N-Myc Antibody [C8B13] | Primary Antibodies

Application: Reactivity: Human, Mouse

Usage Information

Dilution
WB1:1000 IP1:200 IF1:100 - 1:400 FCM1:200 - 1:800 CHIP1:50

Application
WB, IP, IF, FCM

Reactivity
Human, Mouse

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
62 kDa

Positive Control	IMR-32 cells; Neuro-2a cells; BaF3 cells; NTERA-2cl.D1 cells
Negative Control	HeLa cells

Datasheet & SDS

Biological Description

Specificity
N-Myc Antibody [C8B13] detects endogenous levels of total N-Myc protein.

Clone
C8B13

Synonym(s)
N-myc proto-oncogene protein; Class E basic helix-loop-helix protein 37 (bHLHe37); MYCN; BHLHE37; NMYC

Background
N-Myc (MYCN) is a proto-oncogenic transcription factor of the Myc family, characterized by a basic helix-loop-helix leucine zipper (bHLH-LZ) structure that obligately heterodimerizes with Max to bind E-box DNA motifs (CACGTG), thereby activating genes essential for cell proliferation, metabolism, and neural development, a function especially critical in high-risk neuroblastoma, where its amplification is a hallmark. N-Myc features an intrinsically disordered N-terminal transactivation domain (TAD, residues 1–137) containing conserved Myc boxes (MB0, MB1, MBII) for coactivator recruitment, helical segments, and a phosphodegron regulated by kinases (ERK1, GSK3, Aurora-A) for ubiquitin-mediated protein stability, alongside a C-terminal bHLH-LZ domain for Max dimerization and DNA recognition. N-Myc occupies hundreds of euchromatic genomic sites marked by activating histone modifications, recruits chromatin modifiers to open chromatin, alleviates RNA Pol II pausing, and drives expression of genes involved in growth, metabolism, and replication stress response; E-box hypomethylation enables tumor-specific targeting, and inducible downregulation can reverse these effects. N-Myc regulates neural differentiation, hematopoiesis, and stem cell cycling, with antagonism from Mad/Mnt/Max complexes, while its dysregulation, particularly via gene amplification, drives tumorigenesis and poor prognosis.

Background

N-Myc (MYCN) is a proto-oncogenic transcription factor of the Myc family, characterized by a basic helix-loop-helix leucine zipper (bHLH-LZ) structure that obligately heterodimerizes with Max to bind E-box DNA motifs (CACGTG), thereby activating genes essential for cell proliferation, metabolism, and neural development, a function especially critical in high-risk neuroblastoma, where its amplification is a hallmark. N-Myc features an intrinsically disordered N-terminal transactivation domain (TAD, residues 1–137) containing conserved Myc boxes (MB0, MB1, MBII) for coactivator recruitment, helical segments, and a phosphodegron regulated by kinases (ERK1, GSK3, Aurora-A) for ubiquitin-mediated protein stability, alongside a C-terminal bHLH-LZ domain for Max dimerization and DNA recognition. N-Myc occupies hundreds of euchromatic genomic sites marked by activating histone modifications, recruits chromatin modifiers to open chromatin, alleviates RNA Pol II pausing, and drives expression of genes involved in growth, metabolism, and replication stress response; E-box hypomethylation enables tumor-specific targeting, and inducible downregulation can reverse these effects. N-Myc regulates neural differentiation, hematopoiesis, and stem cell cycling, with antagonism from Mad/Mnt/Max complexes, while its dysregulation, particularly via gene amplification, drives tumorigenesis and poor prognosis.

References
https://pubmed.ncbi.nlm.nih.gov/41244073/ https://pubmed.ncbi.nlm.nih.gov/33585251/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%