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1 ding the localized delivery of an epithelial cell growth factor.
2 ls and is thought to be the quintessential T cell growth factor.
3 yrosine kinase that is the receptor for mast cell growth factor.
4 factor, an angiogenesis and Kaposi's-spindle-cell growth factor.
5 Interleukin-2 (IL-2) is recognized as a T cell growth factor.
6 lar permeability and a selective endothelial cell growth factor.
7 ses (MMP-2 and -9), and vascular endothelial cell growth factor.
8 because IL-21 can substitute for IL-2 as a T cell growth factor.
9 ard the chemoattractant vascular endothelial cell growth factor.
10 4 is a cytokine originally identified as a B cell growth factor.
11 leukin-2 (IL-2) is historically known as a T-cell growth factor.
12 the lung expression of Th2 cell-derived mast cell growth factors.
13 n require T cell costimulatory signals and T cell growth factors.
14 ty was largely reversed in the presence of T cell growth factors.
15 ing lymph node macrophages to produce plasma cell growth factors.
16 tentiate Wnt signalling and function as stem-cell growth factors.
17 potentially through induction of paracrine B-cell growth factors.
18 ocompromised mice that express human myeloid cell growth factors.
20 ylase (TYMP; previously known as endothelial cell growth factor 1, ECGF1) as a second key astrocyte-d
28 IL-2, the first cytokine discovered with T cell growth factor activity, is now known to have pleiot
30 lar endothelial growth factor or endothelial cell growth factor-alpha + IGF-1 provided no advantage c
31 cular endothelial growth factor, endothelial cell growth factor-alpha and pancreatic islet neogenesis
32 endothelial biology because some endothelial cell growth factors also exert anti-apoptotic effects.
33 s of endothelial cells, vascular endothelial cell growth factor and basic fibroblast growth factor fu
34 growth factors such as vascular endothelial cell growth factor and basic fibroblast growth factor, i
36 r cancer cells in response to the urothelial cell growth factor and EGFR ligand heparin-binding EGF-l
37 tivity was dependent on vascular endothelial cell growth factor and had an ED50 of 10 microg/ml in me
41 e variance, with type 2, mixed type 1/T(h)17-cell, growth factor, and neutrophil chemoattractant infl
42 --have been engineered from mesenchymal stem cells, growth factor, and/or gene therapy approaches.
44 mitogenic stimulus for ductal and periductal cells, growth factors are necessary for survival, motili
45 direct AAV-mediated in vivo delivery of beta-cell growth factors as a novel therapeutic strategy for
48 e declined lungs from control lungs was stem cell growth factor -beta [P < 0.001, AUC (area under the
49 applied to dendritic cells, UA suppressed T-cell growth factors but up-regulated B cell-activating c
54 atient, one peptide derived from endothelial cell growth factor (ECGF) caused his PBMCs to proliferat
56 tment composed of immune cells, inflammatory cells, growth factors, extracellular matrix, and fibrobl
58 was initially characterized as the primary T-cell growth factor following in vitro activation, less i
59 (dsAAV)-mediated in vivo expression of beta-cell growth factors, glucagon-like peptide-1 (GLP-1) and
62 aling component by receptors for all known T cell growth factors (i.e., IL-2, IL-4, IL-7, IL-9, IL-15
64 by acting as a sensor of the essential Treg cell growth factor IL-2 and its downstream target STAT5.
66 in a marked increase in production of the T cell growth factor IL-2, it does not result in a signifi
71 liferation and accumulation of the primary T cell growth factor, IL-2, by cells stimulated with anti-
72 ytoprotective cytokines vascular endothelial cell growth factor, IL-6, and IL-11 were decreased in th
73 ce that diminished production of the major T cell growth factors, IL-2 and IL-4, is responsible for t
74 ls of other established IFN-gamma inducing T-cell growth factors, IL-2, and IL-12 in this culture sys
77 amino acids may be essential for other beta-cell growth factors in addition to insulin and IGF-I to
80 ased expression of the Th2 cell-derived mast cell growth factors, including IL-4 and IL-9, but not wi
81 kinase-3 (Flt3) ligand (Flt3L), a dendritic cell growth factor, increase the resistance of mice to a
82 y reductions in transformation of fibroblast cells, growth factor independence of hematopoietic cell
83 changes in cellular morphology and rendered cells growth-factor independent by upregulating the MAPK
84 etic experiments showed that both of these T cell growth factors induce a distinct and sustained phas
86 iferation but abrogated vascular endothelial cell growth factor-induced and basic fibroblast growth f
87 RK1/2 but inhibited the vascular endothelial cell growth factor-induced and basic fibroblast growth f
88 n of 15d-PGJ2 inhibited vascular endothelial cell growth factor-induced angiogenesis in the rat corne
89 blast growth factor and vascular endothelial cell growth factor-induced MAPK phosphorylation in endot
92 tors are known to induce the expression of T-cell growth factor interleukin (IL)-2, it is unclear how
100 Expression of the gene is enhanced by the T cell growth factor interleukin-2, suggesting a role for
104 Somatic activating mutations in the mast cell growth factor KIT gene cause cutaneous mastocytosis
105 Stem cell factor (SCF), also known as mast cell growth factor, kit ligand, and steel factor, is the
106 on are strongly induced by the critical mast cell growth factor, kit ligand, which is produced by fib
107 strongly with autoantibodies to endothelial cell growth factor, matrix metalloproteinase 10, and apo
108 blast growth factor and vascular endothelial cell growth factor-mediated cell proliferation and migra
110 tors for hepatocyte and vascular endothelial cell growth factors (MET and VEGFR2, respectively) are c
