not K-Ras(G12V) induced senescence in mouse embryonic fibroblasts.

7 pattern intermediate between pro-B cells and mouse embryonic fibroblasts.

8 he reprogramming potential of Tet2-deficient mouse embryonic fibroblasts.

9 n, and chromatin structure of Ku70-deficient mouse embryonic fibroblasts.

10 te in tumor cells and in the Ras-transformed mouse embryonic fibroblasts.

11 mic key feature of Tet1/Tet2 double-knockout mouse embryonic fibroblasts.

12 he real-time transport of beta-actin mRNA in mouse embryonic fibroblasts.

13 ntoxic to normally dividing Schwann cells or mouse embryonic fibroblasts.

14 arental virus in monkey epithelial cells and mouse embryonic fibroblasts.

15 e are radioresistant compared with wild-type mouse embryonic fibroblasts.

16 reased survival in hyperosmotically stressed mouse embryonic fibroblasts.

17 has no impact on gene expression of arrested mouse embryonic fibroblasts.

18 in various cultured human cell lines and in mouse embryonic fibroblasts.

19 receptor forces in live human platelets and mouse embryonic fibroblasts.

20 of endogenous MS2-tagged beta-actin mRNA in mouse embryonic fibroblasts.

21 of the 42 kDa exon alpha Pol beta variant in mouse embryonic fibroblasts.

22 onocyte-derived macrophages, HeLa cells, and mouse embryonic fibroblasts.

23 and enhance copper accumulation in Ctr1(-/-) mouse embryonic fibroblasts.

24 ing EHD2, and increased caveolar mobility in mouse embryonic fibroblasts.

25 ifferentiation is increased in Id1-deficient mouse embryonic fibroblasts.

26 cell lines: human embryonic kidney cells and mouse embryonic fibroblasts.

27 Here, we analyze de novo DNA methylation in mouse embryonic fibroblasts (2i-MEFs) derived from DNA-h

28 1, Atoh1, Pou4f3, and Gfi1) that can convert mouse embryonic fibroblasts, adult tail-tip fibroblasts

29 ntegration density in transcription units in mouse embryonic fibroblasts also correlated strongly wit

30 In addition, Hipk2 (-/-) neurons and mouse embryonic fibroblasts also show increased expressi

31 Utilizing mouse embryonic fibroblast and cancer cell line models,

32 We found that Plp2-deficient mouse embryonic fibroblast and human fibroblasts carryin

33 to block hypoxia-induced Fbln5 expression in mouse embryonic fibroblasts and 3T3 fibroblasts.

34 Here, using mouse embryonic fibroblasts and an array of biochemical

35 imately 10000 regions of OG enrichment in WT mouse embryonic fibroblasts and approximately 18000 regi

36 We validate our method by imaging mouse embryonic fibroblasts and BON cells.

37 al and reduced colony formation of Fan1(-/-) mouse embryonic fibroblasts and bone marrow mesenchymal

38 Genetic ablation of MST1 in mouse embryonic fibroblasts and bone marrow-derived macr

39 expression is markedly reduced in TAp63-null mouse embryonic fibroblasts and brown adipose tissues an

40 nhibited the Hh pathway in both Hh-dependent mouse embryonic fibroblasts and cultured cancer cells (I

41 found to be SIRT1-dependent in proliferating mouse embryonic fibroblasts and differentiating human SW

42 in cells, we deleted ELMOD2 in immortalized mouse embryonic fibroblasts and discovered a number of c

43 ption assays were performed with IQGAP1-null mouse embryonic fibroblasts and HEK293 cells with IQGAP1

44 upon FGF stimulation at conserved serines in mouse embryonic fibroblasts and HEK293 cells.

45 osteopontin and other FN-type matrix in both mouse embryonic fibroblasts and human melanoma.

46 lted in immortalization of Rb1 (-/-) primary mouse embryonic fibroblasts and in aggressive tumor grow

47 f the mitochondrial respiratory complexes in mouse embryonic fibroblasts and in the striatum, a brain

48 s of mutant Kras homozygous and heterozygous mouse embryonic fibroblasts and lung cancer cells, that

49 rmacological or genetic inhibition of ILK in mouse embryonic fibroblasts and macrophages selectively

50 This phenotype was also seen in both mouse embryonic fibroblasts and mesangial cells.

51 Using genetic deficiencies in mouse embryonic fibroblasts and mouse liver, we identifi

52 K-Ras(G12V))-induced premature senescence in mouse embryonic fibroblasts and normal human bronchial e

53 , Eomes, and Ets2 is sufficient to reprogram mouse embryonic fibroblasts and post-natal tail-tip-deri

54 Cytogenetic analysis of mouse embryonic fibroblasts and pre-malignant B cells de

55 1alpha) stabilization in cultured Pink1(-/-) mouse embryonic fibroblasts and primary cortical neurons

56 adation of IP3R3 is accelerated in Pten(-/-) mouse embryonic fibroblasts and PTEN-null cancer cells.

