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1 ot Radical) inhibited Notch1 activation from Jagged1.
2 in signaling of a mammalian Serrate homolog, Jagged1.
3 of notch activity persists in the absence of Jagged1.
4 s disrupting interactions between Notch3 and Jagged1.
5 an epistatic relationship between Twist1 and Jagged1.
6  augments the interaction between Notch3 and Jagged1.
7 ns in Notch signaling pathway genes, usually JAGGED1.
8 th elevated Wnt signaling displayed elevated Jagged1.
9            TSP2 binds directly to Notch3 and Jagged1.
10 he supporting cells exhibit the Notch ligand Jagged1.
11 ated in tumor angiogenesis, Delta-like 4 and Jagged1.
12 ilization of a soluble extracellular form of Jagged1.
13 -2, was unable to facilitate the shedding of Jagged1.
14  the epidermal growth factor-like repeats of Jagged1.
15 , face, and skeleton, caused by mutations in Jagged1.
16 for Treg expansion and required signaling by Jagged1.
17 ded by Notch1 positive dermal cells, induces Jagged1.
18 1c(+)B220(-)PDCA-1(-), and had low levels 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                            Here we show that JAGGED1, a NOTCH receptor ligand, is significantly more
29 ssed endothelin receptor type B (ETB(R)) and Jagged1, a Notch1 receptor ligand.
30                       Administration of anti-Jagged1 Ab exacerbated clinical disease while that of an
31 sts that express soluble forms of Delta1 and Jagged1 accelerate tumorigenicity in vivo.
32 tors of vascular cells are down-regulated by Jagged1 activation of the Notch1 pathway.
33 dditional support to the proposal that Notch/Jagged1 activity is required for neural stem cell mainte
34 dies will investigate the mechanism in which Jagged1 acts in a cell autonomous and cell non-autonomou
35 ere we show that conditional inactivation of Jagged1 affects neural stem cell maintenance and prolife
36 h hypomorphic mutations in the gene encoding Jagged1 (Alagille syndrome) failed to mount appropriate
37                   Mesodermal inactivation of Jagged1 also results in changes in the identity of sutur
38 nd that the DSL (Delta/Serrate/LAG2) protein Jagged1, an activating ligand for Notch receptor signali
39 e-tune liver inflammation by upregulation of Jagged1 and activation of Notch signaling in Th1 cells.
40 stem cells associated with increased stromal Jagged1 and Angiopoietin-1 expression and reduced primit
41  in EGF12 substantially increases binding to Jagged1 and Delta-like 1 (DLL1) ligands.
42 d monocyte-derived DCs express Notch ligands Jagged1 and Delta-like4, whereas naive CD8(+) T cells ex
43                  We investigated the role of Jagged1 and Delta1 in experimental autoimmune encephalom
44 ound that soluble forms of the Notch ligands Jagged1 and Delta1 induced fibroblast growth factor rece
45 ssion of the NOTCH receptor and its ligands, Jagged1 and Delta1.
46 ncreased affinity of this region for ligands Jagged1 and DLL1.
47  Manic Fringe inhibit Notch1 activation from Jagged1 and enhance activation from Delta-like 1, Radica
48 sed 3T3-L1 preadipocytes to the Notch ligand Jagged1 and found that differentiation was significantly
49 ls of costimulatory molecules, Notch ligands Jagged1 and Jagged2, and CD11b, and produced more Ifnb a
50                          Interaction between Jagged1 and MAGP-2 requires the epidermal growth factor-
51 lls and COS-7 cells coexpressing full-length Jagged1 and MAGP-2.
52 malformations caused by mutations in Serrate/Jagged1 and Notch signaling components.
53 ) enhances Notch signaling and binds to both Jagged1 and Notch3 ectodomains, potentially bridging two
54 owed enhanced expression of the Notch ligand Jagged1 and significantly increased receptor density of
55 e primitive state, and combined signals from Jagged1 and TGF-beta are important in controlling its qu
56 nt by the demonstration of overexpression of Jagged1 and the downstream Notch pathway member Hes1.
