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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
17  EC tip cell phenotype and the expression of jagged-1, a ligand for the notch pathway.
18 Computational analyses identified two genes, Jagged-1, a Notch-receptor ligand, and embryonic-lethal
19                             Mechanistically, JAGGED-1, a transmembrane ligand for the NOTCH receptor,
20   Significantly, exogenously added Wnt-1 and Jagged-1 also stalled MDDC differentiation, suggesting t
21                   Reducing the expression of Jagged 1 and 2 in the Mgp(-/-) mice by crossing them wit
22                       Expression of Notch 2, Jagged 1 and 2, Delta 1 and 4, Hes 1 and 5, and Deltex w
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
27  of the C-terminal extracellular portions of Jagged 1 and Jagged 2.
28           The down-regulation of Notch 1 and Jagged 1 and loss of their osteoprotective function migh
29 lated organ defects occur in mice that carry jagged 1 and notch 2 mutations.
30 mber produce high levels of the Notch ligand jagged 1 and support an increase in the number of haemat
31                                              Jagged-1 and Delta-1 equally activated CBF-1/RBPJkappa t
32            Furthermore, ethanol induced both Jagged-1 and ELAVL2 mRNA.
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
35                        The downregulation of Jagged-1 and Notch-3 was associated with a decrease in C
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
38 iption 3-dependent up-regulation of Notch-3, Jagged-1, and carbonic anhydrase IX.
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-
41 i-NOTCH2 negative regulatory region and anti-jagged 1 antibodies.
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
44        These results obtained in vitro table Jagged 1 as a candidate regulator of stem cell fate in t
45                  In this report, we identify Jagged-1 as the highest expressed Notch ligand in ovaria
46 ts of the Notch pathway, Notch1, Notch2, and Jagged 1, as direct targets of miR-34a.
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
49 dendritic cells that upregulate Notch ligand Jagged-1 but not Delta-4.
50          HDM exposure promoted expression of Jagged 1, but not Jagged 2, on DCs.
51              Hence, transgenic expression of Jagged-1 by antigen-presenting cells can induce antigen-
52                    Upregulation of OX40L and Jagged-1 by mDC resulted in mDC-driven Th2 responses.
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
55          Normal and CML LTHSCs cultured with Jagged-1 demonstrated reduced cell cycling, consistent w
56      Stimulation of CD45RA+ naive T cells by Jagged-1 EBV-LCL reduces production of interferon-gamma,
57 ing cells and overexpressed the Notch ligand Jagged-1 (EBV-LCL J1) by adenoviral transduction.
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
62          On the basis of the array analysis, jagged-1 expression was further evaluated in cultured ce
63                                              Jagged-1 expression was significantly increased in the k
64                            Reintroduction of JAGGED-1 expression within the PTEN-null fibroblasts was
65 nscription factor NF-kB and its induction of Jagged-1 expression, which promoted Notch signaling and
66 f differentiated chondrocytes and failure of Jagged-1 expression.
67 fied extracellular domain of human Jagged-1 (Jagged-1(ext)).
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
71        Causative dominant mutations in human Jagged 1 have been identified in most AGS patients.
72 of investigated molecules (Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1, TNF-alpha, IL-17, RANKL, and OPG
73 Notch activation resulted in upregulation of jagged 1 in both epidermis and dermis.
74 in stimulates expression of the Notch ligand jagged 1 in osteoblasts.
75 stern blotting, we demonstrate expression of Jagged 1 in primary stromal cultures.
76                           Down-regulation of Jagged-1 in BMS substantially increased DC differentiati
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
79 quired for TNF induction of the notch ligand jagged-1 in EC.
80    Here we demonstrate that TNF induction of jagged-1 in human EC is rapid and dependent upon signali
81  activity implying a direct role for stromal JAGGED-1 in regulation of MaSC properties.
82                                Enrichment of jagged-1 in tip cells was confirmed by immunofluorescent
83 , Notch-1 and Notch-2, and one Notch ligand, Jagged-1, in hematopoietic cells.
