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Description
N-Myc Recombinant Rabbit mAb (S-2729-50)Product Specification Host Rabbit Antigen N Myc Synonyms N myc proto oncogene protein; Class E basic helix loop helix protein 37 (bHLHe37); BHLHE37; NMYC; MYCN Immunogen Synthetic Peptide Location Nucleus Accession P04198 Clone Number S 2729 50 Antibody Type Recombinant mAb Isotype IgG Application WB, ICC Reactivity Hu Positive Sample IMR 32 Purification Protein A Concentration 0. 5 mg ml Conjugation Unconjugated Physical Appearance Liquid Storage
Product Specification
| Host | Rabbit |
| Antigen | N-Myc |
| Synonyms | N-myc proto-oncogene protein; Class E basic helix-loop-helix protein 37 (bHLHe37); BHLHE37; NMYC; MYCN |
| Immunogen | Synthetic Peptide |
| Location | Nucleus |
| Accession | P04198 |
| Clone Number | S-2729-50 |
| Antibody Type | Recombinant mAb |
| Isotype | IgG |
| Application | WB, ICC |
| Reactivity | Hu |
| Positive Sample | IMR-32 |
| Purification | Protein A |
| Concentration | 0.5 mg/ml |
| Conjugation | Unconjugated |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 40% Glycerol, 0.05% BSA, 0.03% Proclin 300 |
| Stability & Storage | 12 months from date of receipt / reconstitution, -20 °C as supplied |
Dilution
| application | dilution | species |
| WB | 1:1000-1:2000 | Hu |
| ICC | 1:500 | Hu |
Background
N-Myc is a 64-kDa basic-helix–loop–helix–leucine-zipper transcription factor encoded by MYCN on 2p24 whose amplification or enhancer hijacking defines high-risk subsets of neuroblastoma, medulloblastoma and rhabdomyosarcoma; it heterodimerizes with MAX to bind the E-box CACGTG, recruits TRRAP–TIP60 and p300/CBP to unleash transcription of ribosomal proteins, nucleotide and polyamine biosynthetic enzymes, as well as miR-17-92, thereby driving rapid G1-S transit, metabolic rewiring toward glutaminolysis and serine synthesis, and suppression of differentiation; its intrinsically disordered N-terminus is stabilized by Aurora-A–mediated cis-prolyl isomerization that blocks ubiquitination by FBXW7, while phosphorylation at Ser62 by CDK1 primes subsequent phosphorylation at Thr58 by GSK3β to trigger SCFβ-TrCP-mediated degradation, and BET-bromodomain or HDAC inhibitors can restore this degradation in tumors harboring MYCN amplification, making N-Myc a validated but still elusive therapeutic target.
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