57 d the body of evidence supporting a role for Jagged1 and the Notch signaling pathway in vascular deve
58 rs Notch3 and Notch4, Notch ligands Dll4 and Jagged1, and activated Notch receptors in contrast to un
59 s an association between levels of IL6 mRNA, Jagged1, and Ang2.
60 acellular domain of Notch1 (NIC), its ligand Jagged1, and its target gene Hes1, which were associated
61 f Zeste homologue 2 (EZH2), the Notch ligand Jagged1, and PTK2 were elevated 3- to 4.3-fold in tumor-
62                                 Lastly, both Jagged1- and Delta1-derived tumors contained phenotypica
63 es, and evaluated their ability to transduce Jagged1- and Delta1-mediated signaling in a cell-based a
64      Here we show that Notch1 and its ligand Jagged1 are present at the synapse, and that Notch signa
65 ies showed that Notch1 ligands, particularly Jagged1, are present on Tregs and that, indeed, blockade
66 scent arterial endothelial tube and identify Jagged1 as a direct Notch target.
67   Here we identified the Notch family member Jagged1 as a physiological ligand for CD46.
68 tes involved stimulation of the Notch ligand Jagged1 as well as angiopoietin2 (Ang2).
69  signaling did not correlate with changes in Jagged1 binding as found for Delta1.
70 lthough fringe glycosylation does not reduce Jagged1 binding to Notch1, the resultant ligand-receptor
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                            Furthermore, high JAGGED1 expression in a subset of clinically localized t
108 Cs and enhanced HSPC expansion by increasing Jagged1 expression in BM stromal cells.
109 es, based on immunohistochemical analysis of JAGGED1 expression in human tumor samples from 154 men.
110 ne metastasis to chemotherapy, which induces Jagged1 expression in osteoblasts to provide a survival
111 Cs during remyelination through induction of Jagged1 expression in reactive astrocytes.
112                           In Twist1 mutants, Jagged1 expression in the suture is reduced substantiall
113                                  Conversely, Jagged1 expression is markedly induced by TLR ligation.
114 the mutant dorsal RPE domains, where ectopic JAGGED1 expression may partially counteract the effects
115  cytokines, indicating the critical role for Jagged1 expression on APCs.
116                                              Jagged1 expression on endothelium activates Notch in vas
117              Moreover, in patients, BRD4 and Jagged1 expression positively correlated with the presen
118                                 TLRs induced Jagged1 expression rapidly and independently of new prot
119 r, it remains undetermined whether increased Jagged1 expression reflects a cause for or a consequence
120                      Strikingly, TLR-induced Jagged1 expression was strongly dependent on the Notch m
121 is hypothesis, we found that Jagged2 but not Jagged1 expression, correlates with the ability of DCs t
122 k loop that includes both autoregulation and JAGGED1 expression.
123 eas IFN-gamma, TNF-alpha, and IL-17 decrease Jagged1 expression.
124 JAG1 mouse model that enables spatiotemporal Jagged1 expression.
125          MAGP-2 was found complexed with the Jagged1 extracellular domain shed from 293T cells and CO
126                       MAGP-2 shedding of the Jagged1 extracellular domain was decreased by the metall
127 mooth muscle, and Notch target genes such as Jagged1 fail to activate normally.
128     In vivo treatment of wild-type mice with Jagged1-Fc enhanced AHR and airway inflammation, whereas
129               In contrast, administration of Jagged1-Fc protected from disease, that of Delta1-Fc exa
130                               Treatment with Jagged1-Fc was associated with increased IL-10-producing
131  interactions through excess soluble ligand, Jagged1-Fc.
