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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 angiogenesis factors including Notch ligands Jagged 1/2 and DLL-4 and VEGF were significantly reduced
13 ts ligands (DLL (Delta-like protein)-1/3/4), Jagged 1/2) and Notch-induced transcription factor Hes1
14 t during biliary regeneration, expression of Jagged 1 (a Notch ligand) by myofibroblasts promoted Not
15  EC tip cell phenotype and the expression of jagged-1, a ligand for the notch pathway.
16 Computational analyses identified two genes, Jagged-1, a Notch-receptor ligand, and embryonic-lethal
17                             Mechanistically, JAGGED-1, a transmembrane ligand for the NOTCH receptor,
18   Significantly, exogenously added Wnt-1 and Jagged-1 also stalled MDDC differentiation, suggesting t
19                   Reducing the expression of Jagged 1 and 2 in the Mgp(-/-) mice by crossing them wit
20                       Expression of Notch 2, Jagged 1 and 2, Delta 1 and 4, Hes 1 and 5, and Deltex w
21 inase 1 enhances expression of Notch ligands Jagged 1 and 2, which increases Notch activity and alter
22 g major histocompatibility complex class II, Jagged 1 and interferon-response molecules and upregulat
23 ings, in vitro-differentiated and HDM-pulsed Jagged 1 and Jagged 2 double-deficient DCs lacked the ca
24 sthma mouse model to compare the capacity of Jagged 1 and Jagged 2 single- and double-deficient DCs t
25  of the C-terminal extracellular portions of Jagged 1 and Jagged 2.
26 lated organ defects occur in mice that carry jagged 1 and notch 2 mutations.
27 mber produce high levels of the Notch ligand jagged 1 and support an increase in the number of haemat
28                                              Jagged-1 and Delta-1 equally activated CBF-1/RBPJkappa t
29            Furthermore, ethanol induced both Jagged-1 and ELAVL2 mRNA.
30 eased significantly, along with increases in Jagged-1 and Hes-1 coinciding with the progression and r
31   This study documents the regulation of the Jagged-1 and Notch-3 genes in VSMCs by growth factor sti
32                        The downregulation of Jagged-1 and Notch-3 was associated with a decrease in C
33 , we demonstrated a cooperative influence of Jagged-1 and TGFbeta1 on cholangiocytic differentiation.
34 f the arterial and venous markers (EphB4 and Jagged-1), and showed evidence of arteriovenous shunting
35 iption 3-dependent up-regulation of Notch-3, Jagged-1, and carbonic anhydrase IX.
36 sis with concomitant attenuation of Notch-1, Jagged-1, and its downstream genes such as Hes-1 in vitr
37 uments that the Notch-3 receptor, the ligand Jagged-1, and the downstream transcription factor, HESR-
38 ent study shows that Notch-2 and its ligand, Jagged-1, are highly up-regulated in GR cells, which is
39 at Notch-1 and its ligands, Delta-like-1 and Jagged-1, are overexpressed in many glioma cell lines an
40        These results obtained in vitro table Jagged 1 as a candidate regulator of stem cell fate in t
41                  In this report, we identify Jagged-1 as the highest expressed Notch ligand in ovaria
42 ts of the Notch pathway, Notch1, Notch2, and Jagged 1, as direct targets of miR-34a.
43 these results unveil a novel stromal PTEN-to-JAGGED-1 axis in maintaining the MaSC niche, and subsequ
44 at removing one copy of Rumi in a Jag1(+/-) (jagged 1) background results in severe bile duct morphog
45 dendritic cells that upregulate Notch ligand Jagged-1 but not Delta-4.
46          HDM exposure promoted expression of Jagged 1, but not Jagged 2, on DCs.
47              Hence, transgenic expression of Jagged-1 by antigen-presenting cells can induce antigen-
48                    Upregulation of OX40L and Jagged-1 by mDC resulted in mDC-driven Th2 responses.
49 Down-regulation of Notch-1, Delta-like-1, or Jagged-1 by RNA interference induces apoptosis and inhib
50  In addition, we demonstrated that exogenous Jagged-1, Delta-like 1, and Delta-like 4 within the cell
51          Normal and CML LTHSCs cultured with Jagged-1 demonstrated reduced cell cycling, consistent w
52      Stimulation of CD45RA+ naive T cells by Jagged-1 EBV-LCL reduces production of interferon-gamma,
53 ing cells and overexpressed the Notch ligand Jagged-1 (EBV-LCL J1) by adenoviral transduction.
54  Notch3-expressing ovarian cancer cells with Jagged-1-expressing feeder cells activated the promoter
55 neage differentiation requires Smad3-induced Jagged-1 expression and Notch activation, MEK/Smad3-regu
56    Immunohistochemical analyses demonstrated jagged-1 expression in distal tubules of kidneys from no
57          On the basis of the array analysis, jagged-1 expression was further evaluated in cultured ce
58                                              Jagged-1 expression was significantly increased in the k
59                            Reintroduction of JAGGED-1 expression within the PTEN-null fibroblasts was
60 f differentiated chondrocytes and failure of Jagged-1 expression.
