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anti-Human JAG1 Antikörper:
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Human Monoclonal JAG1 Primary Antibody für CyTOF, FACS - ABIN4900205
Kibbie, Teles, Wang, Hong, Montoya, Krutzik, Lee, Kwon, Modlin, Cruz: Jagged1 Instructs Macrophage Differentiation in Leprosy. in PLoS pathogens 2016
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Rat (Rattus) Polyclonal JAG1 Primary Antibody für CyTOF, ELISA (Capture) - ABIN4900585
Stahl, Uemura, Ge, Shi, Tashima, Stanley: Roles of Pofut1 and O-fucose in mammalian Notch signaling. in The Journal of biological chemistry 2008
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Mouse (Murine) Monoclonal JAG1 Primary Antibody für IHC (fro), FACS - ABIN2480076
McKusick: The Human Genome Project and clinical medicine. in Hospital practice (Office ed.) 1991
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Human Monoclonal JAG1 Primary Antibody für FACS - ABIN4897050
Hoare, Ito, Kang, Weekes, Matheson, Patten, Shetty, Parry, Menon, Salama, Antrobus, Tomimatsu, Howat, Lehner, Zender, Narita: NOTCH1 mediates a switch between two distinct secretomes during senescence. in Nature cell biology 2017
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Human Polyclonal JAG1 Primary Antibody für FM, IHC - ABIN129524
Yabe, Matsumoto, Tsurumoto, Shindo: Immunohistological localization of Notch receptors and their ligands Delta and Jagged in synovial tissues of rheumatoid arthritis. in Journal of orthopaedic science : official journal of the Japanese Orthopaedic Association 2005
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Human Polyclonal JAG1 Primary Antibody für ICC, IF - ABIN269362
Okamoto, Matsuda, Joetham, Lucas, Domenico, Yasutomo, Takeda, Gelfand: Jagged1 on dendritic cells and Notch on CD4+ T cells initiate lung allergic responsiveness by inducing IL-4 production. in Journal of immunology (Baltimore, Md. : 1950) 2009
Human Polyclonal JAG1 Primary Antibody für ELISA, ICC - ABIN337168
Siar, Ha, Aung, Nakano, Tsujigiwa, Nagatsuka, Ng, Kawakami: Immunolocalization of notch signaling protein molecules in a maxillary chondrosarcoma and its recurrent tumor. in European journal of medical research 2010
Human Polyclonal JAG1 Primary Antibody für IHC, IHC (p) - ABIN4327850
Gunin, Petrov, Golubtzova, Vasilieva, Kornilova: Age-related changes in angiogenesis in human dermis. in Experimental gerontology 2014
TR3/Nur77 regulated the expression of DLL4 and Jagged1 in culture endothelial cells. DLL4 and Jagged1 play important roles in the angiogenic responses induced by TR3/Nur77.
miR-539 was downregulated in WT tissues. And miR-539 inhibited the progression of WT through negatively regulating JAG1-Notch1/3 expression. MiR-539 should be a valuable indicator of the diagnosis and prognosis of WT.
Synthetic/secretor aortic smooth muscle cells are apoptosis-prone, and the accruing thrombin-cleaved Jagged1 fragments counteract the otherwise useful effects of Jagged1/NOTCH1 signalling, thus hampering tissue homeostasis/remodelling, and aortic smooth muscle cells adhesion, differentiation, and migration.
Bronchial epithelial cells had the potential to promote the differentiation of Th2 lymphocytes through Jagged-1/Notch-1 signaling.
treatment of Placenta-derived mesenchymal stromal cells with soluble JAG1 significantly enhanced chondrogenesis in culture
Jag1 and Notch2 play a key role in kidney fibrosis development by regulating Tfam expression and metabolic reprogramming.
The JAG1 SNP rs2235811 was associated with the BMD of the total body under the dominant inheritance model (p=0,024). rs2235811 might contribute to the variation in bone mineral density in women from northern Mexico. No significant associations were found for rs6514116, rs2273061, or rs6040061, although some trends were seen.
This study identified a total of 7 JAG1 variants in patients with Alagille syndrome as well as 2 interstitial deletions involving this gene, and among them, the variants c.1977G>A (p.Trp659* ) and c.1106_1107delCC (p.Pro369fs) as well as the 9.24 Mb chromosomal interstitial deletion had not been reported previously.
This study demonstrates that stimulation of macrophages by tumor cell NRG1 can enhance transendothelial migration and intravasation. We also demonstrate that this effect is due to induction of macrophage JAG1, an important ligand of the Notch signaling pathway.
JAG1-induced invasion of Glioma-Initiating Cells through activation of NF-kappa B(p65) pathway.
Four families with Midaortic Syndrome were found to have a likely causal mutation in JAG1.
higher JAG1 expression was found in MCPyV-negative than in MCPyV-positive MCC (p<0.001), and NOTCH3 expression was higher in MCPyV-positive MCC (p=0.062). Kaplan-Meier and multivariate analyses showed that patients with MCC with higher NOTCH3 expression had better overall survival than otherwise (p=0.001 and p=0.033, respectively).
We observe similar stapes defects and hearing loss in one patient with heterozygous JAGGED1 loss, and a diversity of conductive and sensorineural hearing loss in nearly half of Alagille Syndrome patients, many of which carry JAGGED1 mutations
MFNG imposes a negative correlation between Jag1 and Notch, being high Jag1 in the absence of MFNG predictive of poor prognosis.