132 equirement for intact vSMC Notch signals via JAGGED1 for efficient EC Notch1 receptor activation and
133 animals reveals that increased expression of Jagged1 gene, a known regulator of the Notch signaling p
134 15 evolutionary conserved regions within the Jagged1 genomic locus and identify a single Notch respon
135                    Manipulation of Delta1 or Jagged1 had no effect on the frequency of Th17 cells or
136                                 In contrast, Jagged1 has been described as a Notch ligand expressed i
137 the Notch1 decoy, which blocks both Dll4 and Jagged1 has been recently shown to restrict tumor vessel
138 h, Dll4-Notch signaling is enhanced, whereas Jagged1 has weak signaling capacity and competes with Dl
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 autonomous and non-autonomous requirement of Jagged1 in a cell lineage-specific approach during midfa
142  are multiple cellular sources of its ligand Jagged1 in a rodent model of remyelination.
143 R, expression ratios of Notch1, Notch 3, and Jagged1 in dry eye were 0.43, 0.56, and 0.50, respective
144 nced the expression of Notch3 and its ligand Jagged1 in human breast cancer cell lines.
145 ration that heterozygous loss of function of JAGGED1 in humans can cause Alagille syndrome, which has
146 his study demonstrates that thrombin cleaves Jagged1 in its extracellular domain.
147 could promote its own expression and that of JAGGED1 in mural cells.
148                                      Loss of Jagged1 in neural crest impairs vascular smooth muscle d
149                        The overexpression of Jagged1 in PAR1 null cells results in a rapid thrombin-i
150                                     Deleting Jagged1 in the CNC using Wnt1-cre; Jag1 Flox/Flox recapi
151 s study design determines the requirement of Jagged1 in the cranial neural crest (CNC) cells, which e
152 tional gene targeting to examine the role of Jagged1 in the development of the skull vault.
153 ysical engagement of Notch3 and VSMC-derived Jagged1 in the interior of the same cell.
154                 We show that inactivation of Jagged1 in the mesodermal compartment of the coronal sut
155     We conditionally deleted both alleles of Jagged1 in the murine pancreas using Cre-loxP technology
156 ecapitulate aortic arch artery expression of Jagged1 in transgenic mice.
157 ermore, APEX1 expression was associated with Jagged1 in various colon cancer cell lines and in tissue
158 y two specific mutations that reduce ligand (JAGGED1) induced NOTCH1 signaling.
159 esults showed a critical role for OX40L- and Jagged1-induced cosignaling in GM-BMDC-induced Treg expa
160 with low levels of Slc35c2, both Delta1- and Jagged1-induced Notch signaling were reduced, and the fu
161  Notch ligands and low levels of Delta1- and Jagged1-induced Notch signaling.
162                Interestingly, suppression of Jagged1-induced Notch1 signaling did not correlate with
163                                     Although Jagged1-induced signaling was suppressed by LFng and MFn
164 e of bone metastases, mediated by osteoblast Jagged1-induced tumor Notch signaling.
165 h TCR-alphabeta and -gammadelta development, Jagged1 induces mainly alphabeta-lineage differentiation
166                                              Jagged1 induction was augmented by IFN-gamma, was partia
167              Finally, recombinant Notch3 and Jagged1 interact with the LRP1 85-kDa B-chain, a subunit
168 was required for transfer, in which a Notch2-Jagged1 interaction played a decisive role.
169                           Here, we show that Jagged1 is a direct Notch target in smooth muscle, resul
170          Here, we show that the Notch ligand Jagged1 is a potent proangiogenic regulator in mice that
171                Our results thus suggest that Jagged1 is an effector of Twist1 in coronal suture devel
172                                        Thus, Jagged1 is an RBP-J target gene that is activated in a b
173                          We demonstrate that Jagged1 is expressed in a layer of mesoderm-derived sutu
174 ing conditional gene targeting, we show that Jagged1 is required for lens fiber cell genesis, particu
175                  In this study, we show that Jagged1 is up-regulated on bone marrow-derived dendritic
176 dritic cells and B cells after priming while Jagged1 is up-regulated only on dendritic cells.