57 When overexpressed in both mouse embryonic fibroblasts and rat OPCs (rOPCs), cell c

58 carcinogen-driven immortalization of primary mouse embryonic fibroblasts and recapitulates early step

59 duced ATP depletion to incite cell stress in mouse embryonic fibroblasts and renal proximal tubular c

60 Incubation of mouse embryonic fibroblasts and T cells with transformin

61 nia virus replication in both HeLa cells and mouse embryonic fibroblasts and that its influence is ex

62 ockdown of GRB10 in nontumorigenic PTEN null mouse embryonic fibroblasts and tumorigenic PCa cell lin

63 rometric approach showed that ARH3-deficient mouse embryonic fibroblasts are characterized by a speci

64 e detail chromatin accessibility dynamics as mouse embryonic fibroblasts are reprogrammed into induce

65 We used mouse embryonic fibroblasts as a system to determine the

66 en uncovered new roadblocks in reprogramming mouse embryonic fibroblasts as pluripotent stem cells, d

67 mechanistic target of rapamycin signaling in mouse embryonic fibroblasts as well as in muscle and liv

68 a new system to delete FIP200 in transformed mouse embryonic fibroblasts as well as mammary tumor cel

69 oliferation, redox state and migration using mouse embryonic fibroblast Balb/3T3, human dermal fibrob

70 In the case of mouse embryonic fibroblasts, BER of the Sp lesion is str

71 ind that Orai1 is a dimer in resting primary mouse embryonic fibroblasts but displays variable stoich

72 iciently induces the cardiac gene program in mouse embryonic fibroblasts but not adult fibroblasts.

73 f proteomes extracted from Escherichia coli, mouse embryonic fibroblast cell cultures, and Arabidopsi

74 nternal structures of a mitochondrion from a mouse embryonic fibroblast cell line (NIH3T3) were visua

75 d in a Cry1 (-/-) Cry2 (-/-) double knockout mouse embryonic fibroblast cell line.

76 grin beta1 expression, we examined IPMK(-/-) mouse embryonic fibroblast cells and found that integrin

77 through cAMP-CREB signaling pathways both in mouse embryonic fibroblast cells and in urinary and repr

78 MG2 over TEM8 was further demonstrated using mouse embryonic fibroblast cells and mice deficient in t

79 s of 26S proteasomes purified from wild-type mouse embryonic fibroblast cells and those lacking Usp14

80 ntaneously (3T9) or virus-(SV40) transformed mouse embryonic fibroblast cells as targets.

81 Interestingly, in mouse embryonic fibroblast cells derived from CIZ1-null

82 We investigated this question using mouse embryonic fibroblast cells expressing wild-type PK

83 Knockout of GSK3beta in mouse embryonic fibroblast cells increases expression of

84 optosis was not affected in SV40-transformed mouse embryonic fibroblast cells lacking Bak/Bax.

85 Although S187A mouse embryonic fibroblast cells showed normal prolifera

86 ng MyoD-induced differentiation of 4.1R(-/-) mouse embryonic fibroblast cells.

87 y a minor fraction (30-40%) of the 26S in WT mouse embryonic fibroblast cells.

88 ed the glycolytic products in both tumor and mouse embryonic fibroblast cells.

89 Mouse embryonic fibroblasts challenged with TPZ or Cu(OP

90 formation but is dispensable for kidney and mouse embryonic fibroblast ciliary formation.

91 R3/MyD88/IFN-beta promoter stimulator 1(-/-) mouse embryonic fibroblasts completely lacked antiviral

92 ssion of the RIPK1 mutants D325V or D325H in mouse embryonic fibroblasts confers not only increased s

93 Experiments carried out in mouse embryonic fibroblasts corroborated these findings.

94 Additionally, whereas WT mouse embryonic fibroblasts could be reprogrammed to a s

95 Analysis of wounds and mouse embryonic fibroblast cultures showed that EMILIN-1

96 employ cell-based complementation studies in mouse embryonic fibroblast deficient for Esco1 and Esco2

97 nd of WT KRAS to rescue the growth defect of mouse embryonic fibroblasts deficient in all Ras genes.

