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1 ly by haploinsufficiency of the Notch ligand jagged1.
2 for Treg expansion and required signaling by Jagged1.
3 ded by Notch1 positive dermal cells, induces Jagged1.
4 1c(+)B220(-)PDCA-1(-), and had low levels of Jagged1.
5 in signaling of a mammalian Serrate homolog, Jagged1.
6 of notch activity persists in the absence of Jagged1.
7 s disrupting interactions between Notch3 and Jagged1.
8 an epistatic relationship between Twist1 and Jagged1.
9  augments the interaction between Notch3 and Jagged1.
10 ns in Notch signaling pathway genes, usually JAGGED1.
11 th elevated Wnt signaling displayed elevated Jagged1.
12            TSP2 binds directly to Notch3 and Jagged1.
13 ot Radical) inhibited Notch1 activation from Jagged1.
14 he supporting cells exhibit the Notch ligand Jagged1.
15 ated in tumor angiogenesis, Delta-like 4 and Jagged1.
16 ilization of a soluble extracellular form of Jagged1.
17 -2, was unable to facilitate the shedding of Jagged1.
18  the epidermal growth factor-like repeats of Jagged1.
19 linical proof of concept for the use of anti-Jagged1/2 to reprogram MDSC-mediated T-cell suppression
20                                              Jagged1/2 was induced in MDSCs by tumor-derived factors
21 the therapeutic effect of the humanized anti-Jagged1/2-blocking antibody CTX014 on MDSC-mediated T-ce
22   The most highly EBNA-3C-repressed gene was Jagged1, a cell surface ligand and inducer of the Notch
23 ated with downregulation of the Notch ligand Jagged1, a key driver of smooth muscle differentiation i
24          Here we show that the expression of Jagged1, a ligand for canonical Notch signaling, was res
25                                              Jagged1, a ligand in the Notch signaling pathway, has be
26 f APEX1 were mediated by the upregulation of Jagged1, a major Notch ligand.
27                                              Jagged1, a Notch ligand, and Notch have been implicated
28 ssed endothelin receptor type B (ETB(R)) and Jagged1, a Notch1 receptor ligand.
29                       Administration of anti-Jagged1 Ab exacerbated clinical disease while that of an
30 sts that express soluble forms of Delta1 and Jagged1 accelerate tumorigenicity in vivo.
31 tors of vascular cells are down-regulated by Jagged1 activation of the Notch1 pathway.
32 dditional support to the proposal that Notch/Jagged1 activity is required for neural stem cell mainte
33 dies will investigate the mechanism in which Jagged1 acts in a cell autonomous and cell non-autonomou
34 ere we show that conditional inactivation of Jagged1 affects neural stem cell maintenance and prolife
35 h hypomorphic mutations in the gene encoding Jagged1 (Alagille syndrome) failed to mount appropriate
36                   Mesodermal inactivation of Jagged1 also results in changes in the identity of sutur
37 nd that the DSL (Delta/Serrate/LAG2) protein Jagged1, an activating ligand for Notch receptor signali
38 e-tune liver inflammation by upregulation of Jagged1 and activation of Notch signaling in Th1 cells.
39 stem cells associated with increased stromal Jagged1 and Angiopoietin-1 expression and reduced primit
40                    Confirming a link between JAGGED1 and cell survival, transcriptional profiling sho
41  and mouse data, we show that NOTCH1 ligands JAGGED1 and DELTA LIKE-4 are up-regulated secondary to h
42  in EGF12 substantially increases binding to Jagged1 and Delta-like 1 (DLL1) ligands.
43 d monocyte-derived DCs express Notch ligands Jagged1 and Delta-like4, whereas naive CD8(+) T cells ex
44                  We investigated the role of Jagged1 and Delta1 in experimental autoimmune encephalom
45 ound that soluble forms of the Notch ligands Jagged1 and Delta1 induced fibroblast growth factor rece
46 ssion of the NOTCH receptor and its ligands, Jagged1 and Delta1.
47 ncreased affinity of this region for ligands Jagged1 and DLL1.