MiR-26b-5p acts as a tumor suppressor through suppressing cells proliferation and inducing cells apoptosis via directly targeting JAG1 in multiple myeloma
miR-30d may improve TGF-beta1-induced pulmonary fibrosis through direct binding to the 3'UTR of JAG1 and blocking JAG1/Notch signaling
these two lossoffunction JAG1 mutations may be associated with Alagille syndrome manifestations in these patients
Results provide evidence that JAG1 is downregulated by microRNA-128 binding its 3'UTR in glioma cells.
The demonstration that miR-124 inhibits gastric cancer cell growth supports the concept that miR-124 functions as a tumor suppressor by a mechanism that involves translational repression of the JAG1 and the inhibition of Notch signaling pathway.
The c.765C>T JAG1 variant is significantly associated with the pathogenesis of tetralogy of Fallot in the Iranian population.
In vivo, knockdown of Jagged1 could suppress the tumorigenicity of Glioma-Initiating Cells through NF-kappa B(p65) signaling.
Our findings reveal deep conservation of Jagged1-Notch2 signaling in patterning the pharyngeal arches from fish to mouse to man, despite the very different functions of their skeletal derivatives in jaw support and sound transduction.
these findings demonstrate the utility of soluble OX40 L and JAG1 to induce TCR-independent regulatory T-cells proliferation
Missense mutant of Jag1 (Jag1(Ndr)) disrupts bile duct development and is responsible for Alagille syndrome phenotypes in heart, eye, and craniofacial dysmorphology.
These findings demonstrate a critical role of osteolineage Jagged1 in bone homeostasis, where Jagged1 maintains the transition of osteoprogenitor to maturing osteoblasts.
Data (including data from studies in transgenic mice) suggest that signaling via Notch2 and Notch3 plays role in promoting cell differentiation and steroidogenesis in preovulatory granulosa cells; mechanism involves regulation of gene expression of Jag1 and Rbpj. (Notch2 = Notch2 receptor; Notch3 = Notch3 receptor; Jag1 = jagged-1 protein; Rbpj = recombining binding protein suppressor of hairless)
Notch1 signaling is activated in brain endothelial cells cocultured with astrocytes, and astrocytic Jagged1 expression is required for angiogenic enhancement.
loss of Jag1 function in osteoblast lineage cells may contribute to the skeletal phenotype associated with Alagille syndrome.
Epidermal stem cells accelerate diabetic wound healing via the Notch1 signaling pathway; Jag1 overexpression improves diabetic wound healing in vivo.
pre-coated Notch1 protein promotes Notch1-knocked down B cells to produce antibody in LPS-stimulated B cells suggesting that Notch1 in other cells may promote antibody production by binding its ligands Dll1 and Jag1 in B cells.
JAG1 is the main activator of NOTCH signaling and GDNF expression in Sertoli cells.
the effects of two Notch ligands, i.e., Jagged1 and DLL1, on murine and human hematopoiesis in vitro. Our observations indicate that the stromal expression of Notch ligands increases the production of both the total and phenotypically early murine and human hematopoietic cells in the co-culture.
Fringe modifications at EGF8 and EGF12 enhanced Notch1 binding to and activation from Delta-like 1, while modifications at EGF6 and EGF36 (added by Manic and Lunatic but not Radical) inhibited Notch1 activation from Jagged1.
A Jagged1-Hey1 signal might mediate the impairment of angiogenesis induced by Ang II during cardiac hypertrophy.
Data show that Rac1 induced nuclear import of STAT3 by physical binding, and nuclear STAT3 directly activated the transcription of essential oocyte-specific genes, including Jagged1, GDF9 and BMP15.
Diabetes mellitus induces Jagged1 overexpression and suppresses Notch signaling in endothelial cells. Blocking Jagged1 prevented diabetes-induced microvasculopathy and could reverse it even after 4 weeks.
Jagged1 intracellular domain-mediated inhibition of Notch1 signalling regulates cardiac homeostasis in the postnatal heart.
Notch ligands Jagged1b and Jagged2b induce duct cell lineage in the liver and pancreas of the zebrafish.
Results indicate that Jagged-Notch signaling is required for segregation between wt1-expressing cells and differentiated steroidogenic tissue.
Notch pathway is involved in the early steps of thyroid morphogenesis, and Jagged1-Notch signal is required for zebrafish thyroid development and function
Expression of both jagged2 and jagged1b mRNA in the central nervous system suggested that they might be involved in control of differentiating neural progenitors.
Mib-Jag1-Notch signalling regulates patterning and structural roles of the notochord by controlling cell-fate decisions
Jagged and Delta ligands are functionally redundant or required in specific combinations in many differentiation processes
the combination of XSICD-mediated intracellular signaling and the extracellular domain of Notch ligands-mediated activation of Notch receptor is involved in the primary neurogenesis
Results found that JAG1, the miR-199b target gene, promotes PSCs proliferation through activating the Notch1 signal pathway.
The jagged 1 protein encoded by JAG1 is the human homolog of the Drosophilia jagged protein. Human jagged 1 is the ligand for the receptor notch 1, the latter a human homolog of the Drosophilia jagged receptor notch. Mutations that alter the jagged 1 protein cause Alagille syndrome. Jagged 1 signalling through notch 1 has also been shown to play a role in hematopoiesis.
, jagged 1 (Alagille syndrome)
, jagged 1
, protein jagged-1-like
, protein jagged-1b
, protein jagged-1a
, jagged 1 L homeolog
, C-Serate-1 protein