ライフサイエンスコーパス: LIF

1 LIF also induced neuronal plasticity in dorsal root gang

2 LIF at levels found in the C26 CM was sufficient for STA

3 LIF detection allowed quantification of the metabolic co

4 LIF is a sensitive technique and useful in the study of

5 LIF is overexpressed in a large percentage of CRCs.

6 LIF levels are significantly lower in cells with the P72

7 LIF overexpression promotes cellular resistance towards

8 LIF signaling is known to promote self-renewal and pluri

9 LIF was elevated in C26 conditioned medium (CM), but IL-

10 LIF was overexpressed in tumor tissue compared with heal

11 LIF, a cytokine that is required for optimal reproductiv

12 LIF-3i-reverted hPSCs retained normal karyotypes and gen

13 LIF-JAK/STAT3 signalling was recently shown to be a limi

14 or stem cell factor is unnecessary using 2i-LIF.

15 2i/LIF can abrogate persistent-NPC interactions, recover po

16 ore homogeneous undifferentiated culture (2i/LIF), we examine the role of cellular heterogeneity in t

17 mESCs cultured in serum/LIF or serum-free 2i/LIF conditions.

18 ycogen synthase kinase 3 (GSK3) with LIF (2i/LIF) provides an optimal culture environment for mouse E

19 Here we show that 2i/LIF treatment in clonal lines of pre-iPS cells results i

20 F condition was more variable than in the 2i/LIF but mostly consistent across the two conditions.

21 ived from cells cultured in serum/LIF vs. 2i/LIF revealed differential roles for Nanog, Oct4/Pou5f1,

22 ring early development in comparison with 2i/LIF ESCs.

23 several cytokines (TNFalpha, IL-beta, IL-6, LIF), and the density of Iba1(+) microglia in pups with

24 Ablating IL-6, LIF, or gp130 uncouples this cellular cross-talk, and po

25 By quantitative PCR, interleukin-6, LIF, and CNTF mRNA increased but with significantly diff

26 A LIF-blocking antibody abolished C26 CM-induced STAT repo

27 fficient to sustain intrinsic signaling in a LIF-independent manner to promote ES cell pluripotency a

28 with either soluble LIF receptor (sLIFR), a LIF antagonist, or the mTOR inhibitor rapamycin reversed

29 d murine LIF (mLIF) act in mouse cells via a LIF receptor (LIFR)-glycoprotein 130 (gp130) heterodimer

30 remained pluripotent in the absence of added LIF.

31 15 proteins, including IL-1alpha, IL-17, and LIF.

32 uterus increased HLA-G, EGF-Receptor-2, and LIF-Receptor expression on EVT, presumably representing

33 tured with Erk and Gsk3 inhibitors (2i), and LIF, similar to conventional mESCs.

34 -6 promoter after fibroblast activation, and LIF receptor (LIFR) and STAT4 formed a molecular complex

35 lta) and 2 antiapoptotic proteins (FGFR2 and LIF) were authentic targets for miR-494.

36 pathways, such as Notch, Wnt, Hedgehog, and LIF, in progenitor cells compared with differentiated ce

37 ukemia inhibitory factor (LIF), only OSM and LIF were sufficient to activate the STAT reporter in myo

38 asma and GCF IL-1beta, IL-6, IL-11, OSM, and LIF levels were analyzed by enzyme-linked immunosorbent

39 uces sequential mRNA expression of PROK1 and LIF in an in vivo baboon model, in human endometrial epi

40 Anti-LIF completely eliminated lung LIF detection and markedl

41 kine expression was also exaggerated in anti-LIF-treated lungs, albeit after injury had ensued.

42 /6 mice in the presence of neutralizing anti-LIF IgG or control IgG.

43 ups, bacteremia was more prevalent with anti-LIF treatment, suggestive of compromised barrier functio

44 o GCSCs induced ZEB1 expression, attenuating LIF activities.