177 s for missense mutations of the Notch ligand Jagged1 (Jag1) exhibit head-shaking behavior indicative
178  Delta-like ligand 4 (Dll4) while repressing Jagged1 (Jag1) expression.
179 ecifically target Notch1, Notch2, Notch3, or jagged1 (Jag1) in a mouse model of primary liver cancer
180 his work investigates the role of Notch2 and Jagged1 (Jag1) in secondary fiber cell differentiation u
181                             The Notch ligand Jagged1 (Jag1) is essential for vascular remodeling and
182                             The Notch ligand Jagged1 (Jag1) is expressed in the prosensory domains, a
183 NOTCH signaling induced by Delta1 (DLL1) and Jagged1 (JAG1) NOTCH ligands is modulated by the beta3N-
184 ctivating FGFR1 upregulates the Notch ligand Jagged1 (Jag1) on neighboring ECs.
185 with an engineered, high-affinity variant of Jagged1 (Jag1) reveals a binding interface that extends
186 tasis effectors, including Tenascin C (Tnc), Jagged1 (Jag1), and Epiregulin (Ereg).
187  out two of these ligands, Delta1 (Dll1) and Jagged1 (Jag1), in the mouse ear.
188 ptional repressor Hey1, and the Notch-ligand Jagged1 (Jag1), was induced by TGF-beta at the onset of
189  gene for the Notch signaling pathway ligand Jagged1 (JAG1), which are found in 94% of patients.
190  Most cases are associated with mutations in JAGGED1 (JAG1), which encodes a Notch ligand, although i
191  bulk and clonal cultures, we show here that Jagged1 (JAG1)-mediated Notch signaling allows human ETP
192 nd gain-of-function approaches, we show that Jagged1 (JAG1)-mediated Notch signaling is both required
193 ediated mechanism that elevated NOTCH ligand Jagged1 (JAG1).
194 n, E-cadherin, Pdx1, Nkx6.1, Notch1, Notch2, Jagged1, Jagged2, Hes1), hereby describing the kinetics
195 ) receptors and their transmembrane ligands, Jagged1 (JI) and Delta1 (Dl1), mediate signaling events
196            In vitro VSMC lentivirus-mediated Jagged1 knockdown, confocal localization analysis, and c
197                                 Heterozygous Jagged1 knockout mice, a model for Alagille Syndrome (AG
198 Fbeta1-mediated Smad3/Smad2 phosphorylation; Jagged1 level was coordinately reduced.
199 rebral vessels feature reduced Pdgfrbeta and Jagged1 levels and impaired proliferation.
200                  Neurl1 expression decreases Jagged1 levels in cells and blocks signaling from Jagged
201                                     Ex vivo, Jagged1 ligand activates Notch in neural crest explants
202 ES1, the Notch2 and Notch1 receptors and the Jagged1 ligand are induced in meningiomas of all grades,
203 ome Notch signaling components including the Jagged1 ligand are upregulated in advanced human prostat
204 ignaling using Notch intracellular domain or Jagged1 ligand induced smooth muscle alpha-actin (SM act
205                         Notch signaling, via Jagged1 ligand on Sus cells and Notch1 and Notch2 recept
206 active Notch1 in presence of myocardin or by Jagged1 ligand stimulation.
207 in immunoprecipitation studies revealed both Jagged1 ligand- and Notch1-enhanced myocardin/SRF comple
208 inished expression of PDGF receptor beta and JAGGED1 ligand.
209 hile inhibiting signaling induced by Serrate/Jagged1 ligands.