48  Manic Fringe inhibit Notch1 activation from Jagged1 and enhance activation from Delta-like 1, Radica
49 8 and phosphorylated vimentin interacts with Jagged1 and increases Notch activation potential.
50 ls of costimulatory molecules, Notch ligands Jagged1 and Jagged2, and CD11b, and produced more Ifnb a
51                          Interaction between Jagged1 and MAGP-2 requires the epidermal growth factor-
52 lls and COS-7 cells coexpressing full-length Jagged1 and MAGP-2.
53 malformations caused by mutations in Serrate/Jagged1 and Notch signaling components.
54 ) enhances Notch signaling and binds to both Jagged1 and Notch3 ectodomains, potentially bridging two
55 n of PTH signaling through the reestablished Jagged1 and osteopontin levels correlated with the rescu
56 owed enhanced expression of the Notch ligand Jagged1 and significantly increased receptor density of
57 e primitive state, and combined signals from Jagged1 and TGF-beta are important in controlling its qu
58 nt by the demonstration of overexpression of Jagged1 and the downstream Notch pathway member Hes1.
59 rs Notch3 and Notch4, Notch ligands Dll4 and Jagged1, and activated Notch receptors in contrast to un
60 s an association between levels of IL6 mRNA, Jagged1, and Ang2.
61 acellular domain of Notch1 (NIC), its ligand Jagged1, and its target gene Hes1, which were associated
62 cific to DLL1, as other Notch ligands (DLL3, JAGGED1, and JAGGED2) do not influence the clinical outc
63 f Zeste homologue 2 (EZH2), the Notch ligand Jagged1, and PTK2 were elevated 3- to 4.3-fold in tumor-
64                                 Lastly, both Jagged1- and Delta1-derived tumors contained phenotypica
65 es, and evaluated their ability to transduce Jagged1- and Delta1-mediated signaling in a cell-based a
66      Here we show that Notch1 and its ligand Jagged1 are present at the synapse, and that Notch signa
67 ies showed that Notch1 ligands, particularly Jagged1, are present on Tregs and that, indeed, blockade
68 scent arterial endothelial tube and identify Jagged1 as a direct Notch target.
69   Here we identified the Notch family member Jagged1 as a physiological ligand for CD46.
70 tes involved stimulation of the Notch ligand Jagged1 as well as angiopoietin2 (Ang2).
71 is process, presentation of the NOTCH ligand JAGGED1 blunts the capacity of wild-type bone marrow mac
72            Adoptive transfer of only OX40L(+)Jagged1(+) BMDCs led to Treg expansion, increased produc
73    These data demonstrate the requirement of Jagged1, but not Notch1, within the midfacial CNC popula
74 e to activate monoubiquitination in vitro of Jagged1, but not other mammalian Notch ligands.
75 embrane can affect the signaling activity of Jagged1 by directly enhancing its ubiquitination and sub
76 tive fully human monoclonal antibody against Jagged1 (clone 15D11).
77  receptor and DC-Notch ligands (Delta-like1, Jagged1) cluster in their apposed central-supramolecular
78  tumor onset and growth, whereas full-length Jagged1 completely suppressed tumor development.
79                                        Adult Jagged1 conditional mutants completely lack lenses, alon
80                      Therefore, targeting of Jagged1 could be effective in downregulating Notch signa
81 vitro and in vivo, which suggested that CD46-Jagged1 crosstalk is responsible for the recurrent infec
82 ing Ag-specific cells in the CNS, while anti-Jagged1 decreased the frequency of IL-10-producing cells
83  responsible for pancreatic insufficiency in Jagged1-deficient mice and, by corollary, in Alagille sy
84                                              Jagged1-deficient mice displayed malformed pancreatic du
85 signaling pathway (Notch1, Notch 2, Notch 3, Jagged1, Delta1), four Wnt signaling molecules (Wnt4, -5
86  that Notch3 receptor activation in VSMCs is Jagged1-dependent.