45 a positive feedback loop involving autocrine LIF, LIFR, and STAT4 drove sustained IL-6 transcription.

46 lish Tfcp2l1 as the principal bridge between LIF/Stat3 input and the transcription factor core of nai

47 ar patterns of histone modifications between LIF-independent iOCT4 and control ES cells.

48 e of mobilities that are further analyzed by LIF.

49 fcp2l1 at levels similar to those induced by LIF effectively substituted for LIF or Stat3 in sustaini

50 M-conjugated dextran (for pH measurements by LIF).

51 The downregulation of p53 by LIF is mediated by the activation of Stat3, which transc

52 potent stimulation of naive pluripotency by LIF/Stat3 is attributable to parallel and synergistic in

53 etina, rhodopsin protein was also reduced by LIF.

54 Although pregnancy was rescued by LIF and was maintained to term in uterine gland-containi

55 s can be separated by the DMA and studied by LIF.

56 ZEB1 knockdown in GCSCs caused LIF induction commensurate with GCSC self-renewal and in

57 hich is an autophagy marker, to develop a CE-LIF method for the determination of the number of autoph

58 lfonate (APTS) were separated to obtain a CE-LIF profile of the complex glycan mixture, and the profi

59 initrophenylation reaction conditions and CE-LIF parameters were determined and resulted in the limit

60 the sialic acid residues as determined by CE-LIF and offline mass spectrometric analysis.

61 ate that individual organelle analysis by CE-LIF is a powerful technology to investigate the complexi

62 lves derivatization with FITC followed by CE-LIF using 0.5 mM hydroxyl propyl-beta-cyclodextrin in bo

63 0 M(-1) for Ado and 1000 M(-1) for Ino by CE-LIF.

64 ith laser-induced fluorescence detection (CE-LIF) and matrix assisted laser desorption ionization-tim

65 to laser induced fluorescence detection (CE-LIF) has been used previously to count and determine pro

66 sis-laser-induced fluorescence detection (CE-LIF) method that analyzes Ado and Ino by derivatization

67 ith laser-induced fluorescence detection (CE-LIF) was demonstrated.

68 ith laser induced fluorescence detection (CE-LIF) was employed for rapid sialic acid speciation, faci

69 with laser-induced fluorescent detection (CE-LIF) was previously used to count and determine properti

70 ith laser-induced fluorescence detection (CE-LIF).

71 ith laser induced fluorescence detection (CE-LIF).

72 ith laser induced fluorescence detection (CE-LIF).

73 ith laser-induced fluorescence detection (CE-LIF).

74 ectrophoresis-laser-induced fluorescence (CE-LIF) method for the analysis of D-serine (D-Ser) in cell

75 ectrophoresis laser-induced fluorescence (CE-LIF) setup.

76 ectrophoresis-laser-induced fluorescence (CE-LIF), all the procedures, including thrombin injection,

77 ectrophoresis-laser induced fluorescence (CE-LIF), high performance liquid chromatography (HPLC), and

78 This is both the first demonstration of CE-LIF to analyze individual organelles labeled with fluoro

79 first application of individual organelle CE-LIF to measure the properties of autophagy organelles is

80 pared directly with a previously reported CE-LIF technique, concluding that additional or alternative

81 ervations described here demonstrate that CE-LIF of immunolabeled autophagy organelles is a powerful

82 boxylation reaction to completion and the CE-LIF parameters to separate the neutral species by comple

83 The CE-LIF results were validated by bulk ThT fluorescence meas

84 solated from murine liver tissue prior to CE-LIF analysis.

85 n membrane potential), and separated with CE-LIF.

86 ialylated glycans in comparison to common CE/LIF systems.

87 phoresis with laser-induced fluorescence (CE/LIF) using 8-aminopyrene-1,3,6-trisulfonic acid (APTS)-l

88 a migration direction analogue to routine CE/LIF systems.

89 d for both CE/MS methods and two standard CE/LIF approaches.

