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1 tor, vascular endothelial growth factor, and leukemia inhibitory factor).
2 B activation of E-cadherin was responsive to leukemia inhibitory factor.
3 cts of sweat gland-containing footpads or by leukemia inhibitory factor.
4 K2 induced by GH but not interferon-gamma or leukemia inhibitory factor.
5 onists like endothelin-1, phenylephrine, and leukemia inhibitory factor.
6 of the IL-6-type cytokines, IL-6, IL-11, and leukemia inhibitory factor.
7 sufficient to induce both interleukin-6 and leukemia inhibitory factor.
8 ptin sustains pluripotency in the absence of leukemia inhibitory factor.
9 L-17, increasing production of IFN-gamma and leukemia inhibitory factor.
10 f-renewal to differentiation upon removal of leukemia inhibitory factor.
11 , including interleukin 6, oncostatin M, and leukemia inhibitory factor.
12 ertrophic agonists such as phenylephrine and leukemia inhibitory factor.
13 s in the absence of feeder cells, serum, and leukemia inhibitory factor.
14 g conditions, specifically in the absence of leukemia inhibitory factor.
15 IL-6, IL-8, cyclooxygenase 1 (COX-1), COX-2, leukemia inhibitory factor 1, transforming growth factor
17 y, including ciliary neurotrophic factor and leukemia inhibitory factor, also cause a transient initi
18 ytokine receptor gp130 and the receptors for leukemia inhibitory factor and granulocyte colony-stimul
20 ix production but opposite effects regarding leukemia inhibitory factor and insulin-like growth facto
23 potency of mouse ES cells requires both LIF (leukemia inhibitory factor) and unknown factors in serum
24 newal of pluripotent cells in the absence of leukemia inhibitory factor, and directly regulated mouse
25 ctor-alpha, transforming growth factor-beta, leukemia inhibitory factor, and IL-11 did not increase b
26 amily cytokines ciliary neurotrophic factor, leukemia inhibitory factor, and IL-11 have been identifi
27 actors, such as ciliary neurotrophic factor, leukemia inhibitory factor, and insulin, that are essent
29 -JAK/STAT3 signaling pathway, interleukin-6, leukemia inhibitory factor, and oncostatin M were elevat
30 hat stimulate megakaryopoiesis (IL-6, IL-11, leukemia inhibitory factor, and oncostatin M) bind to re
31 rative factors insulin-like growth factor 1, leukemia inhibitory factor, and urokinase-type plasminog
32 mbryonic stem cells by fibronectin, laminin, leukemia-inhibitory factor, and fibroblast growth factor
33 in Q344ter mice was slowed by Axokine and by leukemia inhibitory factor; and the degeneration in a fe
35 both by the induction of an "injury factor," leukemia inhibitory factor, as shown previously, and by
36 c factor (CNTF), Axokine (a mutein of CNTF), leukemia inhibitory factor, basic fibroblast growth fact
37 , application of factors that activate gp130/leukemia inhibitory factor beta (LIFbeta) heterodimeric
40 s containing interleukin-3 (IL-3), IL-6, and leukemia inhibitory factor contained a mean of 75% of un
41 rs of the ciliary neurotrophic factor (CNTF)-leukemia inhibitory factor cytokine family regulate glio
42 HepG2 cells stimulated with oncostatin M or leukemia inhibitory factor, cytokines which also use gp1
48 lia can stably self-renew in the presence of leukemia inhibitory factor, GSK3 inhibitor (CHIR99021),
50 layers in the presence of human recombinant leukemia inhibitory factor, human recombinant basic fibr
51 not proliferate in the absence of exogenous leukemia inhibitory factor in an in vitro methylcellulos
