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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 (6) and many more products for this protein.
Showing 10 out of 98 products:
Human Monoclonal MYCN Primary Antibody for ChIP, CyTOF - ABIN152254
Tasseva, Cole, Vance: N-Myc and SP regulate phosphatidylserine synthase-1 expression in brain and glial cells. in The Journal of biological chemistry 2011
Show all 3 Pubmed References
Mouse (Murine) Polyclonal MYCN Primary Antibody for ICC, IF - ABIN256650
Sjostrom, Finn, Hahn, Rowitch, Kenney: The Cdk1 complex plays a prime role in regulating N-myc phosphorylation and turnover in neural precursors. in Developmental cell 2005
Show all 2 Pubmed References
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
Human Polyclonal MYCN Primary Antibody for IF (p), IHC (p) - ABIN760676
Ramraj, Aravindan, Somasundaram, Herman, Natarajan, Aravindan: Serum-circulating miRNAs predict neuroblastoma progression in mouse model of high-risk metastatic disease. in Oncotarget 2016
PRMT1 (show PRMT1 Antibodies) has a role in regulating MYCN in neuroblastoma (show ARHGEF16 Antibodies)
N-myc levels appear to be modulated by the antagonistic interactions of both miR-17, as a negative regulator, and HuD (show ELAVL4 Antibodies), as a positive regulator in N-myc-amplified neuroblastoma (show ARHGEF16 Antibodies) cells.
We also propose a model for the stabilization mechanism in which binding to Aurora-A (show AURKA Antibodies) alters how N-Myc interacts with SCF (show KITLG Antibodies)(FbxW7 (show FBXW7 Antibodies)) to disfavor the generation of Lys48-linked polyubiquitin (show UBB Antibodies) chains
This study provides a novel insight for miR (show MLXIP Antibodies)-221 in the control of neuroblastoma (show ARHGEF16 Antibodies) cell proliferation and tumorigenesis, suggesting potentials of miR (show MLXIP Antibodies)-221 as a prognosis marker and therapeutic target for patients with MYCN overexpressing neuroblastoma (show ARHGEF16 Antibodies).
N-MYC is in the downstream-regulated gene family in reprogramming cancer metabolism under hypoxia [review]
SNHG1 is up-regulated by MYCN amplification and could be a potential prognostic biomarker for high-risk neuroblastoma (show ARHGEF16 Antibodies) intervention.
MYCN expression is a marker indicative of likely clinical sensitivity to mTOR (show FRAP1 Antibodies) inhibition in neuroblastoma (show ARHGEF16 Antibodies) cells
Results show that MYCN and LSD1 (show KDM1A Antibodies) co-localize at NDRG1 (show NDRG1 Antibodies) promoter and repress its expression in neuroblastoma (show ARHGEF16 Antibodies) cells.
Data indicate cross-talks between MYCN and beta-catenin (show CTNNB1 Antibodies) signalling, which repress normal beta-catenin (show CTNNB1 Antibodies) mediated transcriptional regulation.
Data show that transcription factor activating enhancer binding protein-4 (TFAP4) is a direct transcriptional target of MYCN in neuroblastoma (show ARHGEF16 Antibodies) and that high levels of this transcription factor are associated with poor clinical outcome in this disease.
interactions of NF-kappaB (show NFKB1 Antibodies) and N-myc with GLT-1/EAAT2 (show SLC1A2 Antibodies) promoter sequences was significantly elevated in the ipsi-lateral cortex of both adult and old Traumatic brain injury mice.
beta-catenin (show CTNNB1 Antibodies) cooperates with the transcription factor Myc (show MYC Antibodies) to activate the progenitor renewal program.
we report the isolation and propagation of neuroblastoma (show ARHGEF16 Antibodies) sphere-forming cells with self-renewal and differentiation potential from tumors of the TH-MYCN mouse, an animal model of high-risk neuroblastoma (show ARHGEF16 Antibodies) with MYCN amplification
miR (show MLXIP Antibodies)-34a contributes to the expansion of Myeloid-derived suppressor cells by inhibiting the apoptosis via suppressing the expression of N-myc.
the role of N-myc in mouse lens development, was examined.
Using comparative genomic hybridization, authors found that NCC (show SLC12A3 Antibodies)-derived NBL (show NUMBL Antibodies) tumors in mice acquired copy number gains and losses that are syntenic to those observed in human MYCN-amplified NBL (show NUMBL Antibodies) including 17q gain, 2p gain and loss of 1p36.
a Mycn target gene encoding the miR (show MLXIP Antibodies) cluster miR-17~92, while most retinoblastomas reemerged without clear genetic alterations in either Mycn or known Mycn targets. This Rb/MYCN model recapitulates key genetic driver alterations seen in human retinoblastoma and reveals the emergence of MYCN independence in an initially MYCN-driven tumor.
The findings reveal a PLK1 (show PLK1 Antibodies)-Fbw7 (show FBXW7 Antibodies)-Myc (show MYC Antibodies) signaling circuit that underlies tumorigenesis and validate PLK1 (show PLK1 Antibodies) inhibitors, alone or with Bcl2 (show BCL2 Antibodies) antagonists, as potential effective therapeutics for MYC (show MYC Antibodies)-overexpressing cancers.
ALKR1275Q cooperated with MYCN in the development of aggressive NB, possibly by downregulating the expression of ECM (show MMRN1 Antibodies)/BM-associated genes and by conferring malignant potentials to MYCN-expressing cells.
Reuslts show that N-Myc overexpression leads to the development of poorly differentiated, invasive prostate cancer that is molecularly similar to human NEPC.
In MYCN transgenic fish, Gab2 (show GAB2 Antibodies) overexpression activated the Shp2 (show PTPN11 Antibodies)-Ras (show RAB1A Antibodies)-Erk (show MAPK1 Antibodies) pathway, enhanced neuroblastoma (show ARHGEF16 Antibodies) induction, and increased tumor penetrance.
The authors demonstrate in zebrafish that nf1 (show NF1 Antibodies) loss leads to aberrant activation of RAS (show RAB1A Antibodies) signaling in MYCN-induced neuroblastomas that arise in these precursors, and that the GTPase-activating protein (GAP)-related domain (GRD) is sufficient to suppress the acceleration of neuroblastoma (show ARHGEF16 Antibodies) in nf1 (show NF1 Antibodies)-deficient fish, but not the hypertrophy of sympathoadrenal cells in nf1 (show NF1 Antibodies) mutant embryos.
At somitogenesis stages, nmyc1 expression was detected in the retina, midbrain, posterior hindbrain and presumptive spinal cord. It was also transcribed in the endoderm and its derivatives as well as in branchial arches.
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
, N-myc protein
, neuroblastoma myc-related oncogene 1
, Avian myelocytomatosis viral (v-myc) related oncogene neuroblastoma derived (Nmyc)
, Avian myelocytomatosis viral (v-myc) related oncogene, neuroblastoma derived (Nmyc)
, N-myc-like protein
, v-myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog
, MYCN proto-oncogene, bHLH transcription factor S homeolog
, v-myc avian myelocytomatosis viral oncogene neuroblastoma derived homolog S homeolog
, v-myc myelocytomatosis viral related oncogene, neuroblastoma derived, a