90 r enzymatic protection approach with the CGE-LIF (capillary gel electrophoresis with laser-induced fl

91 CNTF/LIF/STAT3 signaling has been shown to promote their diff

92 Using a four-color LIF detector, 265 bases could be read in 30 min with a 2

93 gh WR is necessary to enable Nanog to confer LIF-independent self-renewal, the mechanism of dimerizat

94 lly eluted with free Man-6-P thus confirming LIF as a bona fide Man-6-P-modified protein.

95 12p70, IL-13, IL-17F, leptin, G-CSF, GM-CSF, LIF, NGF, SCF, and TGF-alpha.

96 The proinflammatory cytokine LIF reprograms fibroblasts into a proinvasive phenotype,

97 . report that NPCs also produce the cytokine LIF, which suppresses Th17 cell-driven inflammation and

98 Our data demonstrate that a single cytokine, LIF, can simultaneously and independently affect both RP

99 Addition of two such cytokines, LIF or VEGF, at levels comparable to those secreted by Z

100 Decreased LIF levels in diseased groups might reflect the possible

101 Analysis of glycan-deleted LIF mutants demonstrated that loss of glycans bearing th

102 ess factor) promoter region, and demonstrate LIF repression by ZEB1.

103 in-line laser-induced fluorecence detection (LIF) determined for the first time the pH of each magnet

104 led to laser-induced fluorescence detection (LIF) has been proposed for the determination of ochratox

105 online laser-induced fluorescence detection (LIF) is reported.

106 use embryonic stem cells (mESCs) by enabling LIF-dependent STAT3 phosphorylation, with E-cadherin nul

107 these findings, we conclude that endogenous LIF facilitates tissue protection during pneumonia.

108 PHLPP-1 knockdown enhances LIF-mediated cardioprotection against doxorubicin and al

109 in latent membrane protein 1 (LMP1) enhances LIF production.

110 Surprisingly, we found that NANOG enhances LIF signal transduction, resulting in elevated pSTAT3.

111 stromal cells in PDAC tissues both expressed LIF, but only stromal cells could secrete it.

112 nd patient biopsy specimens poorly expressed LIF, precluding LIFR lysosomal degradation and OSMR tran

113 withdrawal of the ES cell maintenance factor LIF.

114 t the IL6-related stem cell-promoting factor LIF supports PDAC-associated neural remodeling (PANR).

115 ine how IL-6 and leukemia-inhibiting factor (LIF) affect SVZ cell expansion, proliferation, and self-

116 the presence of leukaemia inhibitory factor (LIF) (hereafter termed 2i/L) induces a naive state in mo

117 by the cytokine leukaemia inhibitory factor (LIF) acting through the transcription factor Stat3.

118 are activated by leukemia inhibitory factor (LIF) and contribute to mouse embryonic stem (mES) cell m

119 kines, including Leukemia inhibitory factor (LIF) and Interleukin 6 (IL-6), in human NPCs.

120 serum levels of leukemia inhibitory factor (LIF) and that higher LIF levels correlated with local tu

121 atin M (OSM) and leukemia inhibitory factor (LIF) are IL-6 family members with a wide range of biolog

122 family cytokine leukemia inhibitory factor (LIF) as a serum predictor of local NPC recurrence follow

123 ted to STAT4 and leukemia inhibitory factor (LIF) as potentially linked.

124 ress IL-6 and/or leukemia inhibitory factor (LIF) cytokines.

125 Leukaemia inhibitory factor (LIF) has been recently identified as a p53 target gene,

126 to determine how leukemia inhibitory factor (LIF) insufficiency affects their response.

127 tin M (OSM), and leukemia inhibitory factor (LIF) levels in patients with different periodontal disea

128 to withdrawal of leukemia inhibitory factor (LIF) or bone morphogenetic protein 4 (BMP4).