210 earing loss in one patient with heterozygous JAGGED1 loss, and a diversity of conductive and sensorin
211  progression and metastasis and suggest that JAGGED1 may be a useful marker in distinguishing indolen
212                                    Moreover, Jagged1 may play a role in CNS homeostasis because murin
213 es the dystrophic phenotype, suggesting that Jagged1 may represent a target for DMD therapy in a dyst
214 ed in significant changes in both Delta1 and Jagged1 mediated signaling, but mutations in less highly
215 inhibition of growth depended on the loss of Jagged1-mediated Notch activation, with signaling throug
216                                Disruption of Jagged1-mediated notch signaling causes a loss of some s
217 h inhibition in cardiac neural crest impairs Jagged1 messenger RNA expression and results in deficien
218  crest explants and results in activation of Jagged1 messenger RNA, a response that is blocked by Not
219 omain implicated in membrane recognition and Jagged1 missense mutations, which affect these loops and
220 suppressed Jagged1 effects and expression of Jagged1 mRNA as well.
221                                              JAGGED1 mutations cause Alagille syndrome, comprising a
222 ly half of AGS patients, many of which carry JAGGED1 mutations.
223 e Syndrome (ALGS), a disease associated with JAGGED1 mutations.
224            Prostate specific upregulation of Jagged1 neither interferes with prostate epithelial home
225 gh percentage of lung cancer lines expressed Jagged1, Notch receptors, and their transcriptional targ
226       Genetic or pharmacologic disruption of Jagged1, Notch, alphavbeta3, or VWF suppresses VSMC cove
227         Our data support the hypothesis that Jagged1-Notch signaling conveys a lateral inductive sign
228  identifies APEX1 as a positive regulator of Jagged1/Notch activity and suggests that it is a potenti
229 strate functional roles for Smad3, Hey1, and Jagged1/Notch in mediating TGF-beta-induced EMT.
230 e data suggest the essential role of miR-26a/Jagged1/Notch pathway in regulating the stem cell-like t
231 nd functions as an upstream activator in the Jagged1/Notch signaling pathway.
232 e effects are mediated through inhibition of Jagged1/Notch signaling.
233 tion or respecification, likely due to local JAGGED1/NOTCH signaling.
234 in colon cancers that exhibit high levels of Jagged1/Notch signaling.
235  new mechanism for functional integration of Jagged1/Notch signalling and coordinated activation of t
236 nt activation, followed by delayed, indirect Jagged1/Notch-dependent activation.
237 nsisting of immediate-early Smad3-dependent, Jagged1/Notch-independent activation, followed by delaye
238  DAPT or by inhibiting the function of Dll4, Jagged1, Notch1, or the canonical Notch transcription fa
239                                     Enhanced Jagged1-Notch1 signaling in KO mice via reduced beta-sec
240 d to TGF-beta1 restricted OPC maturation via Jagged1-Notch1 signaling.
241  and promoter activity assays, we found that Jagged1/Notch1 signaling increased ETB(R) expression ind
242                These results identify a BRD4/Jagged1/Notch1 signaling pathway that is critical for di
243  involving BRD4 and the ligand/receptor pair Jagged1/Notch1 that sustains triple-negative breast canc
244                                 We find that Jagged1-Notch2 signaling functions early to pattern the
245     Our findings reveal deep conservation of Jagged1-Notch2 signaling in patterning the pharyngeal ar
246     Here we show a conserved requirement for Jagged1-Notch2 signaling in patterning the stapes and in
247                                      Whereas Jagged1-Notch2 signaling is known to pattern the sensori
248 ractions between Notch on CD4(+) T cells and Jagged1 on APCs in the initiation of IL-4 production and
249  cell (VSMC) recognition of the Notch ligand Jagged1 on endothelial cells leads to expression of inte
250 opes from the cytoplasmic tail of the ligand Jagged1, one in the intracellular membrane proximal regi
251 her demonstrate that miR-26a directly target Jagged1, one of the Notch ligand, and that its tumor sup
252 d, blockade of Notch1 signaling with an anti-Jagged1 or a blocking anti-Notch1 Ab inhibits Treg suppr
253          OP9 stromal cells expressing either Jagged1 or Delta1 inhibit the differentiation of DN1 thy
254 w that 2 different classes of Notch ligands, Jagged1 or Delta1, transmit distinct signals to T-cell p
255             Activation of Notch receptors by Jagged1 or forced expression of the constitutively activ
256                         Mutations in Notch2, Jagged1 or homologs of the Hairy-related transcriptional
257 show that either absence of the Notch ligand Jagged1 or inhibition of Notch signaling in second heart
258 ith fibroblasts expressing the Notch ligands Jagged1 or Jagged2.
