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Validated All-in-One™ qPCR Primer for JAG1(NM_000214.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
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.
Gene References into function
- a cell surface protein that functions in an ambryologically important signaling pathway
- interaction with Notch1 on tumor cells dramatically induces proliferation and inhibition of apoptosis in vitro
- inhibits proliferation of cd34+ macrophage progenitors
- Familial deafness, congenital heart defects, and posterior embryotoxon caused by cysteine substitution in the first epidermal-growth-factor-like domain of jagged 1.
- JAG1 gene abnormality may be an aggravating factor in extrahepatic biliary atresia
- experiments in vitro showed that Jagged1 signaling inhibited process outgrowth from primary human oligodendrocytes
- Activation of Notch-1 signaling by Jagged-1 induces monocyte-derived dendritic cell maturation in vitro.
- Results of this study are consistent with the proposal that either haploinsufficiency for wild-type JAG1 and/or dominant negative effects produced by mutated JAG1 are responsible for the AGS phenotype.
- identification of C-terminal PDZ-ligand is essential for cellular transformation
- Identification of novel Jagged1 mutations in patients with Alagille syndrome.
- Conditional mutation of this protein shows the developing heart is more sensitive than developing liver to JAG1 dosage.
- suppresses the self-renewal capacity and long-term growth of two myeloblastic leukemia cell lines
- Delta and Jagged undergo ADAM-mediated ectodomain processing followed by PS-mediated intramembrane proteolysis to release signaling fragments
- Notch activation by JAG1 in the presence of alloantigen-presenting cells may therefore be a means of inducing specific regulatory T cells while preserving other T-cell functionality
- Notch receptors 1&2 and their ligand Jagged1 are highly expressed in cultured and primary MM cells, suggesting Notch signaling is involved in the tight interactions between neoplastic plasma cells and their bone marrow microenvironment
- induced an attenuation of cell motility which is accompanied by a decrease in actin stress fibers and an increase in adherence junctions and induces a NIH 3T3 cell tranformed phenotype mediated by FGF signaling.
- Delta-1 and Jagged-1 have roles in growth suppression in two myeloid leukemia cell lines
- soluble form of Jagged1, when present in the cell culture medium, was sufficient to induce keratinocyte differentiation
- upregulated in Papillomavirus-mediated cervical neoplasia and required for notch activation.
- structured in solution, as suggested by circular dichroism and NMR spectroscopy, and displays an EGF-like disulfide bond topology, as determined by disulfide mapping
- Dysregulation of JAGGED1 protein levels plays a role in prostate cancer progression and metastasis and suggest that JAGGED1 may be a useful marker in distinguishing indolent and aggressive prostate cancers.
- 12 new mutations are described: 5 frameshifts, 3 nonsense, 2 missense, and 2 splice site.
- Down-regulation of Notch-1, Delta-like-1, or Jagged-1 by RNA interference induces apoptosis and inhibits proliferation in multiple glioma cell lines.
- Jagged1 and GDNF/Ret/GFRalpha1 interact and have a role in regulating ureteric budding and branching
- observed that Jagged1 is preferentially upregulated in human cervical tumors and sustains tumor progression by HPV 16 oncogenes
- Identification of novel Jagged1 mutations in patients with Alagille syndrome.
- Data describe the immunohistochemical staining pattern of four Notch receptors (Notch1-4) and their ligands (Delta1 and Jagged1) in synovial tissues obtained from rheumatoid arthritis patients.
- Wild-type JAG1 is inhibitory for hepatocyte growth factor gene expression; mutant JAG1 reverses the inhibition
- 83 novel mutations within the JAG1 gene are associated with Alagille syndrome.
- data indicate a role for JAGGED/Notch signaling in the process of thymic involution
- Jagged-1 induces cell growth inhibition and S phase cell cycle arrest in prostate cancer cells.
- Increased expression of Notch3, Jagged1, Hes1, and Hes6 gene transcripts were observed during differentiation of cultured human skeletal muscle cells.
- results reveal that Jagged1, which is regulated by hepatitis B virus X protein, may contribute to the development of hepatocellular carcinoma
- absence of correlation between mutations in specific JAG1 gene exons and clinical features in patients with leukoencephalopathy CADASIL-like phenotype
- patients with tumors expressing high levels of JAG1 protein had a worse outcome than those with tumors expressing low levels
- Mutations in JAGGED1 is associated with Notch signaling inhibition and Alagille syndrome
- Overexpression of jagged1 is associated with breast cancer
- Aberrant expression of Jagged1 and Notch1 are associated with poor outcome in breast cancer
- JAG1 expression is associated with a basal phenotype and recurrence in lymph node-negative breast cancer.
- IL-6 treatment triggered Notch-3-dependent upregulation of the Notch ligand Jagged-1 and promotion of MS and MCF-7-derived spheroid growth
- Notch-1 and the Notch ligand Jagged-1 were expressed at significantly higher levels in CCRCC tumors than in normal human renal tissue, and the growth of primary CCRCC cells was attenuated upon inhibition of Notch signaling.
- The results thus showed that Jag-1-mediated Notch signaling in human bone marrow stromal cells was necessary to initiate chondrogenesis, but it must be switched off for chondrogenesis to proceed.
- This is the first study that explores the possible interaction between JAG1, NOTCH2, and Hey2 in the variable phenotypes observed in patients with Alagille syndrome
- Data show that Jagged1 are abundantly expressed in osteoarthritis.
- Two mutations in the NOTCH1 found in patients with left ventricular outflow tract defects reduce JAGGED1 induced signaling.
- Jagged-1 is the primary Notch3 ligand in ovarian carcinoma and Jagged-1/Notch3 interaction constitutes a juxtacrine loop promoting proliferation and dissemination of ovarian cancer cells within the intraperitoneal cavity
- These data demonstrate the existence of novel cross-talk between thrombin, FGF, and Notch signaling pathways, which play important roles in vascular formation and remodeling.
- NOTCH3 expression is induced in mural cells through an autoregulatory loop that requires endothelial-expressed JAGGED1.
- These hematopoiesis-supportive clones also showed high gene expression of Jaggedl, a Notch ligand, as well as high potential to deposit calcium after osteogenic induction.