129 ctor (CNTF) and leukaemia inhibitory factor (LIF) potently protect axotomised retinal ganglion cells

130 Leukaemia inhibitory factor (LIF) regulates ESCs through Stat3, independently of Gsk3

131 ession, enhanced leukemia inhibitory factor (LIF) sensitivity, and reduced responsiveness to fibrobla

132 tin M (OSM) and leukaemia inhibitory factor (LIF) signal through receptor complexes that are critical

133 between Tet1 and leukemia inhibitory factor (LIF) signaling.

134 that delivery of leukemia inhibitory factor (LIF) to the CNS stimulates the self-renewal of neural st

135 that addition of leukemia inhibitory factor (LIF) together with either serum or bone morphogenetic pr

136 rentiation after leukemia inhibitory factor (LIF) withdrawal but, unlike control ESCs, failed to main

137 rentiation after leukemia inhibitory factor (LIF) withdrawal.

138 Leukemia inhibitory factor (LIF), a critical implantation factor of uterine gland or

139 al regulation of leukemia inhibitory factor (LIF), a cytokine crucial for blastocyst implantation.

140 lation status of leukemia inhibitory factor (LIF), a previously identified high affinity ligand for t

141 Leukemia inhibitory factor (LIF), an interleukin-6 family neurocytokine, is up-regul

142 ostatin M (OSM), leukemia inhibitory factor (LIF), and IL-11, have fibrogenic features.

143 oncentrations of leukemia inhibitory factor (LIF), basic fibroblast growth factor (bFGF), and nerve g

144 tin M (OSM), and leukemia inhibitory factor (LIF), only OSM and LIF were sufficient to activate the S

145 tin M (OSM), and leukemia inhibitory factor (LIF), signal via the common GP130 cytokine receptor subu

146 ing the cytokine leukemia inhibitory factor (LIF), which propagates the pluripotent state by activati

147 ing), which uses leukemia inhibitory factor (LIF)-expressing SNL feeders, frequently had two Xas.

148 y, PI3K-AKT, the leukemia inhibitory factor (LIF)-JAK-STAT3 axis, Wnt-GSK3 signalling, and the transf

149 mone (ACTH) and leukaemia inhibitory factor (LIF).

150 ation of uterine leukemia inhibitory factor (LIF).

151 th the cytokine leukaemia inhibitory factor (LIF).

152 stimulated with leukemia inhibitory factor (LIF).

153 of the cytokine leukemia inhibitory factor (LIF).

154 tivation of the leukaemia inhibitory factor (LIF)/signal transducer and activator of transcription 3

155 unction with the leukemia inhibitory factor (LIF)/Stat3 pathway.

156 echanism for how leukemia inhibitory factor (LIF)/STAT3 signaling reaches across to the MAPK/ERK path

157 ins [mCherry and leukemia inhibitory factor (LIF)].

158 ium supplemented with three cytokines (FGF2, LIF, and IGF1) in combination, so-called "FLI medium," i

159 tilayer network of leaky integrate-and-fire (LIF) spiking neuron models.

160 nction with both laser-induced fluorescence (LIF) and mass spectrometry (MS) detection methods.

161 C) with a tandem laser-induced fluorescence (LIF) and mass spectrometry (MS) detection scheme for the

162 te and robust CE-laser-induced fluorescence (LIF) assay and is generally applicable to any analysis r

163 oresis (CE) with laser-induced fluorescence (LIF) detection.

164 argely relies on laser-induced fluorescence (LIF) detection.

165 with a confocal laser-induced fluorescence (LIF) detector.

166 d detected using laser-induced fluorescence (LIF) in a sheath flow cuvette.

167 d using a simple laser-induced fluorescence (LIF) instrument.

168 raviolet (UV) or laser-induced fluorescence (LIF) signals.

169 croscopy (STEM), laser induced fluorescence (LIF) spectrometry, and ambient-pressure X-ray photoelect

170 lyzer (DMA) with laser-induced fluorescence (LIF) to simultaneously retrieve two-dimensional informat

171 ionally assisted laser-induced fluorescence (LIF).

