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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
16              On this background, T3, NE, and leukemia inhibitory factor activate hypertrophy with dif
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
19 weeks in stromal cultures in the presence of leukemia inhibitory factor and IL-6.
20 ix production but opposite effects regarding leukemia inhibitory factor and insulin-like growth facto
21 -F442A fibroblasts with growth hormone (GH), leukemia inhibitory factor and interferon-gamma.
22 ses to other gp130-signaling cytokines (e.g. leukemia inhibitory factor and interleukin 11).
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
28 de IL-6, IL-11, ciliary neurotrophic factor, leukemia inhibitory factor, and oncostatin M (OSM).
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
34                       Oncostatin M (OSM) and leukemia inhibitory factor are pleiotropic cytokines tha
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
38                                     Notably, leukemia inhibitory factor, but not interferon-gamma, al
39 n of the differentiation-associated cytokine leukemia inhibitory factor by atopic fibroblasts.
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
43             Here we report the production of leukemia inhibitory factor-dependent, so-called naive ty
44                   Supplementation of KM with leukemia inhibitory factor elicited lineage restriction
45                                 In contrast, leukemia inhibitory factor fails to activate Akt or prom
46 of differentiation through the withdrawal of leukemia-inhibitory factor for 6 or more days.
47 n vitro differentiation following removal of leukemia inhibitory factor from the growth media.
48 lia can stably self-renew in the presence of leukemia inhibitory factor, GSK3 inhibitor (CHIR99021),
49                                              Leukemia inhibitory factor has been utilized to maintain
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
53 n osteoblasts, also induce interleukin-6 and leukemia inhibitory factor in these cells.
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
58                        In response to GH and leukemia inhibitory factor, IRS-2 is immediately phospho
59 d transient stimulation of interleukin-6 and leukemia inhibitory factor is inhibited by actinomycin D
60 , but in some experiments minor increases in leukemia inhibitory factor levels were observed.
61      Cortical progenitors begin to interpret leukemia inhibitory factor (LIF) and bone morphogenetic
62 d underlying signal transduction pathways of leukemia inhibitory factor (LIF) and bone-morphogenic pr
63                                     The CDFs leukemia inhibitory factor (LIF) and ciliary neurotrophi
64                       Our data indicate that leukemia inhibitory factor (LIF) and ciliary neurotrophi
65 ranscription factor pathway are activated by leukemia inhibitory factor (LIF) and contribute to mouse
66              Activation of the receptors for leukemia inhibitory factor (LIF) and IL-11 is essential
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)
69                                              Leukemia inhibitory factor (LIF) and LIF receptors are e
70                                              Leukemia inhibitory factor (LIF) and LIF receptors have
71                  We have shown recently that leukemia inhibitory factor (LIF) and oncostatin M (OSM),
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
78                           We have found that leukemia inhibitory factor (LIF) and transforming growth
79                       Oncostatin M (OSM) and leukemia inhibitory factor (LIF) are IL-6 family members
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
84                             The receptor for leukemia inhibitory factor (LIF) consists of two polypep
85  is a new member of the interleukin 6 (IL-6)/leukemia inhibitory factor (LIF) cytokines, which activa
86 ress DeltaEGFR each also express IL-6 and/or leukemia inhibitory factor (LIF) cytokines.
87 nterleukin-6 (IL-6), oncostatin M (OSM), and leukemia inhibitory factor (LIF) direct the formation of
88                                 The cytokine leukemia inhibitory factor (LIF) drives self-renewal of
89                                              Leukemia inhibitory factor (LIF) expression in the uteru
90 hat five of the up-regulated miRNAs targeted leukemia inhibitory factor (LIF) expression.