52 sulin-like growth factor (IGF)-1, IGF-2, and leukemia inhibitory factor in medulloblastoma cells, but
54 he cytokines ciliary neurotrophic factor and leukemia inhibitory factor increases expression of endog
55 (NE) through a beta-adrenergic receptor, and leukemia inhibitory factor induced hypertrophy by a 20%
56 e of its soluble receptor), but not IL-1 nor leukemia inhibitory factor, induced Akt phosphorylation
57 le collagens, matrix metalloproteinases, and leukemia inhibitory factor, insulin-like growth factor 1
59 d transient stimulation of interleukin-6 and leukemia inhibitory factor is inhibited by actinomycin D
62 d underlying signal transduction pathways of leukemia inhibitory factor (LIF) and bone-morphogenic pr
65 ranscription factor pathway are activated by leukemia inhibitory factor (LIF) and contribute to mouse
67 unts of the IL-6 family cytokines, including Leukemia inhibitory factor (LIF) and Interleukin 6 (IL-6
68 the expression of the neuropoietic cytokines leukemia inhibitory factor (LIF) and its receptor (LIFR)
72 rferon (IFN), but retained responsiveness to leukemia inhibitory factor (LIF) and remained LIF depend
73 egulation of cell cycle-associated genes and leukemia inhibitory factor (Lif) and revealed alteration
74 te that cYes kinase activity is regulated by leukemia inhibitory factor (LIF) and serum and is down-r
75 t NPC patients had increased serum levels of leukemia inhibitory factor (LIF) and that higher LIF lev
76 vivo stem cell expansion are the addition of leukemia inhibitory factor (LIF) and the AC6.21 stromal
77 ences of nerve transection: the induction of leukemia inhibitory factor (LIF) and the reduction in th
80 onic stem cells in response to withdrawal of leukemia inhibitory factor (LIF) as a differentiation si
81 r identification of the IL-6 family cytokine leukemia inhibitory factor (LIF) as a serum predictor of
82 y upregulated with IL-6 pointed to STAT4 and leukemia inhibitory factor (LIF) as potentially linked.
83 ve determined the crystal structure of human leukemia inhibitory factor (LIF) bound to the cytokine b
85 is a new member of the interleukin 6 (IL-6)/leukemia inhibitory factor (LIF) cytokines, which activa
87 nterleukin-6 (IL-6), oncostatin M (OSM), and leukemia inhibitory factor (LIF) direct the formation of
91 es of the ciliary neurotrophic factor (CNTF)-leukemia inhibitory factor (LIF) family have been shown
93 -2 mutation (Shp-2(Delta46-110)) demonstrate leukemia inhibitory factor (LIF) hypersensitivity and in
95 Previous work has implicated the cytokine leukemia inhibitory factor (LIF) in cutaneous inflammati
100 ch NPs expand after H-I and to determine how leukemia inhibitory factor (LIF) insufficiency affects t
108 erleukin-11 (IL-11), oncostatin M (OSM), and leukemia inhibitory factor (LIF) levels in patients with
110 which ciliary neurotrophic factor (CNTF) and leukemia inhibitory factor (LIF) negatively regulate the
111 d the effects of overexpressing the cytokine leukemia inhibitory factor (LIF) on adult neurogenesis i
112 differentiation in response to withdrawal of leukemia inhibitory factor (LIF) or bone morphogenetic p
113 be induced in culture either by exposure to leukemia inhibitory factor (LIF) or by deprivation of ne
114 conditioned medium from mice lacking either leukemia inhibitory factor (LIF) or LIF and ciliary neur
115 stem (ES) cells in vitro requires exogenous leukemia inhibitory factor (LIF) or related cytokines.
116 erentiated pluripotent state is dependent on leukemia inhibitory factor (LIF) or related cytokines.
