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Validated All-in-One™ qPCR Primer for NR4A1(NM_001202233.1) Search again
Product ID:
HQP055121
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
GFRP1, HMR, N10, NAK-1, NGFIB, NP10, NUR77, TR3
Gene Description:
nuclear receptor subfamily 4 group A member 1
Target Gene Accession:
NM_001202233.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
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:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
This gene encodes a member of the steroid-thyroid hormone-retinoid receptor superfamily. Expression is induced by phytohemagglutinin in human lymphocytes and by serum stimulation of arrested fibroblasts. The encoded protein acts as a nuclear transcription factor. Translocation of the protein from the nucleus to mitochondria induces apoptosis. Multiple alternatively spliced variants, encoding the same protein, have been identified.
Gene References into function
- Hepatitis B virus X protein induced transcription
- We review here recent studies on the glucocorticoid receptor and the orphan receptors Nur77 and RORgamma
- Promyelocytic leukemia protein PML inhibits Nur77-mediated transcription through specific functional interactions.
- Induction of apoptosis by TPA and VP-16 is through induction of TR3 expression and translocation from nucleus to cytosol, which may be a novel signal pathway for TR, and a new biological function to exert its effect on apoptosis in gastric cancer cells.
- upregulation by Wnt-1
- plays a dual role in selective regulation of apoptosis and cell cycle in gastric cancer cells
- Nur77 drives transcription of PAI-1 through direct binding to an NGFI-B responsive element (NBRE), indicating monomeric binding and a ligand-independent mechanism. Nur77, itself, is transcriptionally up-regulated by TNFalpha.
- TR3 is a modulator of vascular endothelial cell proliferation and arrests endothelial cells in the G1 phase of the cell cycle by influencing cell cycle protein levels.
- TR3 orphan nuclear receptor mediates apoptosis through up-regulating E2F1 in human prostate cancer cells
- TR3/Nur77 translocation from the nucleus may initiate the apoptotic cascade in colon cancer cells by stimulating other cytosolic proapoptotic molecules to associate with mitochondria.
- The genes identified here are novel candidates as key early mediators of VEGF-induced endothelial functions.
- TR3 has a distinct role and functional mode in mediating tretinoin-induced signalling.
- Ectopic expression of TR3 in both H460 and Calu-6 lung cancer cell lines promoted their cell cycle progression and BrdU incorporation.
- In transgenic mice expressing human TR3 orphan receptor, as described in this review, TR3 inhibits formation of smooth muscle cell-rich atherosclerotic lesions.
- Nur77 activated by HIF under hypoxic conditions regulates production of the peptide hormone precursor POMC.
- Nur77, which is regulated by a MAPK pathway activated via arrestin 2, modulates NK(1)R-mediated nonapoptotic programmed cell death
- NUR77 binds to BCL-2 and effects its role and phenotype
- Chenodeoxycholic acid derivative-induced apoptosis of SNU-1 gastric cancer cell lines is mediated by mitochondria and by Nur77.
- P. 743:"Nothern blot analysis of Nur77 mRNA expression revealed that PGF(2alpha) and Butaprost, but not Bimatoprost, induced upregulation of Nur77 mRNA expression in human trabecular meshwork cells."
- NGFIB plays a crucial role in adrenal zonation by regulating 3beta-hydroxysteriod dehydrogenase 2 gene transcription
- Expression of Nurr1 and NGFI-B plays an important role in human adrenal cortex and its neoplasms, including possible regulation of steroidogenesis.
- Nur77 has a role in the stabilization of HIF-1alpha and in tumor progression and metastasis
- The repressive effect of Nur77 on IL-2 promoter activation is mediated through inhibition of the transcription factor complex nuclear factor-kappaB.
- Causal relationship between the rapid decline of aromatase mRNA and induction of orphan nuclear receptors NURR1 and NGFI-B expression, which concomitantly occur upon LH surge at the later stages of ovarian follicular development.