91 es of the ciliary neurotrophic factor (CNTF)-leukemia inhibitory factor (LIF) family have been shown
92                                      Because leukemia inhibitory factor (LIF) has little or no effect
93 -2 mutation (Shp-2(Delta46-110)) demonstrate leukemia inhibitory factor (LIF) hypersensitivity and in
94                     The role of the cytokine leukemia inhibitory factor (LIF) in axotomy-induced spro
95    Previous work has implicated the cytokine leukemia inhibitory factor (LIF) in cutaneous inflammati
96                  PROK1 induces expression of leukemia inhibitory factor (LIF) in endometrial epitheli
97      We recently described the expression of leukemia inhibitory factor (LIF) in human fetal and muri
98             We have investigated the role of leukemia inhibitory factor (LIF) in postnatal neuronal d
99               At these doses, mRNA levels of leukemia inhibitory factor (LIF) increased.
100 ch NPs expand after H-I and to determine how leukemia inhibitory factor (LIF) insufficiency affects t
101                                              Leukemia inhibitory factor (LIF) is a cytokine involved
102                                              Leukemia inhibitory factor (LIF) is a pleiotropic cytoki
103                                              Leukemia inhibitory factor (LIF) is a pleiotropic neuroi
104                     Here we demonstrate that leukemia inhibitory factor (LIF) is a potent endogenous
105                    The uterine expression of leukemia inhibitory factor (LIF) is essential for embryo
106                                              Leukemia inhibitory factor (LIF) is produced by a large
107                                              Leukemia inhibitory factor (LIF) is required, but not su
108 erleukin-11 (IL-11), oncostatin M (OSM), and leukemia inhibitory factor (LIF) levels in patients with
109                                 The cytokine leukemia inhibitory factor (LIF) modulates glial and neu
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
118                                              Leukemia inhibitory factor (LIF) promotes differentiated
119                                              Leukemia inhibitory factor (LIF) promotes giant cell dif
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
124         Bone morphogenetic protein (BMP) and leukemia inhibitory factor (LIF) signaling both promote
125  sets suggested interaction between Tet1 and leukemia inhibitory factor (LIF) signaling.
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
129                              The addition of leukemia inhibitory factor (LIF) to purified CD34(+) thy
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
133                                              Leukemia inhibitory factor (LIF) was critical for prolif
134 IL-6, sIL-6R, oncostatin M (OSM), IL-11, and leukemia inhibitory factor (LIF) was determined by rever
135       Ciliary neurotrophic factor (CNTF) and leukemia inhibitory factor (LIF) were investigated to te
136 ESCs) initiated normal differentiation after leukemia inhibitory factor (LIF) withdrawal but, unlike
137 4 and Dab2, and express much less Fgf5 after leukemia inhibitory factor (LIF) withdrawal.
138 heterogeneous onset of differentiation after leukemia inhibitory factor (LIF) withdrawal.
139                                              Leukemia inhibitory factor (LIF), a critical implantatio
140 n mice through transcriptional regulation of leukemia inhibitory factor (LIF), a cytokine crucial for
141                                 The mRNA for leukemia inhibitory factor (LIF), a neuroimmune signalin
142 igated the mannose phosphorylation status of leukemia inhibitory factor (LIF), a previously identifie
143                   One of these candidates is leukemia inhibitory factor (LIF), a pro-inflammatory cyt
144 onstrated that the proinflammatory cytokine, leukemia inhibitory factor (LIF), affects the hypothalam
145                                              Leukemia inhibitory factor (LIF), an interleukin-6 famil
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
148                          Oncostatin M (OSM), leukemia inhibitory factor (LIF), and interleukin-6 (IL-
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
154               In the presence of recombinant leukemia inhibitory factor (LIF), CAFC cloning efficienc
155       Activating ligands of gp130, including leukemia inhibitory factor (LIF), can block differentiat
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
161                                      Because leukemia inhibitory factor (LIF), like SDF-1, is secrete
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
173                                 The cytokine leukemia inhibitory factor (LIF), which stimulates MEK5
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,
177                                              Leukemia inhibitory factor (LIF)-induced activation of J
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
181 ignals for self-renewal are generated by the leukemia inhibitory factor (LIF).
182  with both epidermal growth factor (EGF) and leukemia inhibitory factor (LIF).
183 s and was identified by mass spectrometry as leukemia inhibitory factor (LIF).