98 Here we show that mouse embryonic fibroblasts deficient in Bax/Bak1 are re

99 in post-myocardial infarction hearts, and in mouse embryonic fibroblasts deleted for GSK-3beta.

100 Nphp5(-/-) mouse embryonic fibroblast developed normal cilia, and N

101 Interestingly, Msh3(-/-) mouse embryonic fibroblasts displayed increased chromati

102 the cII gene from lambda phage in transgenic mouse embryonic fibroblasts during the transition from p

103 and decreased senescence of hepatocytes and mouse embryonic fibroblasts, effects that were blocked b

104 tallin was upregulated in Tsc1-/- or Tsc2-/- mouse embryonic fibroblasts, Eker rat uterine leiomyoma-

105 ively, in Dhrs3(-/-) embryos, and Dhrs3(-/-) mouse embryonic fibroblasts exhibit reduced metabolism o

106 Spry1(-/-) and Spry2(-/-) double mutant mouse embryonic fibroblasts exhibited decreased cell mig

107 show that deletion of Ada3 from Ada3(FL/FL) mouse embryonic fibroblasts exhibited various chromosome

108 Whereas Bok(-/-) mouse embryonic fibroblasts exposed to thapsigargin, A23

109 levant doses; however, in the Ku70-deficient mouse embryonic fibroblasts, exposure to a high dose of

110 Tsc1(-/-) and Tsc2(-/-) mouse embryonic fibroblasts expressed higher uPA levels

111 turally diverse fatty acyl donor analogs and mouse embryonic fibroblasts expressing PORCN protein fro

112 More importantly, mouse embryonic fibroblasts expressing the SMURF2 S384A

113 nct culture platforms: feeder-free Matrigel, mouse embryonic fibroblast feeders, and Matrigel replate

114 Calnexin deficiency as studied in mouse embryonic fibroblasts from calnexin(-/-)mice or in

115 doplasmic reticulum (ER) stress response) in mouse embryonic fibroblasts from Epm2a(-/-), Epm2b(-/-),

116 onferred resistance to cell death, and (iii) mouse embryonic fibroblasts from IFN receptor 1 knockout

117 Similarly, mouse embryonic fibroblasts from Mcub(-/-) mice were mor

118 Here we used mouse embryonic fibroblasts from mice deficient in FAM13

119 Analysis of cultured mesoderm explants and mouse embryonic fibroblasts from null mutants shows that

120 Employing mouse embryonic fibroblasts from wild-type and RGS6(-/-)

121 ated reprogramming factor expression levels, mouse embryonic fibroblasts go through unique epigenetic

122 es induced in Cln3(Deltaex1) (-) (6)-derived mouse embryonic fibroblasts have visibly disorganized me

123 We developed an immortalized mouse embryonic fibroblast (iMEF) line in which full-len

124 duce mitochondrial fission when expressed in mouse embryonic fibroblasts in the absence of additional

125 e expression of HH target genes in Sufu(-/-) mouse embryonic fibroblasts, in which constitutive Gli a

126 mber of RhoA signaling-mediated processes in mouse embryonic fibroblasts, including stress fiber form

127 ressor function because ablation of SRPK1 in mouse embryonic fibroblasts induces cell transformation.

128 letion can sensitize breast cancer cells and mouse embryonic fibroblasts into entering paclitaxel-ind

129 Myc (c-Myc) or Oct4 during reprogramming of mouse embryonic fibroblasts into iPSCs.

130 omised relocation of Xi in CIZ1-null primary mouse embryonic fibroblasts is accompanied by loss of PR

131 show that SV40 TAg-induced transformation in mouse embryonic fibroblasts is independent of activator

132 Furthermore, mouse embryonic fibroblasts isolated from TRPM7 kinase-d

133 AX/BCL2 agonist killer (BAK) double-knockout mouse embryonic fibroblasts, its location was solely cyt

134 We examined mouse embryonic fibroblasts lacking Atg16l1 (ATG16L1 KO

135 Complementation experiments in mouse embryonic fibroblasts lacking beta-arrestins combi

136 Cyclin B1 induces chromosomal instability in mouse embryonic fibroblasts lacking both Tp53 and Rb1.

137 ld-type and NLS-mutated pol beta(R4S,K5S) in mouse embryonic fibroblasts lacking endogenous pol beta.