259                                 Mice lacking Jagged1 or Notch2 in neural crest-derived cells (NCCs) o
260         Functional analyses demonstrate that Jagged1 overexpression ameliorates the dystrophic phenot
261                                Collectively, Jagged1 overexpression does not significantly accelerate
262                                 In addition, Jagged1 overexpression upregulates Tgfbeta signaling in
263 ted by intravitreal or systemic injection of Jagged1 peptide and gamma secretase inhibitor DAPT, resp
264                                              Jagged1 peptide treatment of Akt1DeltaEC;Akt2KO mice and
265 )/3C(low) LCLs expressed increased levels of Jagged1 protein and were able to more efficiently induce
266 gs support a model in which dysregulation of JAGGED1 protein levels plays a role in prostate cancer p
267 tion between TLR and Notch pathways leads to Jagged1-RBP-J-mediated autoamplification of Notch signal
268 ide treatment of Akt1DeltaEC;Akt2KO mice and Jagged1 re-expression in Akt-deficient endothelium resto
269 n the developing CNS, Notch1 and its ligand, Jagged1, regulate oligodendrocyte differentiation and my
270 feration and differentiation in IFE, whereas Jagged1 regulates hair follicle differentiation.
271 estingly, diseased cells exhibited augmented Jagged1 release and Notch1 activation after TLR4 stimula
272                                Tumor-derived Jagged1 represents a central node in mediating tumor-str
273 cell signaling (e.g., down-regulation of the Jagged1 signaling pathway).
274 drocytes through the inhibition of the Notch/Jagged1 signaling pathway.
275 EGF repeat 12 resulted in loss of Delta1 and Jagged1 signaling, while mutation of the O-fucose site i
276 sulted in hyperactivation of both Delta1 and Jagged1 signaling.
277                         During these stages, Jagged1 signals can influence the differentiation of imm
278 gged1 signals, T-cell progenitors respond to Jagged1 signals during a brief window of their developme
279  marrow-derived stem cells do not respond to Jagged1 signals, T-cell progenitors respond to Jagged1 s
280 ble extracellular domain of the Notch ligand Jagged1 (sJ1) inhibits Notch signaling and induces FGF1
281 ith crosslinked soluble delta-like 4 (sDll4)/Jagged1 (sJag1) or constitutive expression of the Notch1
282 hereas the transfer of BMDC transfected with Jagged1 small interfering RNA (siRNA) cells into WT or I
283 They also bound directly to the Notch ligand Jagged1, suggesting that their mechanism of action invol
284 cause murine astrocytes specifically express Jagged1 that is up-regulated by TGF-beta, whereas IFN-ga
285                            In the absence of Jagged1, the anterior growth and equatorial transition z
286        With the exception of the full-length Jagged1 transfectant, all other cell lines, including th
287 st-derived Jagged1 using osteoblast-specific Jagged1 transgenic mouse model.
288 hanced signaling induced by either Delta1 or Jagged1, underscoring the diversity of mammalian fringe
289                                     However, Jagged1 upregulation results in increased inflammatory f
290 sis-promoting function of osteoblast-derived Jagged1 using osteoblast-specific Jagged1 transgenic mou
291    Concurrent signaling induced by OX40L and Jagged1 via OX40 and Notch3 receptors expressed on Tregs
292                                    Increased Jagged1 was also present in intestinal tumors of Apc(163
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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