Normal function · from ai-gene-review (P01106, commit 79fe13b38970) · AI-generated, not KB evidence

MYC (c-Myc) is a nuclear bHLH-leucine zipper transcription factor and major proto-oncogene that regulates cell growth, proliferation, metabolism, and apoptosis. MYC functions primarily through obligate heterodimerization with MAX to bind E-box DNA motifs (CACGTG) at promoters and enhancers, activating transcription of target genes involved in cell cycle progression, ribosome biogenesis, and metabolic programs. MYC can also repress transcription via interaction with MIZ1 (ZBTB17). The protein contains N-terminal transactivation domains with conserved Myc boxes (MBI-MBIV) and a C-terminal bHLH-LZ domain for dimerization and DNA binding. MYC stability is regulated by a phosphodegron at T58/S62 recognized by the E3 ligase FBXW7 for ubiquitin-mediated proteasomal degradation. MYC is deregulated in over 50% of human cancers and regulates approximately 11% of human genes.

DNA-binding transcription factor activity forming heterodimers with MAX to bind E-box sequences and regulate target gene expression
E-box DNA binding activity recognizing CANNTG sequences in target gene promoters and enhancers
Protein dimerization activity forming heterodimers with MAX protein for DNA binding and transcriptional regulation
molecular function: protein dimerization activity · directly involved in: protein-containing complex assembly · locations: nucleus; nucleoplasm · in complex: Myc-Max complex · substrates: MAX protein
In the knowledge base · computed from kb/ at build time

Disorders

Relationship is the entry's genetic[].relationship_type. untyped means the entry has a genetic record for the gene but does not type it; its free-text association is shown instead.

DisorderRelationshipWhere the gene appears
Angiosarcoma somatic driver somatic
mechanism: MYC-Amplified Secondary Angiosarcoma Program
scoped to subtype: Radiation-Associated Angiosarcoma
B-Lymphoblastic Leukemia/Lymphoma With Recurrent Genetic Abnormality somatic driver somatic
scoped to subtype: MYC-rearranged
Blastic Plasmacytoid Dendritic Cell Neoplasm somatic driver somatic
mechanism: MYC Rearrangement at 8q24
Burkitt Lymphoma somatic driver somatic
mechanism: MYC Translocation and Oncogene Activation
Osteosarcoma untyped
Amplification / hyperactivation
Plasma Cell Neoplasm untyped
Somatic
mechanism: Precursor-to-Myeloma Clonal Progression
Small Cell Lung Cancer untyped
Amplification
Aflatoxin-Related Hepatocellular Carcinoma no genetic record
mechanism: R249S-CDK4-PIN1-c-Myc Gain-of-Function
BRAF V600E-Mutant Non-Small Cell Lung Cancer no genetic record
animal model: Mus musculus
Fibrolamellar Hepatocellular Carcinoma no genetic record
mechanism: MYC Protein Accumulation
Hepatocellular Carcinoma no genetic record
discussion: (unnamed)
Pancreatic Ductal Adenocarcinoma no genetic record
mechanism: MYC Amplification-Driven RAS-Independent Proliferation
Primary_Tonsillar_Lymphoma no genetic record
mechanism: Double/Triple-hit High-grade B-cell Lymphoma

Identity from HGNC (snapshot 2026-10-01). Page layers are described in the gene pages documentation.