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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

V-myc myelocytomatosis viral related oncogene, neuroblastoma derived

N-myc, MYCN
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: c-Myc, CAN, HAD, NDRG1, p53
Papers using N-myc antibodies
Papers on N-myc
N-myc downstream-regulated gene 4, up-regulated by tumor necrosis factor-α and nuclear factor kappa B, aggravates cardiac ischemia/reperfusion injury by inhibiting reperfusion injury salvage kinase pathway.
New
Zhang et al., Xi'an, China. In Basic Res Cardiol, Mar 2016
N-myc downstream-regulated gene 4 (NDRG4) is expressed weakly in heart and has been reported to modulate cardiac development and QT interval duration, but the role of NDRG4 in myocardial ischemia/reperfusion (I/R) injury remains unknown.
The Detection of Genetic Parameters for Prognostic Stratification of Neuroblastoma Using Multiplex Ligation-Dependent Probe Amplification Technique.
New
Olgun et al., İzmir, Turkey. In Genet Test Mol Biomarkers, Feb 2016
Group 1 (48 cases, 23.7%) contained tumors with a 1p deletion and/or MYCN gene amplification (MNA).
RUNX3 is down-regulated in glioma by Myc-regulated miR-4295.
New
Liu et al., Shenyang, China. In J Cell Mol Med, Feb 2016
In addition, N-myc protein also could bind to the promoter of pri-miR-4295 and inhibit the expression of RUNX3 in glioma cells.
The Interaction of Myc with Miz1 Defines Medulloblastoma Subgroup Identity.
New
Impact
Roussel et al., Memphis, United States. In Cancer Cell, Feb 2016
c-Myc (Myc) or MycN overexpression in granule neuron progenitors (GNPs) induces Group 3 (G3) or Sonic Hedgehog (SHH) MBs, respectively.
Advances in the translational genomics of neuroblastoma: From improving risk stratification and revealing novel biology to identifying actionable genomic alterations.
Review
New
Maris et al., Philadelphia, United States. In Cancer, Feb 2016
Neuroblastoma is a model pediatric solid tumor in its use of recurrent genomic alterations, such as high-level MYCN (v-myc avian myelocytomatosis viral oncogene neuroblastoma-derived homolog) amplification, for risk stratification.
NDRG2 Expression Decreases Tumor-Induced Osteoclast Differentiation by Down-regulating ICAM1 in Breast Cancer Cells.
New
Lim et al., Seoul, South Korea. In Biomol Ther (seoul), Jan 2016
The N-myc downstream-regulated gene 2 (NDRG2) has been known to contribute to the suppression of tumor growth and metastasis, but the precise role of NDRG2 in osteoclast differentiation induced by cancer cells has not been elucidated.
Interactions between Myc and MondoA transcription factors in metabolism and tumourigenesis.
Review
New
Ayer et al., Salt Lake City, United States. In Br J Cancer, Jan 2016
In contrast, in neuroblastoma, N-Myc requires MondoA for metabolic reprogramming and tumourigenesis.
MYC Disrupts the Circadian Clock and Metabolism in Cancer Cells.
New
Impact
Dang et al., Philadelphia, United States. In Cell Metab, Jan 2016
We report here that deregulated expression of MYC or N-MYC disrupts the molecular clock in vitro by directly inducing REV-ERBα to dampen expression and oscillation of BMAL1, and this could be rescued by knockdown of REV-ERB.
TERT rearrangements are frequent in neuroblastoma and identify aggressive tumors.
New
Impact
Versteeg et al., Amsterdam, Netherlands. In Nat Genet, Dec 2015
TERT rearrangements (23%), ATRX deletions (11%) and MYCN amplifications (37%) identify three almost non-overlapping groups of high-stage neuroblastoma, each associated with very poor prognosis.
Impaired differentiation of macrophage lineage cells attenuates bone remodeling and inflammatory angiogenesis in Ndrg1 deficient mice.
New
Ono et al., Fukuoka, Japan. In Sci Rep, Dec 2015
N-myc downstream regulated gene 1 (NDRG1) is a responsible gene for a hereditary motor and sensory neuropathy-Lom (Charcot-Marie-Tooth disease type 4D).
The molecular effect of metastasis suppressors on Src signaling and tumorigenesis: new therapeutic targets.
Review
New
Richardson et al., Shanghai, China. In Oncotarget, Dec 2015
Particular emphasis is bestowed on the potent metastasis suppressor, N-myc downstream regulated gene 1 (NDRG1) and its interactions with the Src signaling cascade.
Telomerase activation by genomic rearrangements in high-risk neuroblastoma.
New
Impact
Fischer et al., Köln, Germany. In Nature, Nov 2015
These rearrangements occurred only in high-risk neuroblastomas (12/39, 31%) in a mutually exclusive fashion with MYCN amplifications and ATRX mutations, which are known genetic events in this tumour type.
Emerging role of N-myc downstream-regulated gene 2 (NDRG2) in cancer.
Review
New
Yang et al., Xi'an, China. In Oncotarget, Nov 2015
UNASSIGNED: N-myc downstream-regulated gene 2 (NDRG2) is a tumor suppressor and cell stress-related gene.
IGF2BP1 harbors prognostic significance by gene gain and diverse expression in neuroblastoma.
New
Impact
Hüttelmaier et al., Heidelberg, Germany. In J Clin Oncol, May 2015
IGF2BP1 was also associated with MYCN gene amplification and MYCN mRNA abundance.
Neuroblastoma: oncogenic mechanisms and therapeutic exploitation of necroptosis.
Review
Raschellà et al., Roma, Italy. In Cell Death Dis, 2014
High-risk NB frequently displays MYCN amplification, mutations in ALK and ATRX, and genomic rearrangements in TERT genes.
The ALK(F1174L) mutation potentiates the oncogenic activity of MYCN in neuroblastoma.
Impact
GeneRIF
George et al., United Kingdom. In Cancer Cell, 2012
findings demonstrate a pathogenic role for ALK(F1174L) in neuroblastomas overexpressing MYCN and suggest a strategy for improving targeted therapy for ALK-positive neuroblastoma
Segmental chromosome aberrations converge on overexpression of mitotic spindle regulatory genes in high-risk neuroblastoma.
GeneRIF
Quattrone et al., Trento, Italy. In Genes Chromosomes Cancer, 2012
Elevated expression of 14 key genes promoting this function is strongly associated to high-risk neuroblastomas with 1p loss and MYCN amplification in a set of 410 tumor samples.
Distinct neural stem cell populations give rise to disparate brain tumors in response to N-MYC.
Impact
GeneRIF
Weiss et al., San Francisco, United States. In Cancer Cell, 2012
Demonstrate context-dependent transformation of neural stem cells in response to common oncogenic signal N-MYC.
Constitutive gray hair in mice induced by melanocyte-specific deletion of c-Myc.
GeneRIF
Beermann et al., Lausanne, Switzerland. In Pigment Cell Melanoma Res, 2012
Double deletion of c-Myc and N-Myc results in nearly complete loss of the residual pigmentation, indicating that N-Myc is capable of compensating for c-Myc loss of function in melanocytes.
Activated ALK collaborates with MYCN in neuroblastoma pathogenesis.
Impact
GeneRIF
Look et al., Boston, United States. In Cancer Cell, 2012
Coexpression of activated ALK with MYCN provides prosurvival signals that block this apoptotic response and allow continued expansion and oncogenic transformation of hyperplastic neuroblasts, thus promoting progression to neuroblastoma.
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