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1 e S17 and on S17 cells engineered to express Jagged 1.
2 pression of which was dependent on epidermal jagged 1.
3 ic processes were affected, one of which was jagged-1.
4 for a soluble form of a Notch ligand, human Jagged-1.
5 echanisms and prevented the glycosylation of Jagged-1.
6 ed the Notch-1 receptor and the Notch ligand Jagged-1.
7 ulate Notch3 while endothelial cells express Jagged-1.
8 DLL1 and DLL4, but not with the Notch ligand Jagged-1.
9 g and the CSC phenotype by secreting soluble Jagged-1.
10 as suggested by the increased expression in Jagged-1.
11 athway involving inactivation of Notch-1 and Jagged-1.
12 und Notch receptors (Notch 1-4) and ligands (Jagged 1-2 and Delta-like 1, 3, 4), resulting in cell-co
13 ssion of Notch 1-4 receptors, their ligands (Jagged 1-2, DLL1,3,4), gamma-secretase complex proteins
14 angiogenesis factors including Notch ligands Jagged 1/2 and DLL-4 and VEGF were significantly reduced
15 ts ligands (DLL (Delta-like protein)-1/3/4), Jagged 1/2) and Notch-induced transcription factor Hes1
16 t during biliary regeneration, expression of Jagged 1 (a Notch ligand) by myofibroblasts promoted Not
18 Computational analyses identified two genes, Jagged-1, a Notch-receptor ligand, and embryonic-lethal
20 Significantly, exogenously added Wnt-1 and Jagged-1 also stalled MDDC differentiation, suggesting t
23 inase 1 enhances expression of Notch ligands Jagged 1 and 2, which increases Notch activity and alter
24 g major histocompatibility complex class II, Jagged 1 and interferon-response molecules and upregulat
25 ings, in vitro-differentiated and HDM-pulsed Jagged 1 and Jagged 2 double-deficient DCs lacked the ca
26 sthma mouse model to compare the capacity of Jagged 1 and Jagged 2 single- and double-deficient DCs t
30 mber produce high levels of the Notch ligand jagged 1 and support an increase in the number of haemat
33 eased significantly, along with increases in Jagged-1 and Hes-1 coinciding with the progression and r
34 This study documents the regulation of the Jagged-1 and Notch-3 genes in VSMCs by growth factor sti
36 , we demonstrated a cooperative influence of Jagged-1 and TGFbeta1 on cholangiocytic differentiation.
37 f the arterial and venous markers (EphB4 and Jagged-1), and showed evidence of arteriovenous shunting
39 sis with concomitant attenuation of Notch-1, Jagged-1, and its downstream genes such as Hes-1 in vitr
40 uments that the Notch-3 receptor, the ligand Jagged-1, and the downstream transcription factor, HESR-
42 ent study shows that Notch-2 and its ligand, Jagged-1, are highly up-regulated in GR cells, which is
43 at Notch-1 and its ligands, Delta-like-1 and Jagged-1, are overexpressed in many glioma cell lines an
47 these results unveil a novel stromal PTEN-to-JAGGED-1 axis in maintaining the MaSC niche, and subsequ
48 at removing one copy of Rumi in a Jag1(+/-) (jagged 1) background results in severe bile duct morphog
53 Down-regulation of Notch-1, Delta-like-1, or Jagged-1 by RNA interference induces apoptosis and inhib
54 In addition, we demonstrated that exogenous Jagged-1, Delta-like 1, and Delta-like 4 within the cell
58 Notch3-expressing ovarian cancer cells with Jagged-1-expressing feeder cells activated the promoter
59 KL and a significant decrease of Notch 1 and Jagged 1 expression were observed compared to control gr
60 neage differentiation requires Smad3-induced Jagged-1 expression and Notch activation, MEK/Smad3-regu
61 Immunohistochemical analyses demonstrated jagged-1 expression in distal tubules of kidneys from no
65 nscription factor NF-kB and its induction of Jagged-1 expression, which promoted Notch signaling and
68 1-induced Notch signaling (using immobilized Jagged-1 fusion protein) during stimulation of purified
