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Validated All-in-One™ qPCR Primer for MYCN(NM_001293228.2) Search again
Product ID:
HQP117938
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
MODED, MYCNsORF, MYCNsPEP, N-myc, NMYC, ODED, bHLHe37
Gene Description:
MYCN proto-oncogene, bHLH transcription factor
Target Gene Accession:
NM_001293228.2(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.
Summary
This gene is a member of the MYC family and encodes a protein with a basic helix-loop-helix (bHLH) domain. This protein is located in the nucleus and must dimerize with another bHLH protein in order to bind DNA. Amplification of this gene is associated with a variety of tumors, most notably neuroblastomas.
Gene References into function
- N-myc promotes survival and induces S-phase entry of postmitotic sympathetic neurons
- MYCN gene copy number is determined with a real-time quantitative PCR (Q-PCR) assay and fluorescence in situ hybridization (FISH) analysis.
- Minichromosome maintenance protein MCM7 is a direct target of the MYCN transcription factor in neuroblastoma.
- nmyc gene amplification heavily influences survival in neuroblastoma in children.
- experimental N-Myc overexpression results in down-regulation of leukemia inhibitory factor (LIF), a modulator of endothelial cell proliferation
- N-myc gene modulates expression of p73, allowing neuroblastoma cells to escape the growth suppressing properties of p73
- Importance of Sp1 consensus motifs in the MYCN promoter.
- High level amplification of N-MYC is not associated with adverse histology or outcome in primary retinoblastoma tumours.
- data suggest that E2F transcription factors are critical for both the full activation and the repression of MYCN in neuroblastomas
- We found no correlation between MYCN and ID2 expression in neuroblastoma cell lines or tumor specimens. However, we did find a significant positive correlation between MYC and ID2 expressions in both MYCN-amplified and single-copy tumor specimens
- Amplification of MYCN and deletion of TP53 with complex cytogenetic abnormalities in a case of pleuropulmonary blastoma
- Transcriptional regulation of ID2 by the MycN oncoprotein is unlikely to be a seminal molecular event resulting in a highly malignant neuroblastoma phenotype.
- expressed in human neuroblastoma cells in response to retinoic acid
- Data show that the MycN protein activates MDR1 transcription both in exogenous transient MYCN-transfected cells and in endogenous metastatic neuroblasts.
- The identification of coexpressed and coamplified genes associated with MYCN overexpression in neuroblastoma suggests biochemical pathways that contribute to the malignant behavior of these tumors and forms a basis for molecular classification.
- MYCN is not activated in neuroblastoma by E2F and Sp1/Sp3
- overexpression of MYCN abrogates the regulation of the centrosome cycle after DNA damage
- NMYC is inhibited by peptide nucleic acid in N-myc amplified human neuroblastoma cells
- MYCN induction in human NB cells results in increased MRP1 mRNA and protein levels
- N-myc-associated tumor aggressiveness is mediated by nestin
- While survival rates were higher for patients with low N-myc expression, these differences were not statistically significant.
- Low level gain for a segment of 2p was detected in five of the 15 neuroblastomas that had high level MYCN amplification. The possibility that low level gain of distal 2p is a risk factor for high level MYCN amplification is discussed.
- decreased MYCN expression and MYCN DNA-binding is correlated with retarded cell cycle progression
- These data suggest that inappropriate perinatal MycN expression in paravertebral ganglia cells from transgenic MYCN mice initiated tumorigenesis by altering the physiologic process of neural crest cell deletion.
- Clustering of neuroblastoma cell lines on the basis of hypermethylation distinguished lines with MYCN amplification (a negative prognostic factor) from those without it (P =.012).
- Data show that nitric oxide negatively regulates proliferation and promotes neuronal differentiation through N-Myc downregulation.
- characterized MYCN amplification and chromosome 2 aneusomy in 12 patients with neuroblastoma
- mechanistic link between N-Myc and death receptor machinery, which may serve as a checkpoint to guard the cell from N-Myc-initiated tumorigenesis.
- finding that MYCN directly modulates baseline MDM2 levels suggests a mechanism contributing to the pathogenesis of neuroblastoma and other MYC-driven malignancies through inhibition of MYC-stimulated apoptosis
- N-myc is recruited to the EAAT2 promoter with TNFalpha
- N-myc down-regulates the mRNA expression of many genes with a role in cell architecture.
- HMGA1 repression by RNA interference reduced neuroblastoma cell proliferation, indicating that HMGA1 is a novel MYCN target gene relevant for neuroblastoma tumorigenesis.
- propose that haploinsufficiency of HuD due to chromosome #1p deletion in neuroblastoma selects for cells that amplify N-myc genes
- combination of gene dosages of MYCN and Survivin and the expression level of BIN1 using the quantitative polymerase chain reaction method was significantly correlated with the clinical stage and the patients' outcome in neuroblastoma
- Recurrent NMYC copy number gain and high protein expression is associated with basal cell carcinoma
- MycN binds to the promoter of CRABP-II and induces CRABP-II transcription directly in neuroblastoma.
- Rationale to test PI3K inhibitors in MYCN-amplified neuroblastoma represent a therapeutic approach applicable to a broad range of cancers in which transcription factors are stabilize.
- MYCN amplification in any form (HSRs or dmins) is associated with a poor outcome.
- The expression of MYCN in tumor cells, and the sensitivity of detection of MYCN by RT-PCR noted in this and other studies, supports further evaluation of MYCN as a NB marker for molecular detection of minimal residual disease.