172 and detected by laser-induced fluorescence (LIF).

173 during pneumonia, but far more so following LIF neutralization, with gene changes implicating cell d

174 by the addition of neutralizing antibody for LIF, but not for IL-6, revealing a critical role of auto

175 erve density, supporting a critical role for LIF function in PANR.

176 e induced by LIF effectively substituted for LIF or Stat3 in sustaining clonal self-renewal and pluri

177 When media from LIF-overexpressing cells were fractionated using a CI-MP

178 Conversely, GCF LIF levels of the CP and GAgP groups were lower than tho

179 emia inhibitory factor (LIF) and that higher LIF levels correlated with local tumor recurrence.

180 ost, including in the rs713875 MTMR3/HORMAD2/LIF/OSM region, are unknown.

181 Using this HPLC-LIF-MS methodology, the disappearance of doxorubicin and

182 We previously identified LIF as a prominent STAT3-activating cytokine expressed i

183 Correspondingly, upregulation of the IL6/LIF-gp130 pathway accounted for the strong STAT3 activat

184 We discovered that Tet1 depletion impaired LIF-dependent Stat3-mediated gene activation by affectin

185 overy of bleachable rhodopsin was delayed in LIF-injected eyes.

186 Consistent with parallel operation, ESCs in LIF accommodated Esrrb deletion and remained pluripotent

187 fore, we evaluated the NP response to H-I in LIF-haplodeficient mice.

188 ription factor Tfcp2l1 is a common target in LIF/Stat3- and 2i-mediated self-renewal, and forced expr

189 only WNT, MEK/ERK, and tankyrase inhibition (LIF-3i).

190 L-27, and OSM signaling but a largely intact LIF response.

191 oectodermic features, characterized by a low LIF, a high LIFR/OSMR ratio, and high MYC expression.

192 Anti-LIF completely eliminated lung LIF detection and markedly exacerbated lung injury compa

193 ed to PROK1 to demonstrate that hCG-mediated LIF expression in the endometrium is dependent on prior

194 h laser-induced fluorescence detection (MEKC-LIF) making it possible to detect superoxide found in si

195 omatography-laser induced fluorescence (MEKC-LIF) method was developed using sodium dodecylbenzene su

196 Failure to modify LIF in the context of mucolipidosis II and its subsequen

197 Moreover, LIF-independent iOCT4 ES cells retain the capacity to di

198 Human OSM (hOSM) and murine LIF (mLIF) act in mouse cells via a LIF receptor (LIFR)-

199 in the allergic group including RELB, NFKB2, LIF and FAS.

200 th known to maintain mESCs in the absence of LIF, rescued Tet1 depletion, further supporting the depe

201 e self-renewal of ES cells in the absence of LIF.

202 aining MESCM through transient activation of LIF-JAK1-STAT3 signaling that delays eventual nuclear tr

203 Surprisingly, mass spectrometric analysis of LIF glycopeptides enriched on the CI-MPR column revealed

204 letion, further supporting the dependence of LIF/Stat3 signaling on Tet1.

205 transcriptional network acting downstream of LIF, WNT and MAPK-ERK to stabilize mouse embryonic stem

206 Importantly, this effect of LIF on OPC proliferation can be harnessed to enhance the

207 itulate the self-renewal-promoting effect of LIF or either of the 2i components.

208 ired nor sufficient for the potent effect of LIF.

209 t reflect the possible beneficial effects of LIF in the modulation of inflammatory response in gingiv

210 ogether with the known beneficial effects of LIF on OL and neuron survival, suggest that LIF has both

211 Moreover, CNTF elevates the expression of LIF and endothelin 2, thus positively promoting Muller a

212 After intravitreal injection of LIF, we analyzed the expression levels of visual cycle g

213 Notably, injection of LIF-blocking antibody into PDAC-bearing mice reduced int

214 Intriguingly, i.p. injections of LIF initiated blastocyst implantation in the uteri of bo

215 clude that Tfcp2l1 is at the intersection of LIF- and 2i-mediated self-renewal pathways and plays a c

216 on serves to control extracellular levels of LIF.

