cMyc

c-Myc is a transcription factor encoded by the MYC gene in humans. It is a member of the Myc family, which also includes N-Myc and L-Myc. As a basic helix-loop-helix leucine zipper (bHLH-LZ) protein, c-Myc forms heterodimers with MAX and binds to E-box sequences (CACGTG) to regulate transcription of thousands of target genes involved in cell growth, metabolism, and proliferation.

c-Myc activity is tightly regulated at multiple levels. Expression is driven by mitogenic signals; the protein is rapidly turned over, with turnover controlled by phosphorylation at Ser62 and Thr58 and subsequent ubiquitination by the SCF-Fbw7 complex, leading to proteasomal degradation. This dynamic regulation couples external cues to gene expression.

Biological roles: c-Myc promotes cell cycle progression, ribosome biogenesis, and metabolic reprogramming, including upregulation of glycolysis and glutaminolysis. It influences differentiation and, in some contexts, can induce apoptosis if survival signals are insufficient.

Clinical relevance: Deregulation of MYC is a hallmark of many cancers. Mechanisms include gene amplification and chromosomal translocations that place MYC under the control of strong enhancers; the classic example is Burkitt lymphoma, where t(8;14) places MYC next to the IGH locus. Overexpression occurs in various solid tumors as well. Directly targeting c-Myc is challenging, but approaches aim to disrupt Myc-Max dimerization or interfere with its transcriptional programs.

In normal physiology, c-Myc participates in development and stem cell biology, with activity tightly tuned by signaling networks to balance growth and differentiation.