61 fied extracellular domain of human Jagged-1 (Jagged-1(ext)).
62 1-induced Notch signaling (using immobilized Jagged-1 fusion protein) during stimulation of purified
63 We found that main Notch ligands Delta-1 and Jagged-1 had the opposite effect on DC differentiation.
64  To investigate if the stromal expression of Jagged 1 has functional effects on hematopoietic progeni
65        Causative dominant mutations in human Jagged 1 have been identified in most AGS patients.
66 Notch activation resulted in upregulation of jagged 1 in both epidermis and dermis.
67 in stimulates expression of the Notch ligand jagged 1 in osteoblasts.
68 stern blotting, we demonstrate expression of Jagged 1 in primary stromal cultures.
69                           Down-regulation of Jagged-1 in BMS substantially increased DC differentiati
70 dherin, thrombospondin, and the notch ligand jagged-1 in cultured human proximal tubular epithelial (
71 e effects were blocked by immunodepletion of Jagged-1 in EC-conditioned medium or blockade of ADAM17
72 quired for TNF induction of the notch ligand jagged-1 in EC.
73    Here we demonstrate that TNF induction of jagged-1 in human EC is rapid and dependent upon signali
74  activity implying a direct role for stromal JAGGED-1 in regulation of MaSC properties.
75                                Enrichment of jagged-1 in tip cells was confirmed by immunofluorescent
76 , Notch-1 and Notch-2, and one Notch ligand, Jagged-1, in hematopoietic cells.
77             We overexpressed a Notch ligand, Jagged-1, in these cells by adenoviral vector transducti
78                              The presence of Jagged 1 increased the number of colonies formed in subs
79 re of DCs with cells expressing Notch ligand Jagged-1 induced up-regulation of maturation markers, IL
80    In the present report we demonstrate that Jagged-1-induced Notch signaling (using immobilized Jagg
81                             We conclude that jagged 1 is a key mediator of non-cell autonomous Notch
82                                              Jagged 1 is expressed throughout the developing embryo,
83                   These results suggest that jagged-1 is expressed in normal kidneys and that this ex
84        Taken together, our results show that Jagged-1 is the primary Notch3 ligand in ovarian carcino
85        Expression of Notch-1 and its ligand, Jagged-1, is associated with the poorest survival, inclu
86             Activation of Notch signaling by Jagged-1 (Jag-1) in vascular smooth muscle cells (VSMC)
87                      In human primary VSMCs, Jagged-1 (Jag-1) significantly reduced proliferation thr
88 nalysis of expression data, the Notch ligand Jagged-1 (Jag-1) was identified as a downstream target o
89               Expression of the Notch ligand Jagged 1 (JAG1) and Notch activation promote poor-progno
90 DPT), and increased expression of IGFBP5 and jagged 1 (JAG1) are seen only in fibroblasts cultured fr
91 gille syndrome is caused by mutations in the Jagged 1 (JAG1) gene, which encodes a ligand for Notch f
92           Conversely, misexpression of human jagged 1 (JAG1) represses ventral gene expression and do
93          Mutations in the human Notch ligand jagged 1 (JAG1) result in a multi-system disorder called
94                                  Deletion of jagged 1 (Jag1) results in inhibition of the hair growth
95                                 Mutations of Jagged 1 (JAG1), a ligand in the Notch signaling pathway
96 idual genes, multidrug resistant 1a (Mdr1a), jagged 1 (Jag1), and notch homolog 3 (Notch3), were targ
97 omponents of the Notch pathway, most notably Jagged 1 (Jag1), as targets of PM induction in human mon
98 we show that conditional inactivation of the Jagged 1 (Jag1)-Notch2 signaling pathway in the developi
99 gh levels of the Notch ligand family member, Jagged 1 (Jag1).
100 hed the membrane-anchored signaling molecule Jagged 1 (Jag1).Wealso mapped the cleavage sites of Jag1
101 e differentially regulated by Notch ligands: Jagged-1 (Jag1) and Delta-like ligand 1 (Dll1).
102 a vascular niche that produces Notch ligands jagged-1 (JAG1) and delta-like ligand-4 (DLL4) drives de
103 onic enhancer region within the Notch ligand Jagged-1 (JAG1) gene, an event requiring DeltaNp63.
104 teractions, such as angiopoietin-2 (ANGPT2), jagged-1 (JAG1), and notch-4 (NOTCH4), as well as genes
105 IL1B), cysteine-rich protein 61 (CYR61), and jagged-1 (JAG1), that act downstream of p63 as key effec
106 h the purified extracellular domain of human Jagged-1 (Jagged-1(ext)).
107 ch was activated in the absence of epidermal jagged 1, jagged 1 was not upregulated in the dermis, an
108       Notch ligands, Delta-like 1 (Dll1) and Jagged 1 (Jg1), are expressed by follicular dendritic ce
109 arian cancer cells that were cocultured with Jagged-1 knockdown mesothelial and tumor feeder cells.