138 A-Seq, we found that inactivation of Flcn in mouse embryonic fibroblasts leads to changes in multiple

139 arly, experiments in cultured Oma1-deficient mouse embryonic fibroblasts link together impeded superc

140 Herein, we demonstrated that, in mouse embryonic fibroblasts, loss of LKB1 and transducti

141 cription factor EB (TFEB) in RagA/B knockout mouse embryonic fibroblasts, lysosomal acidification is

142 es E6/E7) disrupts circadian oscillations in mouse embryonic fibroblasts, measured using PER2::Luc dy

143 s the biogenesis and function of EVs using a mouse embryonic fibroblast (MEF) cell line that can be i

144 Here we label the endogenous Pol II in mouse embryonic fibroblast (MEF) cells using the CRISPR/

145 In mouse embryonic fibroblast (MEF) cells we show that Prom

146 Using an established mouse embryonic fibroblast (MEF) model combining p53 ina

147 Using mouse embryonic fibroblast (MEF) models that generate in

148 se data spanning nearly two cell cycles from Mouse Embryonic Fibroblast (MEF) primary cells.

149 used an inducible Raptor and Rictor knockout mouse embryonic fibroblast (MEF) system to further defin

150 over, Arpp19 ablation dramatically decreased mouse embryonic fibroblast (MEF) viability by perturbing

151 e H3 K36 trimethyltransferase SETD2 knockout mouse embryonic fibroblasts (MEF) cells.

152 Moreover, primary Rad18(-/-) mouse embryonic fibroblasts (MEF) retained robust Fancd2

153 Cyclin A2 deletion in oncogene-transformed mouse embryonic fibroblasts (MEF) suppressed tumor forma

154 nsulin signaling were restored in ATG16L1 KO mouse embryonic fibroblasts (MEF) upon proteasome inhibi

155 E359K mouse embryonic fibroblasts (MEF) were more sensitive to

156 Here using mouse embryonic fibroblasts (MEF), we investigate the ci

157 transformation using G0s2-null immortalized mouse embryonic fibroblasts (MEF).

158 IL-6 mRNA and protein secretion in wild-type mouse embryonic fibroblasts (MEF).

159 uencing on wild-type and beta-actin knockout mouse embryonic fibroblasts (MEFs) after reprograming to

160 y transfecting MNV-1 RNA into IFN-stimulated mouse embryonic fibroblasts (MEFs) and bone marrow-deriv

161 We characterized CENP-F(+/+) and CENP-F(-/-) mouse embryonic fibroblasts (MEFs) and found drastic dif

162 Mouse embryonic fibroblasts (MEFs) and hepatocytes from

163 morphological state space of a population of mouse embryonic fibroblasts (MEFs) and identify topograp

164 ation impairs the proliferative potential of mouse embryonic fibroblasts (MEFs) and is associated wit

165 trimethylation (H3K27me3) in both Pten null mouse embryonic fibroblasts (MEFs) and Pten null mouse p

166 lates Rb in Cdk4(-/-) pituitary AL cells and mouse embryonic fibroblasts (MEFs) and rescues their pro

167 Mouse embryonic fibroblasts (MEFs) and retinal cells fro

168 e generated PCBP2-deficient mice and primary mouse embryonic fibroblasts (MEFs) and showed that loss

169 olysis and represses fatty acid oxidation in mouse embryonic fibroblasts (MEFs) by targeting the AMP-

170 r unit length over mitochondria in Drp1-null mouse embryonic fibroblasts (MEFs) compared to wild-type

171 coding nonmitochondrial PB2 is attenuated in mouse embryonic fibroblasts (MEFs) compared with an isog

172 Here, we derive mouse embryonic fibroblasts (MEFs) deleted in all three

173 EGR1(-/-) mouse embryonic fibroblasts (MEFs) demonstrated lower su

174 AM20C was absent in the conditioned media of mouse embryonic fibroblasts (MEFs) derived from Fam20a k

175 Here we show that primary adipocytes and mouse embryonic fibroblasts (MEFs) derived from FTO over

176 We demonstrate that mouse embryonic fibroblasts (MEFs) derived from Hace1(-/

177 of AhR was NF-kappaB-dependent, as shown in mouse embryonic fibroblasts (MEFs) derived from Rel null