69 We found that main Notch ligands Delta-1 and Jagged-1 had the opposite effect on DC differentiation.
70 To investigate if the stromal expression of Jagged 1 has functional effects on hematopoietic progeni
72 of investigated molecules (Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1, TNF-alpha, IL-17, RANKL, and OPG
77 dherin, thrombospondin, and the notch ligand jagged-1 in cultured human proximal tubular epithelial (
78 e effects were blocked by immunodepletion of Jagged-1 in EC-conditioned medium or blockade of ADAM17
80 Here we demonstrate that TNF induction of jagged-1 in human EC is rapid and dependent upon signali
86 re of DCs with cells expressing Notch ligand Jagged-1 induced up-regulation of maturation markers, IL
87 In the present report we demonstrate that Jagged-1-induced Notch signaling (using immobilized Jagg
93 erized by overexpression of the NOTCH ligand JAGGED-1 (JAG-1) in small pulmonary artery smooth muscle
96 nalysis of expression data, the Notch ligand Jagged-1 (Jag-1) was identified as a downstream target o
97 tic disease primarily caused by mutations in jagged 1 ( JAG1) , BD paucity often results in severe ch
100 DPT), and increased expression of IGFBP5 and jagged 1 (JAG1) are seen only in fibroblasts cultured fr
101 gille syndrome is caused by mutations in the Jagged 1 (JAG1) gene, which encodes a ligand for Notch f
102 uring cochlear development, the Notch ligand JAGGED 1 (JAG1) plays an important role in the specifica
107 idual genes, multidrug resistant 1a (Mdr1a), jagged 1 (Jag1), and notch homolog 3 (Notch3), were targ
108 omponents of the Notch pathway, most notably Jagged 1 (Jag1), as targets of PM induction in human mon
109 we show that conditional inactivation of the Jagged 1 (Jag1)-Notch2 signaling pathway in the developi
111 hed the membrane-anchored signaling molecule Jagged 1 (Jag1).Wealso mapped the cleavage sites of Jag1
113 a vascular niche that produces Notch ligands jagged-1 (JAG1) and delta-like ligand-4 (DLL4) drives de
114 through their expression of the NOTCH ligand JAGGED-1 (JAG1) at stage VIII of the seminiferous epithe
115 onic enhancer region within the Notch ligand Jagged-1 (JAG1) gene, an event requiring DeltaNp63.
117 teractions, such as angiopoietin-2 (ANGPT2), jagged-1 (JAG1), and notch-4 (NOTCH4), as well as genes
118 IL1B), cysteine-rich protein 61 (CYR61), and jagged-1 (JAG1), that act downstream of p63 as key effec
122 ch was activated in the absence of epidermal jagged 1, jagged 1 was not upregulated in the dermis, an
124 arian cancer cells that were cocultured with Jagged-1 knockdown mesothelial and tumor feeder cells.
125 miR-21 and miR-34a, or addition of Wnt-1 and Jagged-1, led to a decrease in endocytic capacity, a key
126 nds, including increased Delta-4 and reduced Jagged-1 levels, reflecting decreased T(H)2 polarization
127 cell-cell contact for reciprocal binding of Jagged-1 ligands and Notch-1 receptors between adjacent
128 ics of Notch signaling involving Delta-4 and Jagged-1 ligands determines tip cell selection and vesse
129 may result from the inhibition of endogenous Jagged 1-mediated Notch signaling since it was not possi
130 nt and requires the repression of endogenous Jagged 1-mediated Notch signaling, which is tolerant to
132 its effects on CD4+ T cell differentiation, Jagged-1-mediated signaling inhibits T cell cytokine sec
137 nephron remodeling process and induction of jagged 1/NOTCH signaling, which expands the cortical con
139 imary Notch3 ligand in ovarian carcinoma and Jagged-1/Notch3 interaction constitutes a juxtacrine loo
141 further test this possibility, the effect of Jagged-1 on murine marrow precursor cells was assessed b
142 2 in the Mgp(-/-) mice by crossing them with Jagged 1 or 2 deficient mice reduces Notch activity, nor
144 tization and challenge with HDM, DC-specific Jagged 1 or Jagged 2 single- or double-deficient mice ha
145 ) with a 3T3 cell layer that expressed human Jagged-1 or by incubating sorted precursors with beads c
146 creased vascular branching as treatment with Jagged-1 peptide reduced the size of the arterial networ
147 Our data suggest that activation of Notch by Jagged-1 plays an important role in maturation of human
149 Notch signaling in human T cells induced by Jagged-1 promotes a novel form of T cell hyporesponsiven
150 served in vivo, resulted in deceased Notch 1/Jagged 1 protein expression however, DHA supplementation
151 trate significant attenuation of Notch 1 and Jagged 1 protein levels in response to DHA supplementati
152 The interplay between Notch receptors and Jagged 1 protein, as expressed by many cells of the live
155 in the gene encoding the human Notch ligand jagged 1 result in a multisystem autosomal dominant diso
156 ceptor by exposing cells to the Notch ligand Jagged-1 resulted in upregulation of PDGF-B expression.
158 consistent with a possible role for loss of Jagged-1 signals in altered HSC and LSC function after O
159 he transmembrane ligand for Notch receptors, Jagged 1 (sJ1), in NIH 3T3 cells results in the formatio
160 eration of fully differentiated DCs, whereas Jagged-1 stimulated accumulation of DC precursors but pr
161 In Notch3-expressing ovarian cancer cells, Jagged-1-stimulating peptides enhanced cellular prolifer
162 ephros region of day 11 mouse embryos on the Jagged 1(-) stromal cell line S17 and on S17 cells engin
163 our and a half LIM domains protein 2), JAG1 (jagged 1), SULF2 (extracellular sulfatase Sulf-2), and T
164 our and a half LIM domains protein 2), JAG1 (jagged 1), SULF2 (extracellular sulfatase Sulf-2), and T
167 or (PDGF) markedly downregulated Notch-3 and Jagged-1 through ERK-dependent signaling mechanisms and
171 ivated in the absence of epidermal jagged 1, jagged 1 was not upregulated in the dermis, and epiderma
175 beneficial effects of the overexpression of Jagged-1 were described in escaper golden retriever musc
176 on DC differentiation was similar to that of Jagged-1, whereas the effect of SS was similar to the ef