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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
  
    16 Computational analyses identified two genes, Jagged-1, a Notch-receptor ligand, and embryonic-lethal 
  
    18   Significantly, exogenously added Wnt-1 and Jagged-1 also stalled MDDC differentiation, suggesting t
  
  
    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
  
  
    27 mber produce high levels of the Notch ligand jagged 1 and support an increase in the number of haemat
  
  
    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
  
    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
  
    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
  
  
  
    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
  
  
  
  
    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
  
  
  
    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
  
  
  
  
  
    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
  
  
  
  
  
    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 
  
    73    Here we demonstrate that TNF induction of jagged-1 in human EC is rapid and dependent upon signali
  
  
  
  
  
    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
  
  
  
  
  
  
  
    88 nalysis of expression data, the Notch ligand Jagged-1 (Jag-1) was identified as a downstream target o
  
    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
  
  
  
  
    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
  
   100 hed the membrane-anchored signaling molecule Jagged 1 (Jag1).Wealso mapped the cleavage sites of Jag1
  
   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
  
   107 ch was activated in the absence of epidermal jagged 1, jagged 1 was not upregulated in the dermis, an
  
   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 
  
   116  its effects on CD4+ T cell differentiation, Jagged-1-mediated signaling inhibits T cell cytokine sec
  
  
  
  
   121  nephron remodeling process and induction of jagged 1/NOTCH signaling, which expands the cortical con
  
   123 imary Notch3 ligand in ovarian carcinoma and Jagged-1/Notch3 interaction constitutes a juxtacrine loo
  
   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
  
   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 
  
   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
  
  
   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. 
  
   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
  
  
   149 or (PDGF) markedly downregulated Notch-3 and Jagged-1 through ERK-dependent signaling mechanisms and 
  
  
  
   153 ivated in the absence of epidermal jagged 1, jagged 1 was not upregulated in the dermis, and epiderma
  
  
  
   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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