87 nes involved in the Notch signaling pathway (Jagged1, Dll4, Hey1, Hey2, Hes1) and decreased apelin ex
88  Consistent with such a relationship, Twist1-Jagged1 double heterozygotes exhibit a substantial incre
89 ptors (Notch2, Notch3), ligands (Dll1, Dll4, Jagged1), downstream targets (Hey, Hes), and endothelial
90 er Cell, Cao and colleagues identify an FGF4/Jagged1-driven crosstalk between tumor cells and their v
91                         However, the role of JAGGED1 during craniofacial development is poorly unders
92                          Arsenite suppressed Jagged1 effects and expression of Jagged1 mRNA as well.
93  persistent upregulation of the Notch ligand Jagged1 (encoded by Jag1) in PCECs, which in turn stimul
94 activation of Notch1 with a specific ligand, Jagged1, enhanced the LPS-induced inflammatory response
95 p is normally recruited to a tissue-specific Jagged1 enhancer by directly interacting with the Notch
96 e transfer of activated Notch1 or its ligand Jagged1 expanded the proliferative capacity of neonatal
97 n of Notch signaling on HBCs; elimination of Jagged1 expressed by sustentacular cells may be the liga
98                                              Jagged1 expressed by tumor cells may activate Notch sign
99 r, Lfng in NSCs and Notch ligands Delta1 and Jagged1, expressed by their progeny, together influence
100  cells were cocultured with allergen-pulsed, Jagged1-expressing BMDCs and, after the transfer of alle
101 d1 levels in cells and blocks signaling from Jagged1-expressing cells to neighboring Notch-expressing
102  its inhibitory effect on bone metastasis of Jagged1-expressing tumor cells, 15D11 dramatically sensi
103        BRD4, but not BRD2 or BRD3, regulated Jagged1 expression and Notch1 signaling.
104 activity impair its ability to down-regulate Jagged1 expression and to block signaling.
105 ally, the Akt/mTOR axis controls endothelial Jagged1 expression and, thereby, Notch signalling regula
106 aB and MAPK signaling pathways, and elevated Jagged1 expression augmented TLR-induced IL-6 production
107 Cs and enhanced HSPC expansion by increasing Jagged1 expression in BM stromal cells.
108 ne metastasis to chemotherapy, which induces Jagged1 expression in osteoblasts to provide a survival
109 Cs during remyelination through induction of Jagged1 expression in reactive astrocytes.
110                           In Twist1 mutants, Jagged1 expression in the suture is reduced substantiall
111                                  Conversely, Jagged1 expression is markedly induced by TLR ligation.
112 the mutant dorsal RPE domains, where ectopic JAGGED1 expression may partially counteract the effects
113  cytokines, indicating the critical role for Jagged1 expression on APCs.
114                                              Jagged1 expression on endothelium activates Notch in vas
115              Moreover, in patients, BRD4 and Jagged1 expression positively correlated with the presen
116                                 TLRs induced Jagged1 expression rapidly and independently of new prot
117 r, it remains undetermined whether increased Jagged1 expression reflects a cause for or a consequence
118 rough the activation of Wnt/beta-catenin and Jagged1 expression to control EC proliferation in extra-
119                      Strikingly, TLR-induced Jagged1 expression was strongly dependent on the Notch m
120 is hypothesis, we found that Jagged2 but not Jagged1 expression, correlates with the ability of DCs t
121 k loop that includes both autoregulation and JAGGED1 expression.
122 eas IFN-gamma, TNF-alpha, and IL-17 decrease Jagged1 expression.
123 JAG1 mouse model that enables spatiotemporal Jagged1 expression.
124          MAGP-2 was found complexed with the Jagged1 extracellular domain shed from 293T cells and CO
125                       MAGP-2 shedding of the Jagged1 extracellular domain was decreased by the metall
126 mooth muscle, and Notch target genes such as Jagged1 fail to activate normally.
127     In vivo treatment of wild-type mice with Jagged1-Fc enhanced AHR and airway inflammation, whereas
128               In contrast, administration of Jagged1-Fc protected from disease, that of Delta1-Fc exa
129                               Treatment with Jagged1-Fc was associated with increased IL-10-producing
130  interactions through excess soluble ligand, Jagged1-Fc.