217 negative regulator of p53, overexpression of LIF is an important mechanism for the attenuation of p53

218 Overexpression of LIF is associated with a poor prognosis in CRC patients.

219 e showed that the mannose phosphorylation of LIF mediates its internalization thereby reducing extrac

220 ce of bone morphogenetic protein, removal of LIF destabilizes pluripotency.

221 her, these data support an important role of LIF-JAK2-STAT3 in C26 cachexia and point to a therapeuti

222 ng a critical role of autocrine secretion of LIF in TNF-alpha-induced STAT3 activation and astrogliog

223 The use of LIF as detector provided an extremely sensitive method f

224 Withdrawal of LIF leads to differentiation of mESCs.

225 of such samples that typically rely only on LIF detectors.

226 iation of ESCs by retinoic acid treatment or LIF deprivation, PDCD2 levels declined.

227 GCF IL-6, IL-1beta, OSM, LIF, and IL-11 levels were analyzed by enzyme-linked imm

228 expression of OCT4 is sufficient to overcome LIF-dependence.

229 ort that LIF is a negative regulator of p53; LIF downregulates p53 protein levels and function in hum

230 ES cells cultured in conventional serum plus LIF medium phenocopy male ES cells cultured in 2i/L.

231 e ability of PHLPP-1 knockdown to potentiate LIF-mediated increases in p-Akt at mitochondria and an a

232 eeders, and supplementation with recombinant LIF caused reactivation of some of X-linked genes.

233 during implantation to coordinately regulate LIF production.

234 mouse embryonic stem cells (mESCs) requires LIF and serum.

235 s, but axNanog dimers are required to rescue LIF-independent self-renewal.

236 st, or the mTOR inhibitor rapamycin reversed LIF-mediated effects, resulting in growth arrest and inc

237 ds to higher steady-state levels of secreted LIF.

238 In vivo, an increase in serum LIF preceded the increase in IL-6 in mice with C26 tumor

239 tes NPC tumorigenesis and suggest that serum LIF levels may predict local recurrence and radiosensiti

240 stablished that the acutely eliminated serum/LIF ESCs had started to differentiate.

241 fferentiated and differentiating ESCs (serum/LIF) with more homogeneous undifferentiated culture (2i/

242 on measurements from mESCs cultured in serum/LIF or serum-free 2i/LIF conditions.

243 y logic derived from cells cultured in serum/LIF vs. 2i/LIF revealed differential roles for Nanog, Oc

244 ging revealed a drastic elimination of serum/LIF ESCs during early development in comparison with 2i/

245 Overall, gene expression in the serum/LIF condition was more variable than in the 2i/LIF but m

246 onic stem cells (mESCs) cultured under serum/LIF conditions exhibit heterogeneous expression of pluri

247 All groups had similar LIF and IL-11 total amounts (P >0.008).

248 Treatment with either soluble LIF receptor (sLIFR), a LIF antagonist, or the mTOR inhi

249 Taken together, our findings suggest LIF as a candidate serum biomarker and diagnostic tool a

250 domain and the tryptophan repeat can support LIF-independent colony formation.

251 ion demonstrates the potential of the tandem LIF-MS detection scheme in quantification and characteri

252 xpression of OCT4 (iOCT4) supports long-term LIF-independent self-renewal of ES cells cultured in med

253 tripotentiality and was more effective than LIF in promoting self-renewal.

