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 greatly activates STAT4 phosphorylation on multiple

4 LIF induced STAT3 Y705 phosphorylation in infected diffe

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

6 LIF is overexpressed in a large percentage of CRCs.

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-3i-reverted hPSCs retained normal karyotypes and gen

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

13 nd DN for cellular responses to IL-6, IL-11, LIF, and OSM.

14 STAT3 has been also reported to induce E2-2, LIF paradoxically induced its repressor Id2.

15 ESCs is between the E3.25-HNC cells and 2i + LIF ESCs; thus, the developmental transition from 33 to

16 ance with the naive ground state of the 2i + LIF ESCs.

17 mary differentiation of ES cells in 2i or 2i+LIF media without serum or undefined serum substitutes.

18 2i/LIF can abrogate persistent-NPC interactions, recover po

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

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

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

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

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

24 Unlike IL-6, LIF inhibits the activity of the Hippo-signaling pathway

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

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

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

28 ndings indicate that leukocytes expressing a LIF transgene reduce fibrosis by suppressing type 2 immu

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

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

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

32 remained pluripotent in the absence of added LIF.

33 Thus, an LIF-driven STAT3 pathway induces SOCS3, Bcl3, and Id2, w

34 Based on these analyses, LIF, CREG2, CST3, CCBE1, and DPP4 are likely osteoclast-

35 15 proteins, including IL-1alpha, IL-17, and LIF.

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

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

38 -6 promoter after fibroblast activation, and LIF receptor (LIFR) and STAT4 formed a molecular complex

39 e potential regulatory effects on ATXN10 and LIF genes respectively.

40 rian cancer cell STAT3 signaling via IL6 and LIF and increase tumor cell stemness.

41 LIF signaling and the redundancy of IL6 and LIF in activating ovarian cancer STAT3 mediated cancer g

42 In addition, both IL6 and LIF increased the percentage of ALDH+ ovarian cancer ste

43 As expected, we found that both IL6 and LIF induce STAT3 phosphorylation in tumor cells.

44 ESCs cultured with GSK3-, MEK-inhibitors and LIF (2iL) display higher ribosome density on a selective

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

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

47 ng UV broad band absorption spectroscopy and LIF, highly sensitive and spatially resolved quantitativ

48 expression on the infected cell surface, and LIF enhanced the antiviral effects of antibody.

49 ransforming growth factor beta (TGFbeta) and LIF interleukin-6 family cytokine (LIF) signaling pathwa

50 Anti-LIF completely eliminated lung LIF detection and markedl

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

52 /6 mice in the presence of neutralizing anti-LIF IgG or control IgG.

53 extent than treatment with anti-IL6 or anti-LIF antibody alone.

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

55 o GCSCs induced ZEB1 expression, attenuating LIF activities.

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

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

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

59 pria lymphocytes (LPLs), STAT4 activation by LIF blocks STAT3-dependent Il17a/Il17f promoter activati

60 e of mobilities that are further analyzed by LIF.

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

62 This effect was not inhibited by LIF or IL6 blocking antibodies alone, but was prevented

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

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

65 etina, rhodopsin protein was also reduced by LIF.

66 Implantation failure was not rescued by LIF administration.

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

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

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

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

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

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

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

74 0 M(-1) for Ado and 1000 M(-1) for Ino by CE-LIF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 th laser-induced fluorescence detection (CGE-LIF) has become a key method in high-throughput glycan a

98 e the glycan identification precision in CGE-LIF and help to reveal "heavy" glycans, yet undetectable

99 At present, CGE-LIF relies on the green fluorophore 8-aminopyrene-1,3,6-

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

101 is, and changes in the levels of circulating LIF correlate well with tumour response to therapy.

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

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

104 12p70, IL-13, IL-17F, leptin, G-CSF, GM-CSF, LIF, NGF, SCF, and TGF-alpha.

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

106 beta) and LIF interleukin-6 family cytokine (LIF) signaling pathways.

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

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

109 Decreased LIF levels in diseased groups might reflect the possible

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

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

112 Laser-induced fluorescence detection (LIF) is a powerful tool for the quantitative analysis of

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

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

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

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

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

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

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

120 actor (CNTF), and leukemia inhibitor factor (LIF) remains to be elucidated.

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

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

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

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

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

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

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

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

129 Expression of leukemia inhibitory factor (LIF) cytokine mRNA, but not other IL-6 family member mRN

130 ere we show that Leukemia Inhibitory Factor (LIF) expression is induced specifically by oncogenic KRA

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

132 Leukemia inhibitory factor (LIF) injections were given intraperitoneally and implant

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

134 we reveal that leukaemia inhibitory factor (LIF) is a key paracrine factor from activated PSCs actin

135 ansgene in which leukemia inhibitory factor (LIF) is under control of a leukocyte-specific promoter a

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

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

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

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

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

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

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

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

144 rentiation after leukemia inhibitory factor (LIF) withdrawal.