131 equirement for intact vSMC Notch signals via JAGGED1 for efficient EC Notch1 receptor activation and
132 animals reveals that increased expression of Jagged1 gene, a known regulator of the Notch signaling p
133 15 evolutionary conserved regions within the Jagged1 genomic locus and identify a single Notch respon
134                    Manipulation of Delta1 or Jagged1 had no effect on the frequency of Th17 cells or
135                                 In contrast, Jagged1 has been described as a Notch ligand expressed i
136 the Notch1 decoy, which blocks both Dll4 and Jagged1 has been recently shown to restrict tumor vessel
137 h, Dll4-Notch signaling is enhanced, whereas Jagged1 has weak signaling capacity and competes with Dl
138 led that, in the absence of the Notch ligand JAGGED1, Hensen's cells died or converted into Claudius
139  Here, we show that on a C57BL/6 background, jagged1 heterozygous mice (Jag1(+/-) ) exhibit impaired
140                TSP1 also binds to Notch3 and Jagged1; however, only TSP2 augments the interaction bet
141  abrogates the pro-differentiation effect of Jagged1 in a cell autonomous fashion.
142 autonomous and non-autonomous requirement of Jagged1 in a cell lineage-specific approach during midfa
143        These data highlight a novel role for Jagged1 in colorectal cancer tumor biology that may go b
144 R, expression ratios of Notch1, Notch 3, and Jagged1 in dry eye were 0.43, 0.56, and 0.50, respective
145 nced the expression of Notch3 and its ligand Jagged1 in human breast cancer cell lines.
146 ration that heterozygous loss of function of JAGGED1 in humans can cause Alagille syndrome, which has
147 his study demonstrates that thrombin cleaves Jagged1 in its extracellular domain.
148 could promote its own expression and that of JAGGED1 in mural cells.
149                                      Loss of Jagged1 in neural crest impairs vascular smooth muscle d
150                        The overexpression of Jagged1 in PAR1 null cells results in a rapid thrombin-i
151                                     Deleting Jagged1 in the CNC using Wnt1-cre; Jag1 Flox/Flox recapi
152 s study design determines the requirement of Jagged1 in the cranial neural crest (CNC) cells, which e
153 tional gene targeting to examine the role of Jagged1 in the development of the skull vault.
154 ysical engagement of Notch3 and VSMC-derived Jagged1 in the interior of the same cell.
155                 We show that inactivation of Jagged1 in the mesodermal compartment of the coronal sut
156     We conditionally deleted both alleles of Jagged1 in the murine pancreas using Cre-loxP technology
157 ecapitulate aortic arch artery expression of Jagged1 in transgenic mice.
158 ermore, APEX1 expression was associated with Jagged1 in various colon cancer cell lines and in tissue
159 l for targeting the NOTCH pathway (primarily JAGGED1) in conditions characterized by compromised vasc
160 y two specific mutations that reduce ligand (JAGGED1) induced NOTCH1 signaling.
161 esults showed a critical role for OX40L- and Jagged1-induced cosignaling in GM-BMDC-induced Treg expa
162 with low levels of Slc35c2, both Delta1- and Jagged1-induced Notch signaling were reduced, and the fu
163 onal evaluation, and 2 showed a reduction in Jagged1-induced NOTCH signaling.
164  Notch ligands and low levels of Delta1- and Jagged1-induced Notch signaling.
165 e of bone metastases, mediated by osteoblast Jagged1-induced tumor Notch signaling.
166 h TCR-alphabeta and -gammadelta development, Jagged1 induces mainly alphabeta-lineage differentiation
167                                              Jagged1 induction was augmented by IFN-gamma, was partia
168              Finally, recombinant Notch3 and Jagged1 interact with the LRP1 85-kDa B-chain, a subunit
169 was required for transfer, in which a Notch2-Jagged1 interaction played a decisive role.
170                           Here, we show that Jagged1 is a direct Notch target in smooth muscle, resul
171 ignaling was switched on, demonstrating that Jagged1 is a novel target of the Kras signaling pathway.
172          Here, we show that the Notch ligand Jagged1 is a potent proangiogenic regulator in mice that
173                Our results thus suggest that Jagged1 is an effector of Twist1 in coronal suture devel
174                                        Thus, Jagged1 is an RBP-J target gene that is activated in a b
175                          We demonstrate that Jagged1 is expressed in a layer of mesoderm-derived sutu
176 pecifically expressed in beta-cells, whereas JAGGED1 is expressed in alpha-cells.