- These data show that small interfering RNA directed to MYCN, which plays a crucial role in neuroblastoma cell survival, may provide a potential novel therapeutic option for aggressive neuroblastomas.
- Lower levels of p21WAF1 and hypo retionblastoma protein induction and a failure to G1 arrest in MYCN amplified neuroblastoma cell lines after DNA damage.
- Chromosome 1p36 deletion and MYCN amplification status may be reliable parameters in determining unfavorable histology and predicting prognosis in neuroblastoma.
- the N-terminal region of the p14(ARF) protein is involved in binding to c-Myc and N-Myc proteins
- N-MYC induces FAK expression.
- High levels of MYCN expression was useful for distinguishing synovial sarcoma from other childhood-spindled cell sarcomas.
- MYCN may override the G1 checkpoint through down-regulation of SKP2 and TP53INP1 resulting in reduced p21(WAF1) expression in p53 wt cell lines, and in addition may act through the WNT signaling pathway in a p53 independent manner.
- MYCN-amplified and non-amplified cell lines form separate classes according to their metabolite profiles.
- An association was found between MYCN amplifcation and 1p deletion in neuroblastomas with high tumor vascularity.
- MYCN was amplified in one clone of neuroblastoma with an unfavorable histology.
- MYCN retinoic acid response is not mediated solely though the region controlling basal activity.
- Concomitant DDX1 and MYCN gain is associated with neuroblastoma
- MYCN might stimulate cell proliferation by inhibiting the expression of DKK1. DKK1 might exert part of its growth suppressive effect by induction of SYNPO2 expression.
- A truncated form of N-Myc wild type can fully rescue the proliferation defect in myc-null fibroblasts, but rescue is dependent on the highly conserved Myc homology box II.
- MYCN-mediated immune escape mechanism, which we believe to be novel, is operative in metastatic cancer and should be considered in tumor immunobiology
- strong and specific immune responses against MYCN expressing tumours are possible in patients with the most common HLA class 1 type in the Caucasian population.
- Analysis of 2 neuroblastoma cell lines with inducible activity of MYCN showed that DKK3 is down-regulated by MYCN. MYCN expression is inversely correlated with expression of DKK3.
- keratoepithelin induces elevated TFPI2 transcript levels in neuroblastoma cells without alterations of MYCN expression.
- besides MYCN and ALK, other genes proximal and distal to MYCN are highly expressed in neuroblastoma
- These data represent the first example of a role for a Myc family member in retinal development and the first characterization of a mouse model in which the hypocellular retina is properly proportioned to the other ocular structures
- N-myc is a novel regulator of PI3K-mediated VEGF expression in neuroblastoma
- Tumor cell ploidy may be a clinically useful factor for prognostication and treatment stratification in children with MYCN-amplified, favorable-stage NB tumors.
- The PAX3-FKHR protein acts directly on the MYCN gene at the transcriptional level. PAX3-FKHR contributes to the expression of MYCN and in turn MYCN collaborates with PAX3-FKHR in tumorigenesis.
- MYCN genomic copy number from 44 human brain tumors (22 medulloblastomas and 22 neurocytomas) was determined.
- cyclin E expression in 2 t(11;14)-negative mantle cell lymphomas characterized by a cryptic t(2;14)(p24;q32) and identification of MYCN as a new lymphoma oncogene associated with a blastoid mantle cell lymphoma
- report 11 novel mutations in MYCN-related Feingold syndrome, including seven mutations in exon 2 that result in a premature termination codon in the long MYCN transcript, and review the clinical features of these patients
- Huwe1 links destruction of N-Myc to the quiescent state that complements differentiation in the neural tissue
- identified that three out of the five microRNAs target MYCN and of these miR-34a caused the most significant suppression of cell growth through increased apoptosis and decreased DNA synthesis in neuroblastoma cell lines with MYCN amplification
- N-MYC promotes cell proliferation through a direct transactivation of neuronal leucine-rich repeat protein-1 (NLRR1) gene in neuroblastoma.
- Transcription levels of the MYCN gene in blood cell subpopulations of Patients with leukemia
- Two novel MYCN mutations in sporadic and familial cases of Feingold syndrome are described.
- Binomial segregation at cell division explains the high degree of MYCN copy-number variability in neuroblastoma.
- MYCN gain is associated with the late stage of retinoblastoma.
- Vasoactive intestinal peptide decreases MYCN expression and synergizes with retinoic acid in a human MYCN-amplified neuroblastoma cell line.
- MycN and DNA methylation are responsible for CRABP-II expression in pediatric tumors and demethylation of CRABP-II may be an early event in tumor development.
- In neuroblastic tumors, MYCN amplification was detected in 35.3% of the cases, whereas 1p36 deletion and 17q23 gain was observed in 46.8% and 58.3% of the cases
- Findings support a new dual model for Myc chromatin function with important implications for the role of Myc in cancer and stem cell biology, including that of induced pluripotent stem cells.
- Transcriptome analyses show that MYCN-amplified neuroblastomas have coordinately deregulated myriad polyamine enzymes (including ODC1, SRM, SMS, AMD1, OAZ2, and SMOX) to enhance polyamine biosynthesis.
- findings show MYCN amplification was not correlated with centrosome amplification in sporadic neuroblastomas
- Aurora A interacts with both N-Myc and the SCF(Fbxw7) ubiquitin ligase that ubiquitinates N-Myc and counteracts degradation of N-Myc, thereby uncoupling N-Myc stability from growth factor-dependent signals