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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 n require T cell costimulatory signals and T cell growth factors.
13 ing lymph node macrophages to produce plasma cell growth factors.
14 ty was largely reversed in the presence of T cell growth factors.
15 tentiate Wnt signalling and function as stem-cell growth factors.
16 ocompromised mice that express human myeloid cell growth factors.
17 potentially through induction of paracrine B-cell growth factors.
18 the lung expression of Th2 cell-derived mast cell growth factors.
20 ylase (TYMP; previously known as endothelial cell growth factor 1, ECGF1) as a second key astrocyte-d
26 IL-2, the first cytokine discovered with T cell growth factor activity, is now known to have pleiot
28 lar endothelial growth factor or endothelial cell growth factor-alpha + IGF-1 provided no advantage c
29 cular endothelial growth factor, endothelial cell growth factor-alpha and pancreatic islet neogenesis
30 endothelial biology because some endothelial cell growth factors also exert anti-apoptotic effects.
31 s of endothelial cells, vascular endothelial cell growth factor and basic fibroblast growth factor fu
32 growth factors such as vascular endothelial cell growth factor and basic fibroblast growth factor, i
34 r cancer cells in response to the urothelial cell growth factor and EGFR ligand heparin-binding EGF-l
35 tivity was dependent on vascular endothelial cell growth factor and had an ED50 of 10 microg/ml in me
39 --have been engineered from mesenchymal stem cells, growth factor, and/or gene therapy approaches.
41 mitogenic stimulus for ductal and periductal cells, growth factors are necessary for survival, motili
42 direct AAV-mediated in vivo delivery of beta-cell growth factors as a novel therapeutic strategy for
45 e declined lungs from control lungs was stem cell growth factor -beta [P < 0.001, AUC (area under the
46 applied to dendritic cells, UA suppressed T-cell growth factors but up-regulated B cell-activating c
50 atient, one peptide derived from endothelial cell growth factor (ECGF) caused his PBMCs to proliferat
53 was initially characterized as the primary T-cell growth factor following in vitro activation, less i
54 (dsAAV)-mediated in vivo expression of beta-cell growth factors, glucagon-like peptide-1 (GLP-1) and
57 aling component by receptors for all known T cell growth factors (i.e., IL-2, IL-4, IL-7, IL-9, IL-15
59 by acting as a sensor of the essential Treg cell growth factor IL-2 and its downstream target STAT5.
61 in a marked increase in production of the T cell growth factor IL-2, it does not result in a signifi
66 liferation and accumulation of the primary T cell growth factor, IL-2, by cells stimulated with anti-
67 ytoprotective cytokines vascular endothelial cell growth factor, IL-6, and IL-11 were decreased in th
68 ce that diminished production of the major T cell growth factors, IL-2 and IL-4, is responsible for t
69 ls of other established IFN-gamma inducing T-cell growth factors, IL-2, and IL-12 in this culture sys
72 amino acids may be essential for other beta-cell growth factors in addition to insulin and IGF-I to
75 ased expression of the Th2 cell-derived mast cell growth factors, including IL-4 and IL-9, but not wi
76 kinase-3 (Flt3) ligand (Flt3L), a dendritic cell growth factor, increase the resistance of mice to a
77 y reductions in transformation of fibroblast cells, growth factor independence of hematopoietic cell
78 changes in cellular morphology and rendered cells growth-factor independent by upregulating the MAPK
79 etic experiments showed that both of these T cell growth factors induce a distinct and sustained phas
81 iferation but abrogated vascular endothelial cell growth factor-induced and basic fibroblast growth f
82 RK1/2 but inhibited the vascular endothelial cell growth factor-induced and basic fibroblast growth f
83 n of 15d-PGJ2 inhibited vascular endothelial cell growth factor-induced angiogenesis in the rat corne
84 blast growth factor and vascular endothelial cell growth factor-induced MAPK phosphorylation in endot
86 tors are known to induce the expression of T-cell growth factor interleukin (IL)-2, it is unclear how
94 Expression of the gene is enhanced by the T cell growth factor interleukin-2, suggesting a role for
98 Stem cell factor (SCF), also known as mast cell growth factor, kit ligand, and steel factor, is the
99 on are strongly induced by the critical mast cell growth factor, kit ligand, which is produced by fib
100 strongly with autoantibodies to endothelial cell growth factor, matrix metalloproteinase 10, and apo
101 blast growth factor and vascular endothelial cell growth factor-mediated cell proliferation and migra
103 tors for hepatocyte and vascular endothelial cell growth factors (MET and VEGFR2, respectively) are c
104 ontain either structural alterations in mast cell growth factor (Mgf) or regulatory mutations that af
106 e, KIT, and require its cognate ligand, Mast cell growth factor (MGF), for survival and differentiati
108 r, endothelial cells by vascular endothelial cell growth factor, neuronal cells by nerve growth facto
110 ent of PVR without the addition of exogenous cells, growth factors, or cytokines typically found in P