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

146 However, leukemia inhibitory factor (LIF), an IL-6 family cytokine, restricts inflammation by

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

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

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

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

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

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

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

154 of the cytokine leukemia inhibitory factor (LIF).

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

156 d genes, such as leukemia inhibitory factor (LIF).

157 related cytokine leukemia inhibitory factor (LIF).

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

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

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

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

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

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

164 oresis (CE) with 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 ed measurements, laser-induced fluorescence (LIF) of SO(2) excited by a 266 nm laser was investigated

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

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

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

171 se pDCs selectively express the receptor for LIF that signals through STAT3.

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

173 related cytokine IL-6 cannot substitute for LIF, suggesting that LIF mediates KRAS-driven malignanci

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

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

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

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

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

179 /Il17f promoter activation, whereas in IECs, LIF bypasses the extraordinarily low level of STAT4 to i

180 ibodies alone, but was prevented by dual IL6/LIF blockade or JAK2 inhibition.

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

182 idua transcriptome was noticeably altered in LIF-replaced FOXA2 cKO mice.

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

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

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

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

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

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

189 indings identify activation of the NF-kappaB/LIF/STAT3 signaling cascade as involved in inducing anti

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

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

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

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

194 Moreover, LIF-neutralizing antibodies synergize with gemcitabine t

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

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

197 out ESCs passaged in defined media alone (no LIF or inhibitors) and in wild-type cells passaged in me

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

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

200 ddition, we found that the administration of LIF is sufficient to restore microbiome homeostasis.

201 riven pancreatic cancer and that blockade of LIF by neutralizing antibodies represents an attractive

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

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

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

205 ired nor sufficient for the potent effect of LIF.

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

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

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

209 Depletion of YAP inhibits the function of LIF in human PDAC cells.

210 ctively, these findings reveal a function of LIF in PDAC tumorigenesis, and suggest its translational

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

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

213 However, intraperitoneal injections of LIF can initiate embryo implantation in the uterus of ad

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 e embryo implantation arising from a lack of LIF, a critical implantation factor of uterine gland ori

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 em cells (mESCs) cultured in the presence of LIF occupy a ground state with highly active pluripotenc

220 odels and human PDAC, aberrant production of LIF in the pancreas is restricted to pathological condit

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

222 Our data suggest a crucial role of LIF in KRAS-driven pancreatic cancer and that blockade o

223 Less is known about the role of LIF, which can similarly activate STAT3, in ovarian canc

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

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

226 Withdrawal of LIF leads to differentiation of mESCs.

227 pin RNA (shRNA)-mediated reduction of IL6 or LIF in CA-MSC partially decreased but could not complete

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

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

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

231 the tumorigenic effects of CA-MSC paracrine LIF signaling and the redundancy of IL6 and LIF in activ

232 Both pharmacologic LIF blockade and genetic Lifr deletion markedly slow tum

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

234 eport that microbiota dysregulation promotes LIF secretion by intestinal epithelial cells (IECs) in a

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

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

237 At elevated temperatures, spatially resolved LIF SO(2) detection up to a few ppm sensitivity was achi

238 Spectrally resolved LIF signal was analyzed at different temperatures.

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

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

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

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

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

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

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

246 ectopic transcription factors, but not serum/LIF alone, rapidly revert cells to pluripotency with nea

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

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

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

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

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

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

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

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

255 cifically by oncogenic KRAS in PDAC and that LIF depletion by genetic means or by neutralizing antibo

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

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

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

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

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

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

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

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

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

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

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

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

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

269 6 cannot substitute for LIF, suggesting that LIF mediates KRAS-driven malignancies through a non-STAT

270 The LIF network was used to encapsulate mouse embryonic stem

271 The LIF signal showed strong dependence on temperature, whic

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

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

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

275 However, anti-E2 antibody localized the LIF receptor to areas of E2 expression on the infected c

276 dometrial receptivity from disruption of the LIF-STAT3-EGR1 pathway.

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

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

279 Thus, LIF effectively inhibits Th17 accumulation and promotes

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

281 pDCs less efficiently after being exposed to LIF, consistent with the induction of Id2.

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

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

284 Stat3 mediates the self-renewal response to LIF.

285 2l1 profoundly compromised responsiveness to LIF.

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

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

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

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

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

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

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

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

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

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

296 Combination of DMA with LIF is simple and robust.

297 Stimulation of pDCs with LIF inhibited IFN-I, TNF, and IL-6 responses to CpG and

298 ration times after repeated analysis by xCGE-LIF.

299 o laser-induced fluorescence detection (xCGE-LIF).

300 lls (hiPSCs) and hiPSC-CMs by employing xCGE-LIF.