178 we show that positioning of mitochondria in mouse embryonic fibroblasts (MEFs) determines the shape

179 Moreover, PGAM5 deficient mouse embryonic fibroblasts (MEFs) exhibited decreased p

180 Mechanistically, Tmem30a-mutant mouse embryonic fibroblasts (MEFs) exhibited diminished

181 In this study, we show that, in mouse embryonic fibroblasts (MEFs) from Fut8(-/-) mice,

182 ts in cell cycle progression in immortalized mouse embryonic fibroblasts (MEFs) from PINK1(-/-) mice,

183 Mouse embryonic fibroblasts (MEFs) from the double knock

184 Using mouse embryonic fibroblasts (MEFs) from Tpcn1(-/-) and T

185 ecrease SRSF6 levels further, we established mouse embryonic fibroblasts (MEFs) from wild type, zQ175

186 of Sall4, Nanog, Esrrb, and Lin28 (SNEL) in mouse embryonic fibroblasts (MEFs) generated high-qualit

187 Consistent with these results, Atf3(-/-) mouse embryonic fibroblasts (MEFs) had more aberrant chr

188 ting protein kinase 2 (HIPK2) in neurons and mouse embryonic fibroblasts (MEFs) has a broad protectiv

189 show that lysates from Nedd4-1 knockout (KO) mouse embryonic fibroblasts (MEFs) have significantly di

190 ned the late mitotic stages NPCs in vivo and mouse embryonic fibroblasts (MEFs) in vitro from Pafah1b

191 on in both breast cancer (BC) cell lines and mouse embryonic fibroblasts (MEFs) induces oversized cel

192 letion can sensitize breast cancer cells and mouse embryonic fibroblasts (MEFs) into entering epirubi

193 imidine tract binding protein PTB to convert mouse embryonic fibroblasts (MEFs) into functional neuro

194 multifaceted effect on the reprogramming of mouse embryonic fibroblasts (MEFs) into induced pluripot

195 Proliferation of primary Ola1(-/-) mouse embryonic fibroblasts (MEFs) is impaired due to de

196 the G50DblKo virus was rescued by growth on mouse embryonic fibroblasts (MEFs) isolated from IFN-alp

197 We examined glutamine metabolism in mouse embryonic fibroblasts (MEFs) isolated from mice th

198 Primary mouse embryonic fibroblasts (MEFs) lacking the ARF tumor

199 Mouse embryonic fibroblasts (MEFs) or primary adult card

200 Cebpg(-/-) mouse embryonic fibroblasts (MEFs) proliferate poorly an

201 from affected individuals and Cdk10-knockout mouse embryonic fibroblasts (MEFs) proliferated normally

202 Ectopic expression of DNMT3L in late-passage mouse embryonic fibroblasts (MEFs) recruited cytoplasmic

203 C1qbp(-/-) mouse embryonic fibroblasts (MEFs) resembled the human d

204 ction of PDAC cancer cells and SerpinB2(-/-) mouse embryonic fibroblasts (MEFs) resulted in increased

205 we report that Cdc14B knockout (Cdc14B(-/-)) mouse embryonic fibroblasts (MEFs) showed defects in rep

206 the generations, and immortalized TIN2(+/DC) mouse embryonic fibroblasts (MEFs) showed telomere short

207 s, we compared gene expression in STAT3-null mouse embryonic fibroblasts (MEFs) stably expressing wil

208 MPK inhibitor to either mouse macrophages or mouse embryonic fibroblasts (MEFs) suppressed IFN-beta a

209 tebrate cells, maintain the DHS landscape of mouse embryonic fibroblasts (MEFs) synergistically.

210 Here, we show in mouse embryonic fibroblasts (MEFs) that this MNNG-depend

211 onic day 18.5 BAT3(-/-) mouse embryos and in mouse embryonic fibroblasts (MEFs) through the modulatio

212 t of this transcription factor complex, from mouse embryonic fibroblasts (MEFs) to examine the role o

213 9 knockout screen in Kras(G12D) immortalized mouse embryonic fibroblasts (MEFs) to search for genes t

214 the first genome-scale map of murine NADs in mouse embryonic fibroblasts (MEFs) via deep sequencing o

215 Mouse embryonic fibroblasts (MEFs) were isolated from Sp

216 infectious EBOV derived from SOCS3 knockout mouse embryonic fibroblasts (MEFs) were significantly re