254 R were overexpressed in tumor cells and that LIF expression correlated with the presence of the activ

255 I alters the composition of the SVZ and that LIF is a key regulator for a subset of intermediate prog

256 vo xenograft mouse studies demonstrated that LIF critically contributes to NPC tumor growth and radio

257 ents and mouse models of PDAC, we found that LIF titers positively correlated with intratumoral nerve

258 Using these model systems, we found that LIF treatment activated the mTORC1/p70S6K signaling path

259 Taken together, our data indicate that LIF and BMP4 are not sufficient to maintain self-renewal

260 immunofluorescence experiments indicate that LIF is targeted directly to lysosomes following its bios

261 Together, our findings indicate that LIF promotes NPC tumorigenesis and suggest that serum LI

262 We also observed that LIF exerted an antagonistic effect on BMP4-induced XEN c

263 We observed that LIF induces rapid, robust, and sustained activation of S

264 Here we report that LIF is a negative regulator of p53; LIF downregulates p5

265 analyses of human NPC biopsies revealed that LIF and LIFR were overexpressed in tumor cells and that

266 Global expression analysis revealed that LIF-independent iOCT4 ES cells and control ES cells exhi

267 e (OL) progenitor cells (OPCs) and show that LIF delivery stimulates their proliferation through the

268 Biological investigations showed that LIF promoted the differentiation of glial nerve sheath S

269 LIF on OL and neuron survival, suggest that LIF has both reparative and protective activities that m

270 The LIF network was used to encapsulate mouse embryonic stem

271 The LIF-STAT3 axis is identified in this study as a critical

272 s initial finding to discover a role for the LIF/LIFR/mTORC1 signaling axis in NPC tumor cell growth

273 However, the LIF-induced down-regulation of RPE65 required a function

274 nd might also be a critical component of the LIF and BMP signaling pathways essential for maintenance

275 art, by suppression of the expression of the LIF/STAT3 negative regulator SOCS3.

276 We identified ZEB1 binding sites within the LIF (stemness factor) promoter region, and demonstrate L

277 Addition of PKA agonists to LIF-induced nephrons (previously shown to be a Wnt/beta-

278 Here we unveil that exposure to LIF initiates an epigenetic switch leading to the consti

279 expression is also increased in response to LIF withdrawal and Fgf/Mek/Erk stimulation.

280 to ES-cell-like cells (rESCs) in response to LIF-STAT3 signalling.

281 Stat3 mediates the self-renewal response to LIF.

282 2l1 profoundly compromised responsiveness to LIF.

283 o Day 42 by switching EGF-containing SHEM to LIF/bFGF-containing MESCM through transient activation o

284 Taken together, LIF is a novel negative regulator of p53, overexpression

285 CI-MPR affinity column, 35-45% of the total LIF molecules were bound and specifically eluted with fr

286 eed, while Klf2-null mESCs can survive under LIF/Serum, they are not viable under 2i, demonstrating t

287 esoderm, endoderm and ectoderm lineages upon LIF withdrawal.

288 e was demonstrated to produce higher uterine LIF levels during implantation than the proline allele.

289 up-regulation of AMCFII, IL-8, IL-15, VEGFA, LIF, FASL, CXCL11, CCL4, CCL25 and down-regulation of IL

290 trices, which are mediated predominantly via LIF induction.

291 Further neuralization of spheres via LIF supplementation and attachment selection on CELLstar

292 iled to maintain stable differentiation when LIF was reintroduced to the growth medium.

293 Here, we tested whether LIF-induced STAT3 activation within the RPE can down-reg

294 f Oct4, Klf4, and Klf2 factors combined with LIF and inhibitors of glycogen synthase kinase 3beta (GS

295 h significantly different time courses, with LIF expression correlating best with NP expansion.

296 nsform into ES-like cells when cultured with LIF-containing medium.

297 DMA with LIF detection can be used for studies of gas-phase fluor

298 Combination of DMA with LIF is simple and robust.

299 ) and glycogen synthase kinase 3 (GSK3) with LIF (2i/LIF) provides an optimal culture environment for

300 mming in serum-free medium supplemented with LIF, a culture condition which does not support induced