117 on-promoting conditions by the withdrawal of Leukemia Inhibitory Factor (LIF) or treatment with retin
120 eceptor complex, glycoprotein130 (gp130) and leukemia inhibitory factor (LIF) receptor, on cardiac fi
121 rophage chemoattractant protein-1 (MCP-1) or leukemia inhibitory factor (LIF) reduced this activity t
122 oid potential has indicated that exposure to leukemia inhibitory factor (LIF) results in the upregula
123 o exhibit increased Wnt expression, enhanced leukemia inhibitory factor (LIF) sensitivity, and reduce
126 how here that treatment of 3T3-L1 cells with leukemia inhibitory factor (LIF) stimulated Raf-1 activi
127 em (ES) cells, in which BMP4 synergizes with leukemia inhibitory factor (LIF) to maintain self-renewa
128 ations of basic fibroblast growth factor and leukemia inhibitory factor (LIF) to proliferate and unde
130 linked to the luciferase reporter, we showed leukemia inhibitory factor (LIF) to strongly potentiate
131 Previously, we reported that delivery of leukemia inhibitory factor (LIF) to the CNS stimulates t
132 gh it is generally accepted that addition of leukemia inhibitory factor (LIF) together with either se
134 IL-6, sIL-6R, oncostatin M (OSM), IL-11, and leukemia inhibitory factor (LIF) was determined by rever
136 ESCs) initiated normal differentiation after leukemia inhibitory factor (LIF) withdrawal but, unlike
140 n mice through transcriptional regulation of leukemia inhibitory factor (LIF), a cytokine crucial for
142 igated the mannose phosphorylation status of leukemia inhibitory factor (LIF), a previously identifie
144 onstrated that the proinflammatory cytokine, leukemia inhibitory factor (LIF), affects the hypothalam
146 ell types and includes interleukin-6 (IL-6), leukemia inhibitory factor (LIF), and granulocyte-colony
147 tokines, including IL-6, oncostatin M (OSM), leukemia inhibitory factor (LIF), and IL-11, have fibrog
149 erleukin 6 (IL-6) family of cytokines, IL-6, leukemia inhibitory factor (LIF), and oncostatin M, act
150 itors were identified as oncostatin M (OSM), leukemia inhibitory factor (LIF), and transforming growt
151 gp130-signaling cytokines, IL-6, IL-11, and leukemia inhibitory factor (LIF), as well as with up-reg
152 in G418 and engineered to express zebrafish leukemia inhibitory factor (Lif), basic fibroblast growt
153 F) and significantly lower concentrations of leukemia inhibitory factor (LIF), basic fibroblast growt
156 cells or by one of the following cytokines: leukemia inhibitory factor (LIF), ciliary neurotrophic f
157 d by an excess of antibodies to IL-6, IL-11, leukemia inhibitory factor (LIF), gp130, stromal cell de
158 kin (IL)-6 family of cytokines (IL-6, IL-11, leukemia inhibitory factor (LIF), granulocyte colonystim
159 ting factor (G-CSF), stem cell factor (SCF), leukemia inhibitory factor (LIF), granulocyte-macrophage
160 uding ciliary neurotrophic factor (CNTF) and leukemia inhibitory factor (LIF), induce the same phenot
162 he interleukin-6 (IL-6) family of cytokines, leukemia inhibitory factor (LIF), oncostatin M (OSM) and
163 e to interleukin-6 and -11 (IL-6 and IL-11), leukemia inhibitory factor (LIF), oncostatin M (OSM), an
164 lly related proteins, including IL-6, IL-11, leukemia inhibitory factor (LIF), oncostatin M (OSM), ci
165 6 (IL-6) family of cytokines, which includes Leukemia Inhibitory Factor (LIF), Oncostatin M (OSM), Ci
166 ocused on the activation of STATs 1 and 3 by leukemia inhibitory factor (LIF), oncostatin-M (OSM), an
167 members IL-11, IL-6, oncostatin M (OSM), and leukemia inhibitory factor (LIF), only OSM and LIF were
168 an undifferentiated state in the presence of leukemia inhibitory factor (LIF), or differentiate into
169 s for the receptors for growth hormone (GH), leukemia inhibitory factor (LIF), or interferon-gamma (I
170 ation of TNF, IL-1, and, to a lesser extent, leukemia inhibitory factor (LIF), produced a prompt and
171 IL-6), IL-11, IL-27, oncostatin M (OSM), and leukemia inhibitory factor (LIF), signal via the common
172 in vitro with media containing the cytokine leukemia inhibitory factor (LIF), which propagates the p
174 during delayed implantation and in pregnant, leukemia inhibitory factor (LIF)-deficient mice with imp