217 onic fibroblasts lacking Atg16l1 (ATG16L1 KO mouse embryonic fibroblasts (MEFs)), an essential autoph

218 se rates for 176 miRNAs in contact-inhibited mouse embryonic fibroblasts (MEFs), 182 miRNAs in dividi

219 cient mouse bone marrow-derived macrophages, mouse embryonic fibroblasts (MEFs), and human HeLa cells

220 reduced in Ras(V12)-expressing p19(Arf) null mouse embryonic fibroblasts (MEFs), and overall Egr DNA-

221 overage and histone methylation occupancy in mouse embryonic fibroblasts (MEFs), induced pluripotent

222 In eEF2K(-/-) mouse embryonic fibroblasts (MEFs), inhibition of HSP90

223 In mouse embryonic fibroblasts (MEFs), inhibition of mitoch

224 1 and -2 can be cell surface-biotinylated on mouse embryonic fibroblasts (mEFs), revealing that endog

225 In mouse embryonic fibroblasts (MEFs), Sirt6 knockout (KO)

226 Similarly, in Kif3a null mouse embryonic fibroblasts (MEFs), the overall TonEBP-d

227 Using knockout mouse embryonic fibroblasts (MEFs), we demonstrate that

228 g studies in Xenopus laevis egg extracts and mouse embryonic fibroblasts (MEFs), we show here that NC

229 s and oxidative stress-induced senescence of mouse embryonic fibroblasts (MEFs), whereas overexpressi

230 ssion in p53 (-/-) and INK4a (-/-)/Arf (-/-) mouse embryonic fibroblasts (MEFs), which failed to inhi

231 types-Schlemm's canal endothelial cells and mouse embryonic fibroblasts (MEFs)-using four different

232 se pluripotent stem cells in comparison with mouse embryonic fibroblasts (MEFs).

233 , using a SILAC approach, of PDGF-stimulated mouse embryonic fibroblasts (MEFs).

234 methyltransferase for PP2A, PP4, and PP6 in mouse embryonic fibroblasts (MEFs).

235 cancer cell lines, ex vivo tumor tissue, and mouse embryonic fibroblasts (MEFs).

236 is using an inducible knockout (KO) model of mouse embryonic fibroblasts (MEFs).

237 escence in wild-type but not caveolin-1 null mouse embryonic fibroblasts (MEFs).

238 ons in two different cell types, B cells and mouse embryonic fibroblasts (MEFs).

239 methyltransferase PRMT5 controls H4R3me2s in mouse embryonic fibroblasts (MEFs).

240 igenic epithelial breast cells (MCF10A), and mouse embryonic fibroblasts (MEFs).

241 H2AX and DNA damage checkpoint activation in mouse embryonic fibroblasts (MEFs).

242 e ER stress responses, within WT or PERK -/- Mouse Embryonic Fibroblasts (MEFs).

243 ls as well as in eEF2K-knockout (eEF2K(-/-)) mouse embryonic fibroblasts (MEFs).

244 slation initiation factor 2alpha (eIF2alpha) mouse embryonic fibroblasts (MEFs); moreover, ECD mRNA l

245 ll (RAW264.7 cells, primary macrophages, and mouse embryonic fibroblasts [MEFs]) apoptosis induced by

246 cient cell lines (A20.2J, CH12.LX, HAP1, and mouse embryonic fibroblasts [MEFs]) reconstituted with w

247 and in mouse, non-cancerous, primary cells (mouse embryonic fibroblasts, MEFs), to assess different

248 In a mouse embryonic fibroblast model, Drp1 C452F cells exhib

249 ment similarly inhibited nuclear import in a mouse embryonic fibroblast model.

250 sonance energy transfer; 3) in MPC1 depleted mouse embryonic fibroblasts, MPC1L rescues the loss of p

251 icroscopy were performed in prkar1 knock-out mouse embryonic fibroblasts, neonatal myocytes, or adult

252 Using mouse embryonic fibroblast nuclei with normal or reduced

253 Expressing core in livers or mouse embryonic fibroblasts of ATGL(-/-) mice no longer

254 ally mimicked by inactivation of IR alone in mouse embryonic fibroblasts or in vivo in brown fat in m

255 and human glioblastoma cells but not that of mouse embryonic fibroblasts or neonatal astrocytes.

