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MiR (show MLXIP Proteins)-26b-5p acts as a tumor suppressor through suppressing cells proliferation and inducing cells apoptosis via directly targeting JAG1 in multiple myeloma
miR (show MLXIP Proteins)-30d may improve TGF-beta1 (show TGFB1 Proteins)-induced pulmonary fibrosis through direct binding to the 3'UTR of JAG1 and blocking JAG1/Notch (show NOTCH1 Proteins) 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 (show MLXIP Proteins)-124 inhibits gastric cancer cell growth supports the concept that miR (show MLXIP Proteins)-124 functions as a tumor suppressor by a mechanism that involves translational repression of the JAG1 and the inhibition of Notch (show NOTCH1 Proteins) 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 (show NOTCH3 Proteins), and target genes was down-regulated with strain.
This study identifies the unique role of JAG1-induced Notch (show NOTCH1 Proteins) activation in the pathogenesis of multiple myeloma
is an autosomal dominant disorder found to be linked to the Notch ligand (show JAG2 Proteins) 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 (show NFKB1 Proteins)-induced miR (show MLXIP Proteins)-506 suppression and JAG1 upregulation upon IL-1beta (show IL1B Proteins) induction.
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 (show STK38 Proteins))) 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 (show NOTCH2 Proteins) and Notch3 (show NOTCH3 Proteins) plays role in promoting cell differentiation and steroidogenesis in preovulatory granulosa cells; mechanism involves regulation of gene expression of Jag1 and Rbpj (show RBPJ Proteins). (Notch2 (show NOTCH2 Proteins) = Notch2 (show NOTCH2 Proteins) receptor; Notch3 (show NOTCH3 Proteins) = Notch3 (show NOTCH3 Proteins) receptor; Jag1 = jagged-1 protein; Rbpj (show RBPJ Proteins) = recombining binding protein suppressor of hairless (show RBPJ Proteins))
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 (show NOTCH1 Proteins) signaling pathway; Jag1 overexpression improves diabetic wound healing in vivo.
pre-coated Notch1 (show NOTCH1 Proteins) protein promotes Notch1 (show NOTCH1 Proteins)-knocked down B cells to produce antibody in LPS (show TLR4 Proteins)-stimulated B cells suggesting that Notch1 (show NOTCH1 Proteins) in other cells may promote antibody production by binding its ligands Dll1 (show DLL1 Proteins) and Jag1 in B cells.
JAG1 is the main activator of NOTCH signaling and GDNF expression in Sertoli cells.
the effects of two Notch (show NOTCH1 Proteins) ligands, i.e., Jagged1 and DLL1 (show DLL1 Proteins), on murine and human hematopoiesis in vitro. Our observations indicate that the stromal expression of Notch (show NOTCH1 Proteins) ligands increases the production of both the total and phenotypically early murine and human hematopoietic cells in the co-culture.
Notch ligands Jagged1b and Jagged2b induce duct cell lineage in the liver and pancreas of the zebrafish.
Results indicate that Jagged-Notch (show NOTCH1 Proteins) signaling is required for segregation between wt1 (show WT1 Proteins)-expressing cells and differentiated steroidogenic tissue.
Notch (show NOTCH1 Proteins) pathway is involved in the early steps of thyroid morphogenesis, and Jagged1-Notch (show NOTCH1 Proteins) 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 (show NOTCH1 Proteins) 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 (show NOTCH1 Proteins) ligands-mediated activation of Notch (show NOTCH1 Proteins) receptor is involved in the primary neurogenesis
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