177 ing conditional gene targeting, we show that Jagged1 is required for lens fiber cell genesis, particu
178                  In this study, we show that Jagged1 is up-regulated on bone marrow-derived dendritic
179 dritic cells and B cells after priming while Jagged1 is up-regulated only on dendritic cells.
180 s for missense mutations of the Notch ligand Jagged1 (Jag1) exhibit head-shaking behavior indicative
181  Delta-like ligand 4 (Dll4) while repressing Jagged1 (Jag1) expression.
182 ecifically target Notch1, Notch2, Notch3, or jagged1 (Jag1) in a mouse model of primary liver cancer
183 his work investigates the role of Notch2 and Jagged1 (Jag1) in secondary fiber cell differentiation u
184                             The Notch ligand Jagged1 (Jag1) is essential for vascular remodeling and
185                             The Notch ligand Jagged1 (Jag1) is expressed in the prosensory domains, a
186 NOTCH signaling induced by Delta1 (DLL1) and Jagged1 (JAG1) NOTCH ligands is modulated by the beta3N-
187 ctivating FGFR1 upregulates the Notch ligand Jagged1 (Jag1) on neighboring ECs.
188 with an engineered, high-affinity variant of Jagged1 (Jag1) reveals a binding interface that extends
189 d endothelial cells provide the Notch ligand Jagged1 (Jag1) to neighboring breast CSCs, leading to No
190 tasis effectors, including Tenascin C (Tnc), Jagged1 (Jag1), and Epiregulin (Ereg).
191  out two of these ligands, Delta1 (Dll1) and Jagged1 (Jag1), in the mouse ear.
192 ptional repressor Hey1, and the Notch-ligand Jagged1 (Jag1), was induced by TGF-beta at the onset of
193  gene for the Notch signaling pathway ligand Jagged1 (JAG1), which are found in 94% of patients.
194  Most cases are associated with mutations in JAGGED1 (JAG1), which encodes a Notch ligand, although i
195  bulk and clonal cultures, we show here that Jagged1 (JAG1)-mediated Notch signaling allows human ETP
196 nd gain-of-function approaches, we show that Jagged1 (JAG1)-mediated Notch signaling is both required
197 ediated mechanism that elevated NOTCH ligand Jagged1 (JAG1).
198 n, E-cadherin, Pdx1, Nkx6.1, Notch1, Notch2, Jagged1, Jagged2, Hes1), hereby describing the kinetics
199            In vitro VSMC lentivirus-mediated Jagged1 knockdown, confocal localization analysis, and c
200                                 Heterozygous Jagged1 knockout mice, a model for Alagille Syndrome (AG
201 Fbeta1-mediated Smad3/Smad2 phosphorylation; Jagged1 level was coordinately reduced.
202 rebral vessels feature reduced Pdgfrbeta and Jagged1 levels and impaired proliferation.
203                       Shear stress increases Jagged1 levels and Notch activation in a vimentin-depend
204                  Neurl1 expression decreases Jagged1 levels in cells and blocks signaling from Jagged
205                                     Ex vivo, Jagged1 ligand activates Notch in neural crest explants
206 ES1, the Notch2 and Notch1 receptors and the Jagged1 ligand are induced in meningiomas of all grades,
207 ome Notch signaling components including the Jagged1 ligand are upregulated in advanced human prostat
208 ignaling using Notch intracellular domain or Jagged1 ligand induced smooth muscle alpha-actin (SM act
209                         Notch signaling, via Jagged1 ligand on Sus cells and Notch1 and Notch2 recept
210 active Notch1 in presence of myocardin or by Jagged1 ligand stimulation.
211 in immunoprecipitation studies revealed both Jagged1 ligand- and Notch1-enhanced myocardin/SRF comple
212 inished expression of PDGF receptor beta and JAGGED1 ligand.