110 miR-21 and miR-34a, or addition of Wnt-1 and Jagged-1, led to a decrease in endocytic capacity, a key
111 nds, including increased Delta-4 and reduced Jagged-1 levels, reflecting decreased T(H)2 polarization
112  cell-cell contact for reciprocal binding of Jagged-1 ligands and Notch-1 receptors between adjacent
113 may result from the inhibition of endogenous Jagged 1-mediated Notch signaling since it was not possi
114 nt and requires the repression of endogenous Jagged 1-mediated Notch signaling, which is tolerant to
115 osis was required for selectively activating Jagged-1-mediated Notch3 signaling.
116  its effects on CD4+ T cell differentiation, Jagged-1-mediated signaling inhibits T cell cytokine sec
117 ted OX40 ligand (OX40L) and the Notch ligand Jagged-1 mRNA and expression on mDC.
118                            The expression of jagged-1 mRNA and protein was observed to be significant
119        Recombinant human TGF-beta1 increased jagged-1 mRNA levels at concentrations between 10(-11) a
120 R-335, -21, and -153 significantly increased Jagged-1 mRNA.
121  nephron remodeling process and induction of jagged 1/NOTCH signaling, which expands the cortical con
122                       Ang-1 also upregulated Jagged-1, Notch3 and apelin expression followed by incre
123 imary Notch3 ligand in ovarian carcinoma and Jagged-1/Notch3 interaction constitutes a juxtacrine loo
124             Upregulation of OX40L as well as Jagged-1 on mDC required HBEC and did not occur in the p
125 further test this possibility, the effect of Jagged-1 on murine marrow precursor cells was assessed b
126 2 in the Mgp(-/-) mice by crossing them with Jagged 1 or 2 deficient mice reduces Notch activity, nor
127 M-driven asthma model but that expression of Jagged 1 or Jagged 2 on DCs is not required.
128 tization and challenge with HDM, DC-specific Jagged 1 or Jagged 2 single- or double-deficient mice ha
129 ) with a 3T3 cell layer that expressed human Jagged-1 or by incubating sorted precursors with beads c
130 creased vascular branching as treatment with Jagged-1 peptide reduced the size of the arterial networ
131 Our data suggest that activation of Notch by Jagged-1 plays an important role in maturation of human
132                                We found that Jagged-1, presented both on the cell surface and on bead
133  Notch signaling in human T cells induced by Jagged-1 promotes a novel form of T cell hyporesponsiven
134 served in vivo, resulted in deceased Notch 1/Jagged 1 protein expression however, DHA supplementation
135 trate significant attenuation of Notch 1 and Jagged 1 protein levels in response to DHA supplementati
136    The interplay between Notch receptors and Jagged 1 protein, as expressed by many cells of the live
137                                              Jagged-1 protein expression was increased in tubules not
138         There was a commensurate increase in jagged-1 protein levels, as assessed by Western blotting
139  in the gene encoding the human Notch ligand jagged 1 result in a multisystem autosomal dominant diso
140 ceptor by exposing cells to the Notch ligand Jagged-1 resulted in upregulation of PDGF-B expression.
141 cellular domain significantly suppressed the Jagged-1 shRNA-mediated growth inhibitory effect.
142  consistent with a possible role for loss of Jagged-1 signals in altered HSC and LSC function after O
143 he transmembrane ligand for Notch receptors, Jagged 1 (sJ1), in NIH 3T3 cells results in the formatio
144 eration of fully differentiated DCs, whereas Jagged-1 stimulated accumulation of DC precursors but pr
145   In Notch3-expressing ovarian cancer cells, Jagged-1-stimulating peptides enhanced cellular prolifer
146 ephros region of day 11 mouse embryos on the Jagged 1(-) stromal cell line S17 and on S17 cells engin
147 MS expressed a substantially higher level of Jagged-1 than Delta-1.
148                Because MAGP-2 interacts with Jagged-1 that controls cell-matrix interaction and cell
149 or (PDGF) markedly downregulated Notch-3 and Jagged-1 through ERK-dependent signaling mechanisms and
150  find that TNF also induces the notch ligand jagged-1, through an NFkappaB-dependent mechanism.
151                       Furthermore, OX40L and Jagged-1 upregulation was inhibited when HBEC expression
152               An EC-derived, soluble form of Jagged-1, via ADAM17 proteolytic activity, led to Notch
153 ivated in the absence of epidermal jagged 1, jagged 1 was not upregulated in the dermis, and epiderma
154                             The notch ligand Jagged-1 was overexpressed on CML OBs.
155                                     However, Jagged-1 was seen in cultured primary murine fetal liver
156                            The Notch ligand, Jagged-1, was not detected in whole marrow or in precurs
157 on DC differentiation was similar to that of Jagged-1, whereas the effect of SS was similar to the ef

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