MYC

MYC (Myc proto-oncogene protein) is a nuclear protein that acts as a transcription factor, driving cell growth, self-renewal, proliferation, differentiation and death under normal conditions. Deregulation of MYC is associated with the initiation and maintenance of many cancers.

Products
Background
Literature
Pathways
Gene Data

Inhibitors

Cat No Product Name / Activity
4406 10058-F4
Inhibits c-Myc-Max dimerization
5306 KJ Pyr 9
High affinity Myc inhibitor

MYC (Myc proto-oncogene protein) is a nuclear protein that acts as a transcription factor, driving cell growth, self-renewal, proliferation and differentiation under normal conditions. MYC belongs to a family of transcription factors that includes N-Myc and L-Myc, and is a subgroup of the larger class of bHLHZ (basic-helix loop-helix leucine zipper domain) transcription factors. MYC heterodimerizes with MAX, enabling DNA binding and transcriptional regulation. MYC is the endpoint for numerous signal transduction pathways, such as MAPK and PI 3-kinase, and acts to integrate different cellular signals.

MYC-MAX is able to bind to 10-15% of the human genome, regulating both protein-coding and non-protein-coding genes. Many of the genes that MYC regulates are involved in the cell cycle and metabolism, including cyclins, CDK4, Cdc25 and more. MYC can also stimulate differentiation and has a crucial role in apoptosis. MYC is also of interest in stem cell research owing to the critical role of the protein in self-renewal and pluripotency, and was originally used by Takahashi and Yamanaka (2006) in combination with other transcription factors, Oct4, Sox2 and Klf4, to reprogram mature cells to become pluripotent.

MYC proteins are very unstable, having a half-life of around 20-30 minutes in many normal cells. The stability of MYC is controlled by numerous ubiquitin ligases, and increased stability of MYC has been shown to be associated with its deregulation and increased tumorigenicity. Phosphorylation at Ser62 increases MYC stability, so prolonging its actions, whereas phosphorylation by GSK-3 at Thr58 promotes MYC ubiquitination and proteasomal degradation. A mutated version of Myc, the gene encoding MYC, is found in many cancers, which causes the gene to be constitutively expressed.

Literature for MYC

Cancer

Cancer Research Product Guide

A collection of over 750 products for cancer research, the guide includes research tools for the study of:

  • Cancer Metabolism
  • Epigenetics in Cancer
  • Receptor Signaling
  • Cell Cycle and DNA Damage Repair
  • Angiogenesis
  • Invasion and Metastasis
Stem Cells

Stem Cells Scientific Review

Written by Kirsty E. Clarke, Victoria B. Christie, Andy Whiting and Stefan A. Przyborski, this review provides an overview of the use of small molecules in the control of stem cell growth and differentiation. Key signaling pathways are highlighted, and the regulation of ES cell self-renewal and somatic cell reprogramming is discussed. Compounds available from Tocris are listed.

Pathways for MYC

MAPK

MAPK Signaling Pathway

The mitogen-activated protein kinase pathway evokes an intracellular signaling cascade in response to extracellular stimuli such as heat and stress. It can influence cell division, metabolism and survival.

MYC Gene Data

Gene Species Gene Symbol Gene Accession No. Protein Accession No.
MYC Human MYC NM_002467 P01106
Mouse Myc NM_010849 P01108
Rat Myc NM_012603 P09416
MYCN Human MYCN NM_005378 P04198
Mouse Mycn NM_008709 P03966
Rat Mycn NM_001013096 Q63379
MYCL Human MYCL NM_001033082 P12524
Mouse Mycl NM_008506 P10166
Rat Mycl NM_001191763 NP_001178692