84             We overexpressed a Notch ligand, Jagged-1, in these cells by adenoviral vector transducti
85                              The presence of Jagged 1 increased the number of colonies formed in subs
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
88                             We conclude that jagged 1 is a key mediator of non-cell autonomous Notch
89                                              Jagged 1 is expressed throughout the developing embryo,
90                   These results suggest that jagged-1 is expressed in normal kidneys and that this ex
91        Taken together, our results show that Jagged-1 is the primary Notch3 ligand in ovarian carcino
92        Expression of Notch-1 and its ligand, Jagged-1, is associated with the poorest survival, inclu
93 erized by overexpression of the NOTCH ligand JAGGED-1 (JAG-1) in small pulmonary artery smooth muscle
94             Activation of Notch signaling by Jagged-1 (Jag-1) in vascular smooth muscle cells (VSMC)
95                      In human primary VSMCs, Jagged-1 (Jag-1) significantly reduced proliferation thr
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
98               Expression of the Notch ligand Jagged 1 (JAG1) and Notch activation promote poor-progno
99 K) signaling, which induces the Notch ligand Jagged 1 (Jag1) and promotes cell differentiation.
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
103           Conversely, misexpression of human jagged 1 (JAG1) represses ventral gene expression and do
104          Mutations in the human Notch ligand jagged 1 (JAG1) result in a multi-system disorder called
105                                  Deletion of jagged 1 (Jag1) results in inhibition of the hair growth
106                                 Mutations of Jagged 1 (JAG1), a ligand in the Notch signaling pathway
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
110 gh levels of the Notch ligand family member, Jagged 1 (Jag1).
111 hed the membrane-anchored signaling molecule Jagged 1 (Jag1).Wealso mapped the cleavage sites of Jag1
112 e differentially regulated by Notch ligands: Jagged-1 (Jag1) and Delta-like ligand 1 (Dll1).
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.
116           Cotreatment with soluble OX40L and Jagged-1 (JAG1) proteins increased Tregs, TFR cells, and
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
119 he JAG1-3'UTR and inhibits the expression of Jagged-1 (JAG1).
120  regeneration via the Notch signaling ligand Jagged-1 (Jag1).
121 h the purified extracellular domain of human Jagged-1 (Jagged-1(ext)).
122 ch was activated in the absence of epidermal jagged 1, jagged 1 was not upregulated in the dermis, an
123       Notch ligands, Delta-like 1 (Dll1) and Jagged 1 (Jg1), are expressed by follicular dendritic ce
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
131 osis was required for selectively activating Jagged-1-mediated Notch3 signaling.
132  its effects on CD4+ T cell differentiation, Jagged-1-mediated signaling inhibits T cell cytokine sec
133 ted OX40 ligand (OX40L) and the Notch ligand Jagged-1 mRNA and expression on mDC.
134                            The expression of jagged-1 mRNA and protein was observed to be significant
135        Recombinant human TGF-beta1 increased jagged-1 mRNA levels at concentrations between 10(-11) a
136 R-335, -21, and -153 significantly increased Jagged-1 mRNA.
137  nephron remodeling process and induction of jagged 1/NOTCH signaling, which expands the cortical con
138                       Ang-1 also upregulated Jagged-1, Notch3 and apelin expression followed by incre
139 imary Notch3 ligand in ovarian carcinoma and Jagged-1/Notch3 interaction constitutes a juxtacrine loo
140             Upregulation of OX40L as well as Jagged-1 on mDC required HBEC and did not occur in the p
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
143 M-driven asthma model but that expression of Jagged 1 or Jagged 2 on DCs is not required.
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
148                                We found that Jagged-1, presented both on the cell surface and on bead
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
153                                              Jagged-1 protein expression was increased in tubules not
154         There was a commensurate increase in jagged-1 protein levels, as assessed by Western blotting
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.
157 cellular domain significantly suppressed the Jagged-1 shRNA-mediated growth inhibitory effect.
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
165 MS expressed a substantially higher level of Jagged-1 than Delta-1.
166                Because MAGP-2 interacts with Jagged-1 that controls cell-matrix interaction and cell
167 or (PDGF) markedly downregulated Notch-3 and Jagged-1 through ERK-dependent signaling mechanisms and
168  find that TNF also induces the notch ligand jagged-1, through an NFkappaB-dependent mechanism.
169                       Furthermore, OX40L and Jagged-1 upregulation was inhibited when HBEC expression
170               An EC-derived, soluble form of Jagged-1, via ADAM17 proteolytic activity, led to Notch
171 ivated in the absence of epidermal jagged 1, jagged 1 was not upregulated in the dermis, and epiderma
172                             The notch ligand Jagged-1 was overexpressed on CML OBs.
173                                     However, Jagged-1 was seen in cultured primary murine fetal liver
174                            The Notch ligand, Jagged-1, was not detected in whole marrow or in precurs
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

 
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