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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.
Vascular smooth muscle cells were cyclically stretched on flexible membranes, as quantified via video tracking, demonstrating that the expression of Jagged1, Notch3, and target genes was down-regulated with strain.
This study identifies the unique role of JAG1-induced Notch activation in the pathogenesis of multiple myeloma
is an autosomal dominant disorder found to be linked to the Notch ligand JAG1.5 Approximately 90 percent of patients presenting with Alagille Syndrome have a mutation on the JAG1 gene that is located on chromosome 20p12.
These data indicate a process of NF-kappaB-induced miR-506 suppression and JAG1 upregulation upon IL-1beta induction.
In subjects with Alagille syndrome, incomplete clinical features of Alagille syndrome and biliary atresia, the frequency of mutations was as follows: single nucleotide variants (51.9%), small insertion or deletion (29.6%) and gross deletion (18.5%).
The Jagged1-Notch pathway showed elevated expression in AI-resistant breast cancer cells, resulting in macrophage differentiation towards M2 TAMs and there contributing to the acquisition of AI resistance.
Data show that Delta-like 4 (DLL4) and Jagged1 (JAG1) displayed equal potency in stimulating Notch target genes in HMEC-1 dermal microvascular endothelial cells but had opposing effects on sprouting angiogenesis in vitro.
Missense mutant of Jag1 (Jag1(Ndr)) disrupts bile duct development and is responsible for Alagille syndrome phenotypes in heart, eye, and craniofacial dysmorphology.
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
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.
endothelial Jagged1 has a role in promoting solid tumor development
Jag1 expression in pulmonary capillary endothelial cells is upregulated after repeated lung injury and contributes to lung fibrosis.
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