213 earing loss in one patient with heterozygous JAGGED1 loss, and a diversity of conductive and sensorin
214 vival, transcriptional profiling showed that JAGGED1 maintains genes critical for mitochondrial funct
215                                    Moreover, Jagged1 may play a role in CNS homeostasis because murin
216 es the dystrophic phenotype, suggesting that Jagged1 may represent a target for DMD therapy in a dyst
217 ed in significant changes in both Delta1 and Jagged1 mediated signaling, but mutations in less highly
218 inhibition of growth depended on the loss of Jagged1-mediated Notch activation, with signaling throug
219                                Disruption of Jagged1-mediated notch signaling causes a loss of some s
220 h inhibition in cardiac neural crest impairs Jagged1 messenger RNA expression and results in deficien
221  crest explants and results in activation of Jagged1 messenger RNA, a response that is blocked by Not
222 omain implicated in membrane recognition and Jagged1 missense mutations, which affect these loops and
223 suppressed Jagged1 effects and expression of Jagged1 mRNA as well.
224                                              JAGGED1 mutations cause Alagille syndrome, comprising a
225 e Syndrome (ALGS), a disease associated with JAGGED1 mutations.
226 ly half of AGS patients, many of which carry JAGGED1 mutations.
227            Prostate specific upregulation of Jagged1 neither interferes with prostate epithelial home
228 gh percentage of lung cancer lines expressed Jagged1, Notch receptors, and their transcriptional targ
229       Genetic or pharmacologic disruption of Jagged1, Notch, alphavbeta3, or VWF suppresses VSMC cove
230         Our data support the hypothesis that Jagged1-Notch signaling conveys a lateral inductive sign
231                                      Reduced Jagged1-Notch transactivation strength disrupts lateral
232  identifies APEX1 as a positive regulator of Jagged1/Notch activity and suggests that it is a potenti
233 e data suggest the essential role of miR-26a/Jagged1/Notch pathway in regulating the stem cell-like t
234 nd functions as an upstream activator in the Jagged1/Notch signaling pathway.
235 tion or respecification, likely due to local JAGGED1/NOTCH signaling.
236 in colon cancers that exhibit high levels of Jagged1/Notch signaling.
237 e effects are mediated through inhibition of Jagged1/Notch signaling.
238 nt activation, followed by delayed, indirect Jagged1/Notch-dependent activation.
239 nsisting of immediate-early Smad3-dependent, Jagged1/Notch-independent activation, followed by delaye
240  DAPT or by inhibiting the function of Dll4, Jagged1, Notch1, or the canonical Notch transcription fa
241                                     Enhanced Jagged1-Notch1 signaling in KO mice via reduced beta-sec
242 d to TGF-beta1 restricted OPC maturation via Jagged1-Notch1 signaling.
243  and promoter activity assays, we found that Jagged1/Notch1 signaling increased ETB(R) expression ind
244                These results identify a BRD4/Jagged1/Notch1 signaling pathway that is critical for di
245  involving BRD4 and the ligand/receptor pair Jagged1/Notch1 that sustains triple-negative breast canc
246                                 We find that Jagged1-Notch2 signaling functions early to pattern the
247     Our findings reveal deep conservation of Jagged1-Notch2 signaling in patterning the pharyngeal ar
248     Here we show a conserved requirement for Jagged1-Notch2 signaling in patterning the stapes and in
249                                      Whereas Jagged1-Notch2 signaling is known to pattern the sensori
250         Increased expression of Notch ligand Jagged1 occurs in several human malignancies, including
251 ractions between Notch on CD4(+) T cells and Jagged1 on APCs in the initiation of IL-4 production and
252  cell (VSMC) recognition of the Notch ligand Jagged1 on endothelial cells leads to expression of inte
253 opes from the cytoplasmic tail of the ligand Jagged1, one in the intracellular membrane proximal regi
254 her demonstrate that miR-26a directly target Jagged1, one of the Notch ligand, and that its tumor sup
255 d, blockade of Notch1 signaling with an anti-Jagged1 or a blocking anti-Notch1 Ab inhibits Treg suppr
256             Activation of Notch receptors by Jagged1 or forced expression of the constitutively activ
257                         Mutations in Notch2, Jagged1 or homologs of the Hairy-related transcriptional
258 show that either absence of the Notch ligand Jagged1 or inhibition of Notch signaling in second heart
259 ith fibroblasts expressing the Notch ligands Jagged1 or Jagged2.
