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MYCN is a member of the MYC family and encodes a protein with a basic helix-loop-helix (bHLH) domain. Additionally we are shipping MYCN Proteins (7) and MYCN Kits (5) and many more products for this protein.
Showing 10 out of 66 products:
Human Polyclonal MYCN Primary Antibody for EIA, WB - ABIN453206
Alvarez-Rodríguez, Pons: Expression of the proneural gene encoding Mash1 suppresses MYCN mitotic activity. in Journal of cell science 2009
Show all 2 references for ABIN453206
Dog (Canine) Polyclonal MYCN Primary Antibody for WB - ABIN2779428
Hansford, Thomas, Keating, Burkhart, Peaston, Norris, Haber, Armati, Weiss, Marshall: Mechanisms of embryonal tumor initiation: distinct roles for MycN expression and MYCN amplification. in Proceedings of the National Academy of Sciences of the United States of America 2004
Human Polyclonal MYCN Primary Antibody for WB - ABIN391590
Li, Sun, Chen, Squires, Nowroozizadeh, Liang, Huang: p53 Mutation Directs AURKA Overexpression via miR-25 and FBXW7 in Prostatic Small Cell Neuroendocrine Carcinoma. in Molecular cancer research : MCR 2015
N-Myc and activated AKT1 (show AKT1 Antibodies) are sufficient to transform human prostate epithelial cells to prostate adenocarcinoma and neuroendocrine carcinoma. N-Myc is required for tumor maintenance.
This study strongly suggests that AT7519 is a promising drug for the treatment of high-risk neuroblastoma (show ARHGEF16 Antibodies) patients with MYCN amplification.
the MNA (MYCN amplification)subclone appears to be constraint by the tumor environment and thus less relevant for tumor behavior in aggressive tumors with a high genomic instability and many segmental aberrations
SOX2 (show SOX2 Antibodies), KCNMB4 (show KCNMB4 Antibodies), FOS, GLI3 (show GLI3 Antibodies) and GLI1 (show GLI1 Antibodies) may be involved in the pathogenesis of neuroblastoma (show ARHGEF16 Antibodies), with the expression of SOX2 (show SOX2 Antibodies) downregulating the expression of MYCN.
let-7 disruption by LIN28B (show LIN28B Antibodies), MYCN sponging, or genetic loss is a unifying mechanism of neuroblastoma (show ARHGEF16 Antibodies) development with broad implications for cancer pathogenesis
Suppression of MycN in human neural crest stem cells inhibits cell growth and cell cycle progression.
Data indicate that suberoylanilide hydroxamic acid (SAHA) blocked the expression of MYCN protein and, by doing so, reduced the effects mediated by this protein.
Three novel genes were identified as recurrently mutated; MYCN, MYO5B and VCL (show VCL Antibodies), and mutations in these genes were exclusively found in malignant sympathetic paraganglioma tumors.
MYCN gene amplification (MNA) is strongly associated with other clinical and biological variables in neuroblastoma (show ARHGEF16 Antibodies). Recursive partitioning has identified subgroups of neuroblastoma (show ARHGEF16 Antibodies) patients with highly disparate rates of MNA.
The results do not support our hypothesis that common germline genetic variants in the MYCN genes is associated with the risk of developing medulloblastoma.
Loss of N-myc significantly impairs the Sonic hedgehog (show SHH Antibodies) signaling pathway and disrupts the expression of cell cycle effectors with a significant reduction of Ccnd2 (show CCND2 Antibodies).
Study shows that ground-state embryonic stem cells express low Myc (show MYC Antibodies) levels. Deletion of both c-myc (show MYC Antibodies) and N-myc activity strongly decreases transcription, splicing, and protein synthesis, leading to proliferation arrest; process is reversible and occurs without affecting pluripotency, suggesting that Myc (show MYC Antibodies)-depleted stem cells enter a state of dormancy.
MYCN overexpression is not sufficient for these cells to form tumors in nude mice
ITGA4 (show ITGA4 Antibodies) expression enhances metastasis in MYCN low neuroblastoma (show ARHGEF16 Antibodies).
MYCN plays a critical role in expansion and survival of aggressive medulloblastoma-propagating cells.
SUMOylation may be part of a quality-control mechanism acting on misfolded Myc (show MYC Antibodies) proteins.
The results of this study provided evidence that N-myc deficiency in the olfactory epithelium progressively diminishes proliferation and neurogenesis with negative consequences at structural and cellular levels.
MYCN/LIN28B/Let-7/HMGA2 pathway implicated by meta-analysis of GWAS in suppression of post-natal proliferation thereby potentially contributing to aging
The above results induced by overexpression of MYCN closely resemble the main aspects of human AML (show RUNX1 Antibodies), suggesting that MYCN plays a role in the etiology of AML (show RUNX1 Antibodies).
a general mechanism for p53 (show TP53 Antibodies) inactivation in some embryonal cell types and consequent susceptibility to MycN oncogenesis at the point of embryonal tumor initiation
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.
N-myc proto-oncogene protein
, class E basic helix-loop-helix protein 37
, neuroblastoma MYC oncogene
, neuroblastoma-derived v-myc avian myelocytomatosis viral related oncogene
, oncogene NMYC
, v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived
, v-myc myelocytomatosis viral related oncogene, neuroblastoma derived
, Avian myelocytomatosis viral (v-myc) related oncogene neuroblastoma derived (Nmyc)
, Avian myelocytomatosis viral (v-myc) related oncogene, neuroblastoma derived (Nmyc)
, N-myc protein
, neuroblastoma myc-related oncogene 1