175 nic sympathetic axotomy leads to a prolonged leukemia inhibitory factor (LIF)-dependent activation of
176 viral or episomal reprogramming), which uses leukemia inhibitory factor (LIF)-expressing SNL feeders,
178 h factor (FGF)-ERK1/2 pathway, PI3K-AKT, the leukemia inhibitory factor (LIF)-JAK-STAT3 axis, Wnt-GSK
179 SOCS-3 is a novel intracellular regulator of leukemia inhibitory factor (LIF)-mediated proopiomelanoc
180 early points of differentiation, conducting leukemia inhibitory factor (LIF)-stimulated biochemical
199 yer of ES cell aggregates independent of the leukemia inhibitory factor (LIF)/STAT3 pathway, it is la
201 Moreover, it provides a mechanism for how leukemia inhibitory factor (LIF)/STAT3 signaling reaches
205 TGF-beta plus EGF synergistically increased leukemia-inhibitory factor (LIF), additively increased I
207 Here, we report that four other cytokines (leukemia inhibitory factor [LIF], oncostatin M [OSM], in
208 tiated when cultured in the presence of LIF (leukemia inhibitory factor), little metabolism of exogen
210 cultured in standard conditions (serum plus leukemia inhibitory factor) or ground-state conditions,
213 gnal using heterodimers of gp130 with either leukemia inhibitory factor receptor (LIFR) (type I) or o
214 receptor complexes, glycoprotein 130 (gp130)/leukemia inhibitory factor receptor (LIFR) alpha and gp1
215 described that consists of a heterodimer of leukemia inhibitory factor receptor (LIFR) and gp130.
216 studies and clinical validation, we identify leukemia inhibitory factor receptor (LIFR) as a breast c
217 ed a placenta-specific enhancer in the human leukemia inhibitory factor receptor (LIFR) gene and now
219 ytokine family and signals through the gp130/leukemia inhibitory factor receptor (LIFR) heterodimer.
220 igodendrocyte survival through activation of leukemia inhibitory factor receptor (LIFR) signaling is
221 ophic factor receptor alpha (CNTFRalpha) and leukemia inhibitory factor receptor (LIFR) was studied i
223 th induction by OSM depends on both types I [leukemia inhibitory factor receptor (LIFR)] and II [OSM
224 rious cytoplasmic domains of either gp130 or leukemia inhibitory factor receptor alpha (LIFR) were us
226 link between the PTEN-Akt-FOXO axis and the leukemia inhibitory factor receptor beta (LIFRbeta)-STAT
227 phosphorylation of glycoprotein 130 (gp130), leukemia inhibitory factor receptor beta, and signal tra
228 ressive effect by directly targeting p63 and leukemia inhibitory factor receptor in RMS cells, which
231 We further demonstrate that one of these, leukemia inhibitory factor receptor, can initiate functi
234 of granulocyte colony-stimulating factor and leukemia inhibitory factor receptors, which are normally
235 identify TFE3 and TFEB as cell type-specific leukemia inhibitory factor-responsive activators of E-ca
236 newal of embryonal stem cells in response to leukemia inhibitory factor signaling and for proliferati
238 by the bone morphogenetic protein (BMP) and leukemia inhibitory factor signaling pathways and the ex
239 rocal relationship between PPARdelta-AKT and leukemia inhibitory factor-STAT3 signaling pathways serv
240 Shp2 deficiency leads to upregulation of leukemia inhibitory factor-stimulated phosphatidylinosit
241 of mouse ES cells by removal of the cytokine leukemia inhibitory factor, there is a global increase i
243 rgy with host ciliary neurotrophic factor or leukemia inhibitory factor to promote neuronal survival
244 biquitously when cultured in the presence of leukemia inhibitory factor to suppress differentiation.
246 g hematopoietic lineages after withdrawal of leukemia inhibitory factor, using in vitro colony format
247 the fundamental role of fibroblast-secreted leukemia inhibitory factor was assessed by using small i
249 actor alpha, interleukin 1 (IL-1), IL-6, and leukemia inhibitory factor, was markedly enhanced during
252 When PI3K/AKT1 signaling declines following leukemia inhibitory factor withdrawal, active GSK3beta a
253 f Cdk2ap1 in mESCs resulted in abrogation of leukemia inhibitory factor withdrawal-induced differenti
254 pression by osteoblasts of interleukin-6 and leukemia inhibitory factor without affecting the 16 othe
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