260                                 Mice lacking Jagged1 or Notch2 in neural crest-derived cells (NCCs) o
261 nant mutations of the canonical Notch ligand Jagged1 (or JAG1) as a cause of peripheral nerve disease
262         Functional analyses demonstrate that Jagged1 overexpression ameliorates the dystrophic phenot
263                                Collectively, Jagged1 overexpression does not significantly accelerate
264                                 In addition, Jagged1 overexpression upregulates Tgfbeta signaling in
265 ted by intravitreal or systemic injection of Jagged1 peptide and gamma secretase inhibitor DAPT, resp
266                                              Jagged1 peptide treatment of Akt1DeltaEC;Akt2KO mice and
267 )/3C(low) LCLs expressed increased levels of Jagged1 protein and were able to more efficiently induce
268 tion between TLR and Notch pathways leads to Jagged1-RBP-J-mediated autoamplification of Notch signal
269 ide treatment of Akt1DeltaEC;Akt2KO mice and Jagged1 re-expression in Akt-deficient endothelium resto
270 n the developing CNS, Notch1 and its ligand, Jagged1, regulate oligodendrocyte differentiation and my
271 feration and differentiation in IFE, whereas Jagged1 regulates hair follicle differentiation.
272 estingly, diseased cells exhibited augmented Jagged1 release and Notch1 activation after TLR4 stimula
273                                Tumor-derived Jagged1 represents a central node in mediating tumor-str
274  Finally, auditory phenotyping revealed that JAGGED1's function in supporting cells is necessary for
275 cell signaling (e.g., down-regulation of the Jagged1 signaling pathway).
276 drocytes through the inhibition of the Notch/Jagged1 signaling pathway.
277 EGF repeat 12 resulted in loss of Delta1 and Jagged1 signaling, while mutation of the O-fucose site i
278 sulted in hyperactivation of both Delta1 and Jagged1 signaling.
279 ble extracellular domain of the Notch ligand Jagged1 (sJ1) inhibits Notch signaling and induces FGF1
280 ith crosslinked soluble delta-like 4 (sDll4)/Jagged1 (sJag1) or constitutive expression of the Notch1
281 hereas the transfer of BMDC transfected with Jagged1 small interfering RNA (siRNA) cells into WT or I
282 They also bound directly to the Notch ligand Jagged1, suggesting that their mechanism of action invol
283 cause murine astrocytes specifically express Jagged1 that is up-regulated by TGF-beta, whereas IFN-ga
284                            In the absence of Jagged1, the anterior growth and equatorial transition z
285        With the exception of the full-length Jagged1 transfectant, all other cell lines, including th
286 st-derived Jagged1 using osteoblast-specific Jagged1 transgenic mouse model.
287                             The Notch ligand Jagged1 triggers differentiation when presented on an ad
288                                     However, Jagged1 upregulation results in increased inflammatory f
289 sis-promoting function of osteoblast-derived Jagged1 using osteoblast-specific Jagged1 transgenic mou
290    Concurrent signaling induced by OX40L and Jagged1 via OX40 and Notch3 receptors expressed on Tregs
291                                    Increased Jagged1 was also present in intestinal tumors of Apc(163
292                 Herein, we demonstrated that Jagged1 was constitutively processed in colorectal cance
293 use tumors Notch signaling was elevated when Jagged1 was elevated.
294 ibrosus, mRNA expression of the Notch ligand Jagged1 was induced by hypoxia, while Jagged2 mRNA expre
295                                 NOTCH ligand JAGGED1 was overexpressed and associated with loss of Cp
296 NOTCH3 expression, and endothelial-expressed JAGGED1 was required for its induction.
297    The in vivo expression of Dll4 but not of Jagged1 was well correlated with expression of IL-33 in
298                          Notch1, Notch3, and Jagged1 were immunolocalized throughout the conjunctival
299 NA-205 (miR-205), is repressed by the ligand jagged1, which is secreted from the tumor stroma to prom
300 to an active peptide from the Notch1 ligand, Jagged1, with increased levels of differentiation marker

 
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