111 ontain either structural alterations in mast cell growth factor (Mgf) or regulatory mutations that af
113 e, KIT, and require its cognate ligand, Mast cell growth factor (MGF), for survival and differentiati
115 r, endothelial cells by vascular endothelial cell growth factor, neuronal cells by nerve growth facto
117 ent of PVR without the addition of exogenous cells, growth factors, or cytokines typically found in P
120 ; also known as platelet-derived endothelial cell growth factor, PD-ECGF) is an angiogenic factor tha
121 ine kinase inhibitor of vascular endothelial cell growth factor, platelet-derived growth factor, and
123 nce coexpression of a T-cell chemokine and T-cell growth factor potentiates antitumor responses in vi
128 lar mutations causing activation of the mast cell growth factor receptor are found in children appare
129 Studies using mice with defective mast/stem cell growth factor receptor c-Kit have suggested key rol
131 helial tyrosine kinase, vascular endothelial cell growth factor receptor type 2, phosphatidylinositol
132 al cells down-regulates vascular endothelial cell growth factor receptor-2 (VEGFR2) mRNA levels and b
133 th factor B (PDGFB) and vascular endothelial cell growth factor receptor-2 (VEGFR2), while at the sam
135 , bone marrow lineage-negative (lin(-)) stem cell growth factor receptor-positive (c-kit(+)) Sca-1(-)
136 reduced mRNA levels of vascular endothelial cell growth factor receptors 1 (Flt-1) and 2 (Flk/KDR) a
137 s discussed include the vascular endothelial cell growth factor receptors, Eph receptors, Tie1, and T
138 induced by contact inhibition (NIH 3T3 mouse cells), growth factor removal (bromodeoxyuridine-blocked
139 g strategies, whereby the traditional triad (cells, growth factors, scaffolds) or a combination there
142 pigment (hemozoin [PfHz]) revealed that stem cell growth factor (SCGF; also called C-type lectin doma
143 leukin 14 (IL-14) or high molecular weight B cell growth factor secreted by activated T and B cells a
146 ed in the regulation of vascular endothelial cell growth factor signaling, offers a unique opportunit
148 ression was regulated negatively by the mast cell growth factor stem cell factor (SCF), and its expre
149 nase is Kit ligand (Kitl; also known as mast cell growth factor, stem cell factor, and Steel factor),
150 s is Kit ligand (or Kitl; also known as mast cell growth factor, stem cell factor, and Steel factor),
152 actors inhibited basal, vascular endothelial cell growth factor-stimulated, and fibroblast growth fac
155 al signaling component shared by all known T cell growth factor (TCGF) receptors (i.e., IL-2, IL-4, I
158 n (gamma(c)) that is activated by multiple T-cell growth factors (TCGFs) such as IL-2, -4, and -7.
159 n (IL)-2, IL-4, IL-7, IL-9, and IL-15, all T-cell growth factors (TCGFs), utilize the common IL-2 rec
163 tance is associated with a circulating islet cell growth factor that is independent of glucose and ob
165 -15 is a proinflammatory and antiapoptotic T-cell growth factor that plays an important role in a var
172 We investigated the ability of IL-15, a T cell growth factor, to modulate prenyl phosphate-induced
173 e phosphorylase/platelet-derived endothelial cell growth factor (TP/PD-ECGF) has diverse functions wi
174 ecific antibody that targets the endothelial cell growth factors vascular endothelial growth factor-A
175 ce lacking the vascular-specific endothelial cell growth factor VEGF or its receptor Flt-1, both of w
176 al stimulating factors, vascular endothelial cell growth factor (VEGF) and basic fibroblast growth fa
182 tors were examined with vascular endothelial cell growth factor (VEGF) homodimers and VEGF/placental
183 duced the expression of vascular endothelial cell growth factor (VEGF) in a time- and Src-STAT-3-depe
185 been demonstrated that vascular endothelial cell growth factor (VEGF) induction of angiogenesis requ
189 -glutamine (Arg-Gln) on vascular endothelial cell growth factor (VEGF) levels in primary human retina
192 rowth factor (bFGF) and vascular endothelial cell growth factor (VEGF) present within the tumor micro
195 growth factor (HGF) and vascular endothelial cell growth factor (VEGF) regulate normal development an
196 zes the contribution of vascular endothelial cell growth factor (VEGF) to the angiogenic environment
198 etes, oxidative stress, vascular endothelial cell growth factor (VEGF), and intercellular adhesion mo
199 f the EC growth factor, vascular endothelial cell growth factor (VEGF), is stimulated by a variety of
200 s of the major inducer, vascular endothelial cell growth factor (VEGF), that were also produced.
201 KDR-IC), a receptor for vascular endothelial cell growth factor (VEGF), was identified by two-hybrid
203 Tumor production of vascular endothelial cell growth factor (VEGF)-C is associated with tumor lym
204 dly increased basal and vascular endothelial cell growth factor (VEGF)-stimulated NO release compared
211 lar permeability factor/vascular endothelial cell growth factor (VPF/VEGF) can both potently enhance
212 of amphiregulin, a potent mammary epithelial cell growth factor was down regulated in mammary glands
213 permeability induced by vascular endothelial cell growth factor was potently reversed by FTY720-P.
214 differentiation in the presence of different cell growth factors, we have determined that the populat
215 yrosine phosphatase and vascular endothelial cell growth factor were significantly decreased in trans
216 elopment of mast cells is stimulated by mast cell growth factor, which is also known as kit ligand be
217 suggest that there could be a hierarchy of T-cell growth factors with regard to their ability to bloc
218 sympathetic neurons, unlike most nonneuronal cells, growth factor withdrawal-induced apoptosis requir