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Validated All-in-One™ qPCR Primer for NR4A3(NM_173200.3) Search again
Powered by BiozBy 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.
Summary
This gene encodes a member of the steroid-thyroid hormone-retinoid receptor superfamily. The encoded protein may act as a transcriptional activator. The protein can efficiently bind the NGFI-B Response Element (NBRE). Three different versions of extraskeletal myxoid chondrosarcomas (EMCs) are the result of reciprocal translocations between this gene and other genes. The translocation breakpoints are associated with Nuclear Receptor Subfamily 4, Group A, Member 3 (on chromosome 9) and either Ewing Sarcome Breakpoint Region 1 (on chromosome 22), RNA Polymerase II, TATA Box-Binding Protein-Associated Factor, 68-KD (on chromosome 17), or Transcription factor 12 (on chromosome 15). Four transcript variants encoding three distinct isoforms have been identified for this gene. [provided by RefSeq].
Gene References into function
- The homeotic protein Six3 is a coactivator of the nuclear receptor NOR-1 and a corepressor of the fusion protein EWS/NOR-1 in human extraskeletal myxoid chondrosarcomas.
- The genes identified here are novel candidates as key early mediators of VEGF-induced endothelial functions.
- In vascular smooth muscle cells, LDL-induced mitogenesis involves NOR-1 upregulation through a CREB-dependent mechanism. Mutation of specific CRE sites in the NOR-1 promoter abolishes LDL-induced NOR-1 promoter activity.
- Aberrant coexpression of NOR1 and SIX3 is a potential alternative mechanism underlying the development of extraskeletal myxoid chondrosarcomas
- different SIX3 mutations in HPE2 may affect different signaling pathways, and that one of these pathways may involve the nuclear receptor NOR1
- Neuron-derived orphan receptor-1 (NOR-1) is a transcription factor over-expressed in human atherosclerotic plaques that is involved in vascular smooth muscle cell proliferation.
- NR4A nuclear receptors NR4A1, NR4A2, NR4A3 are potential transcriptional mediators of inflammatory signals in activated macrophages
- Nur77, Nurr1, and NOR-1 are expressed in human atherosclerotic lesion macrophages and reduce human macrophage lipid loading and inflammatory responses, providing further evidence for a protective role of these factors in atherogenesis.
- platelet-derived growth factor-induced NOR1 transcription in smooth muscle cell is mediated through cAMP-response element-binding protein-dependent transactivation of the NOR1 promoter
- NOR-1 is a critical tumor suppressor of myeloid leukemogenesis that is downregulated in leukemic blasts from acute myeloid leukemia patients.
- NOR-1 up-regulation plays a key role in thrombin-induced endothelial cell growth
- NOR-1 is over-expressed in human atherosclerotic plaques and in porcine arteries subjected to angioplasty, is induced by growth factors in vascular cells and it has been involved in cell migration and proliferation
- NOR-1 is necessary for oxidative metabolism in skeletal muscle.