256 tionally, we show that in kindlin-2 knockout mouse embryonic fibroblasts, overactivation of Ras, Akt,

257 Primary mouse embryonic fibroblasts (pMEFs) expressing caveolin

258 Plk1 overexpression in mouse embryonic fibroblasts prepared from the transgenic

259 CYLD forms were expressed in mouse embryonic fibroblasts, primary T cells, and HEK293

260 SIRT3-null mouse embryonic fibroblasts produced significantly more

261 ckdown of AMPK and the use of AMPKalpha(-/-) mouse embryonic fibroblasts provided further evidence th

262 consumption, and decreased ATP production in mouse embryonic fibroblasts, providing insights into the

263 f canonical autophagy: both WT and Atg5(-/-) mouse embryonic fibroblasts responded similarly.

264 genetic ablation of MPC1 in hepatocytes and mouse embryonic fibroblasts resulted in reduced resting

265 Deletion of USP9X in mouse embryonic fibroblasts resulted in significant down

266 However, paradoxically loss of LKB1 in mouse embryonic fibroblast results in resistance to onco

267 pletion of Spartan from conditional knockout mouse embryonic fibroblasts results in impaired lesion b

268 of Wrn, alone or in combination with Trf2 in mouse embryonic fibroblasts results in increased telomer

269 Transcriptome analysis using mouse embryonic fibroblasts revealed deregulation in the

270 In vitro investigations with mouse embryonic fibroblasts revealed factors, in additio

271 Furthermore, Fkbp10(-/-) mouse embryonic fibroblasts show retention of procollage

272 Rb1-deficient mouse embryonic fibroblasts showed increased levels of O

273 ection of ID8 mouse ovarian tumor cells with mouse embryonic fibroblasts showed that CD73 expression

274 striking decrease seen in cultured Tsc2(-/-) mouse embryonic fibroblasts, suggesting one mechanism th

275 nctions are abrogated in lamin A/C-deficient mouse embryonic fibroblasts that recapitulate the defect

276 In contrast, in mouse embryonic fibroblasts the coding segment is deplet

277 tional responses of embryonic stem cells and mouse embryonic fibroblasts to amber codon suppression.

278 We demonstrate that adaptation of mouse embryonic fibroblasts to cell culture results in a

279 l1, and Myt1l genes (BAM factors) to convert mouse embryonic fibroblasts to induced neuronal cells.

280 points to dissect direct reprogramming from mouse embryonic fibroblasts to induced neuronal cells.

281 ribing the reprogramming routes leading from mouse embryonic fibroblasts to induced pluripotency.

282 he resulting knock-out animals, we also used mouse embryonic fibroblasts to investigate the associate

283 onist Gamitrinib strongly sensitizes primary mouse embryonic fibroblasts to mPT and permeability tran

284 iptional changes during the reprogramming of mouse embryonic fibroblasts to pluripotent stem cells.

285 Here, we use wild-type and vimentin-null mouse embryonic fibroblasts to show that VIFs regulate n

286 Here, we take advantage of mouse embryonic fibroblasts transformed by oncogenic Dbl

287 in tumor cell lines, mouse lung tumors, and mouse embryonic fibroblasts undergoing RAS-induced senes

288 induction of iNOS decreases cell survival in mouse embryonic fibroblasts via mechanisms involving nit

289 Using knockout mouse embryonic fibroblasts we show that Miro1 and Miro2

290 In wild type and FAK knock-out mouse embryonic fibroblasts, we found by immunoblotting,

291 Using mouse embryonic fibroblasts, we genetically dissected th

292 For endogenous beta-actin genes in mouse embryonic fibroblasts, we observe that short-lived

293 Mitochondria in C452F mouse embryonic fibroblasts were depolarized and had red

294 larized recycling of alpha5beta1-integrin in mouse embryonic fibroblasts, which enables persistent fi

295 sis, we examined the Hh signaling pathway in mouse embryonic fibroblasts, which readily responds to t

296 The use of Ada3(FL/FL) mouse embryonic fibroblasts with deletion of Ada3 using

297 Mouse embryonic fibroblasts with genetic ablations of TS

298 Mouse embryonic fibroblasts with Ptpn11 GOF mutations sh

299 linositol (3,4,5)-trisphosphate (PIP3), from mouse embryonic fibroblasts with serum stimulation.

300 lear translocation was observed in wild-type mouse embryonic fibroblasts (WT MEFs), Tg2576 MEFs, and