- RXRalpha is responsible for TR3 nucleocytoplasmic translocation
- Nur77 is an important regulator of HSD3B2 promoter activity
- nongenotropic function of RXRalpha and its involvement in the regulation of the Nur77-dependent apoptotic pathway
- NGFI-B-dependent transcription of proopiomelanocortin gene is antogonized by glucocorticoid receptor.
- Nur77 activation and its apoptotic activity are regulated by small heterodimer partner protein.
- ligand-dependent activation of Nur77 through nuclear pathways induces cell death
- NR4A nuclear receptors NR4A1, NR4A2, NR4A3 are potential transcriptional mediators of inflammatory signals in activated macrophages
- results show that Nur77 can modulate apoptosis through NF-kappaB crosstalk
- Menin's dynamic regulation of histone modifiers with JunD is responsible for PKC theta-synergistic effect on Nur77 expression in T cell
- Both activation of JNK and inhibition of Akt play a role in translocation of Nur77 from the nucleus to the cytoplasm. mutation of an Akt phosphorylation residue Ser351 in Nur77 abolished the effect of Akt or the PI3-K inhibitor.
- Thus, the human INSL3 promoter constitutes a novel target for the orphan nuclear receptor Nur77.
- Formation of Nur77 nuclear bodies might be involved in programmed cell death modulation upon exposure to DNA damaging agents.
- Mutation analysis of the GIOT-1 promoter and overexpression analysis of dominant-negative Nur77 revealed that luteinizing hormone activates GIOT-1 gene expression through Nur77
- TR3 represents inhibitory mechanisms to restrict venous SMC proliferation and may contribute to prevention of vein-graft disease
- 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.
- Nur77 is a physiological binding partner of protein kinase C (PKC) and regulates PKC activity via direct inhibition of its catalytic activity.
- JNK-induced phosphorylation blocked the DNA binding property of TR3 and hence diminished its transactivation activity
- p53 mediates the suppression of TR3 on MDM2 at both transcriptional and post-transcriptional level and suggest TR3 as a potential target to develop new anticancer agents that restrict MDM2-induced tumor progression.
- TR3 is an important apoptosis inducing factor in melanoma cells.
- Plays an important role in the apoptotic actions of IGFBP-3.
- NUR77 is a critical tumor suppressor of myeloid leukemogenesis that is downregulated in leukemic blasts from acute myeloid leukemia patients.
- cross-talk between NR3B and NR4A receptors is a mechanism modulating the transcriptional activities of these orphan nuclear receptors
- The research identified a novel distribution of TR3 in the ER and defined two parallel mitochondrial- and ER-based pathways that ultimately result in apoptotic cell death.
- up-regulated by insulin in cultured L6 skeletal muscle cells, protein accumulated in the nucleus where it functions as a transcription factor, without translocation to the cytoplasm to promote apoptosis
- demonstrate the distinct regulatory mechanisms of p300 and TR3 on retinoid X receptor-alpha acetylation
- In T lymphoma cells, STS induces the expression of the pro-apoptotic orphan receptor Nur77 that overcomes the anti-apoptotic effect of Bcl-2, thus enabling GCinduced apoptosis. However, in the myelogenic leukemia cells, STS does not upregulate Nur77.
- MEF2C consistently inhibits expression of NR4A1/NUR77, which regulates apoptosis via BCL2 transformation.
- an increase in the synthesis of TR3 and the accumulation of TR3 in mitochondria and in nuclei might be involved in the induction of apoptosis by vitamin K(2)
- Nur77 overexpression and RNA interference-mediated Nur77 gene knockdown analysis confirmed that SerpinA3 is indeed a novel Nur77-targeted gene.
- These data identify the NR4A receptor family as potential mediators of an MC1R-coordinated DNA damage response to ultraviolet rays exposure in melanocytic cells.
- data demonstrate a unique role for Akt in inhibiting TR3 functions that are not related to transcriptional activity but that correlate with the regulation of its mitochondrial association