184 ing intermediates following stimulation with leukemia inhibitory factor (LIF).
185 ophy and antiapoptotic phenotypes induced by leukemia inhibitory factor (LIF).
186 quencing of one such factor identified it as leukemia inhibitory factor (LIF).
187  by ciliary neurotrophic factor (CNTF) or by leukemia inhibitory factor (LIF).
188 an undifferentiated state in the presence of leukemia inhibitory factor (LIF).
189 to the differentiation suppressing effect of leukemia inhibitory factor (LIF).
190 ukin-6, interleukin-11, cardiotrophin-1, and leukemia inhibitory factor (LIF).
191 rleukin (IL)-3, IL-6, c-kit ligand (KL), and leukemia inhibitory factor (LIF).
192 ugh transcriptional up-regulation of uterine leukemia inhibitory factor (LIF).
193  but not at Thr308, in NRVMs stimulated with leukemia inhibitory factor (LIF).
194 c stem (ES) cells downstream of the cytokine leukemia inhibitory factor (LIF).
195 renewal and alleviates their requirement for leukemia inhibitory factor (LIF).
196 r pluripotency by the supplementation of the leukemia inhibitory factor (LIF).
197 ty in axons that is mediated by the cytokine leukemia inhibitory factor (LIF).
198  autocrine/paracrine pathway mediated by the leukemia inhibitory factor (LIF)/JAK/STAT pathway.
199 yer of ES cell aggregates independent of the leukemia inhibitory factor (LIF)/STAT3 pathway, it is la
200 ncy, which may occur in conjunction with the leukemia inhibitory factor (LIF)/Stat3 pathway.
201    Moreover, it provides a mechanism for how leukemia inhibitory factor (LIF)/STAT3 signaling reaches
202                     Both cell types secreted leukemia inhibitory factor (Lif); however, whereas Stat3
203 d full-length globular proteins [mCherry and leukemia inhibitory factor (LIF)].
204                                              Leukemia-inhibitory factor (LIF) is a member of the inte
205  TGF-beta plus EGF synergistically increased leukemia-inhibitory factor (LIF), additively increased I
206 related cytokines (i.e., oncostatin M [OSM], leukemia inhibitory factor [LIF], and IL-11).
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
209                            In the absence of leukemia inhibitory factor, mouse ES cells give rise to
210  cultured in standard conditions (serum plus leukemia inhibitory factor) or ground-state conditions,
211                                              Leukemia inhibitory factor plays a major role in the ute
212 ther as a homodimer or as a heterodimer with Leukemia Inhibitory Factor Receptor (LIF-R).
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
218                              Knockout of the leukemia inhibitory factor receptor (LIFR) gene results
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
222 ocyte cell surface, but failed to detect the leukemia inhibitory factor receptor (LIFR).
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
225        The cytokine receptor subunits gp130, leukemia inhibitory factor receptor alpha (LIFRalpha), a
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
229 was caused by placental defect with enhanced leukemia inhibitory factor receptor signaling.
230                                 Similarly, a leukemia inhibitory factor receptor subunit beta (LIFRbe
231    We further demonstrate that one of these, leukemia inhibitory factor receptor, can initiate functi
232 cluded adiponectin, lumican, plasminogen and leukemia inhibitory factor receptor.
233 opment, including GATA4, c-kit receptor, and leukemia inhibitory factor receptor.
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
237                        They are dependent on leukemia inhibitory factor signaling for maintenance of
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
242             We conclude that LIGHT overrides Leukemia inhibitory factor to induce ES cell differentia
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.
245              Ciliary neurotrophic factor and leukemia inhibitory factor, two cytokines critical to th
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
248                        Although no change in leukemia inhibitory factor was observed throughout the d
249 actor alpha, interleukin 1 (IL-1), IL-6, and leukemia inhibitory factor, was markedly enhanced during
250             Levels of oncostatin M (OSM) and leukemia inhibitory factor were analyzed in patients wit
251             Two cytokines, interleukin-6 and leukemia inhibitory factor, which can induce phosphoryla
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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