113 ; also known as platelet-derived endothelial cell growth factor, PD-ECGF) is an angiogenic factor tha
114 ine kinase inhibitor of vascular endothelial cell growth factor, platelet-derived growth factor, and
116 nce coexpression of a T-cell chemokine and T-cell growth factor potentiates antitumor responses in vi
121 lar mutations causing activation of the mast cell growth factor receptor are found in children appare
122 Studies using mice with defective mast/stem cell growth factor receptor c-Kit have suggested key rol
124 al cells down-regulates vascular endothelial cell growth factor receptor-2 (VEGFR2) mRNA levels and b
125 th factor B (PDGFB) and vascular endothelial cell growth factor receptor-2 (VEGFR2), while at the sam
127 , bone marrow lineage-negative (lin(-)) stem cell growth factor receptor-positive (c-kit(+)) Sca-1(-)
128 reduced mRNA levels of vascular endothelial cell growth factor receptors 1 (Flt-1) and 2 (Flk/KDR) a
129 s discussed include the vascular endothelial cell growth factor receptors, Eph receptors, Tie1, and T
130 induced by contact inhibition (NIH 3T3 mouse cells), growth factor removal (bromodeoxyuridine-blocked
131 g strategies, whereby the traditional triad (cells, growth factors, scaffolds) or a combination there
134 pigment (hemozoin [PfHz]) revealed that stem cell growth factor (SCGF; also called C-type lectin doma
135 leukin 14 (IL-14) or high molecular weight B cell growth factor secreted by activated T and B cells a
138 ed in the regulation of vascular endothelial cell growth factor signaling, offers a unique opportunit
140 ression was regulated negatively by the mast cell growth factor stem cell factor (SCF), and its expre
141 nase is Kit ligand (Kitl; also known as mast cell growth factor, stem cell factor, and Steel factor),
142 s is Kit ligand (or Kitl; also known as mast cell growth factor, stem cell factor, and Steel factor),
144 actors inhibited basal, vascular endothelial cell growth factor-stimulated, and fibroblast growth fac
147 al signaling component shared by all known T cell growth factor (TCGF) receptors (i.e., IL-2, IL-4, I
150 n (gamma(c)) that is activated by multiple T-cell growth factors (TCGFs) such as IL-2, -4, and -7.
151 n (IL)-2, IL-4, IL-7, IL-9, and IL-15, all T-cell growth factors (TCGFs), utilize the common IL-2 rec
155 tance is associated with a circulating islet cell growth factor that is independent of glucose and ob
157 -15 is a proinflammatory and antiapoptotic T-cell growth factor that plays an important role in a var
163 We investigated the ability of IL-15, a T cell growth factor, to modulate prenyl phosphate-induced
164 e phosphorylase/platelet-derived endothelial cell growth factor (TP/PD-ECGF) has diverse functions wi
165 ce lacking the vascular-specific endothelial cell growth factor VEGF or its receptor Flt-1, both of w
166 al stimulating factors, vascular endothelial cell growth factor (VEGF) and basic fibroblast growth fa
172 tors were examined with vascular endothelial cell growth factor (VEGF) homodimers and VEGF/placental
173 duced the expression of vascular endothelial cell growth factor (VEGF) in a time- and Src-STAT-3-depe
175 been demonstrated that vascular endothelial cell growth factor (VEGF) induction of angiogenesis requ
179 -glutamine (Arg-Gln) on vascular endothelial cell growth factor (VEGF) levels in primary human retina
182 rowth factor (bFGF) and vascular endothelial cell growth factor (VEGF) present within the tumor micro
185 growth factor (HGF) and vascular endothelial cell growth factor (VEGF) regulate normal development an
186 zes the contribution of vascular endothelial cell growth factor (VEGF) to the angiogenic environment
188 etes, oxidative stress, vascular endothelial cell growth factor (VEGF), and intercellular adhesion mo
189 f the EC growth factor, vascular endothelial cell growth factor (VEGF), is stimulated by a variety of
190 s of the major inducer, vascular endothelial cell growth factor (VEGF), that were also produced.
191 KDR-IC), a receptor for vascular endothelial cell growth factor (VEGF), was identified by two-hybrid
193 Tumor production of vascular endothelial cell growth factor (VEGF)-C is associated with tumor lym
194 dly increased basal and vascular endothelial cell growth factor (VEGF)-stimulated NO release compared
201 lar permeability factor/vascular endothelial cell growth factor (VPF/VEGF) can both potently enhance
202 of amphiregulin, a potent mammary epithelial cell growth factor was down regulated in mammary glands
203 permeability induced by vascular endothelial cell growth factor was potently reversed by FTY720-P.
204 differentiation in the presence of different cell growth factors, we have determined that the populat
205 yrosine phosphatase and vascular endothelial cell growth factor were significantly decreased in trans
206 elopment of mast cells is stimulated by mast cell growth factor, which is also known as kit ligand be
207 suggest that there could be a hierarchy of T-cell growth factors with regard to their ability to bloc
208 sympathetic neurons, unlike most nonneuronal cells, growth factor withdrawal-induced apoptosis requir
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