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| c-Myc | |
|---|---|
| Name | c-Myc |
| Uniprot | P01106 |
| Organism | Homo sapiens |
| Gene | MYC |
c-Myc c-Myc is a transcription factor encoded by the human MYC proto-oncogene, central to regulation of cell proliferation, metabolism, and apoptosis. It integrates signals from growth factor receptors and oncogenic pathways to control expression of genes involved in cell cycle progression and biosynthesis, and is implicated in many cancers and developmental processes. Historical and contemporary research has linked c-Myc activity to major figures and institutions in molecular biology and oncology, including laboratories at Cold Spring Harbor Laboratory, Massachusetts Institute of Technology, Howard Hughes Medical Institute, National Institutes of Health, and investigators associated with Francis Crick, James Watson, and Harold Varmus.
c-Myc was discovered through studies of avian myelocytomatosis viruses and human chromosomal translocations by researchers affiliated with Johns Hopkins University, University of California, San Francisco, University of Cambridge, Stanford University, and University of Chicago. Its importance was rapidly recognized by the cancer research community, with connections to work at Dana-Farber Cancer Institute, Memorial Sloan Kettering Cancer Center, Fred Hutchinson Cancer Research Center, University of Pennsylvania, and Columbia University. Seminal publications and conferences at Royal Society, Cold Spring Harbor Laboratory, and American Association for Cancer Research helped establish c-Myc as a paradigm for oncogenic transcription factors, intersecting with the research of Harold Varmus, J. Michael Bishop, Elizabeth Blackburn, Carol Greider, and Bert Vogelstein.
The c-Myc protein contains a basic helix-loop-helix leucine zipper (bHLH-LZ) domain required for dimerization and DNA binding, and intrinsically disordered N-terminal transactivation domains targeted by ubiquitin ligases and kinases studied at Max Planck Society, European Molecular Biology Laboratory, National Cancer Institute, and Institut Pasteur. Post-translational modification and turnover involve enzymes and complexes researched at Yale University, University of Oxford, Harvard Medical School, and University of California, San Diego, including phosphorylation by kinases linked to PI3K/Akt pathway, MAPK/ERK pathway, and regulation by phosphatases investigated at Rockefeller University and Scripps Research. Promoter elements and enhancer regulation of the MYC locus were illuminated through genomic technologies developed at Broad Institute, Wellcome Sanger Institute, European Bioinformatics Institute, and collaborations with Stanford Genome Technology Center and Johns Hopkins Bloomberg School of Public Health.
c-Myc controls transcriptional programs that drive ribosomal biogenesis, mitochondrial function, nucleotide synthesis, and glycolysis, with mechanistic links to studies at Carnegie Institution for Science, University of Cambridge Department of Pathology, Imperial College London, and University of Toronto. c-Myc coordinates cell cycle entry through regulation of cyclins and CDKs, informed by research from Mount Sinai School of Medicine, University of Michigan, University of California, Irvine, and University of Washington. Its roles in embryonic development and stem cell biology intersect with laboratories at Salk Institute for Biological Studies, Whitehead Institute, Riken, and Kyoto University, and with investigators such as Shinya Yamanaka and James Thomson in the context of pluripotency.
Aberrant MYC activation is a hallmark of many malignancies including Burkitt lymphoma, neuroblastoma, lung carcinoma, breast carcinoma, and hepatocellular carcinoma, as characterized by clinical centers such as Mayo Clinic, Cleveland Clinic, University College London Hospitals, and Karolinska Institute. Chromosomal translocations, gene amplification, and enhancer hijacking involving the MYC locus have been documented in cooperative studies involving Memorial Sloan Kettering Cancer Center, Vanderbilt University Medical Center, University of Texas MD Anderson Cancer Center, and Fred Hutchinson Cancer Research Center. The oncogenic potency of c-Myc has been modeled in genetically engineered mice developed at Roswell Park Comprehensive Cancer Center, Fred Hutchinson Cancer Research Center, The Jackson Laboratory, and European Molecular Biology Laboratory mouse facilities, contributing to translational efforts at National Cancer Institute and clinical programs at Stanford Health Care.
c-Myc functions downstream of receptor tyrosine kinases studied at Genentech, Amgen, Roche, and Pfizer research programs, integrating inputs from pathways characterized at Cold Spring Harbor Laboratory, Salk Institute for Biological Studies, Harvard Medical School, and Massachusetts General Hospital. It forms heterodimers with Max, interacts with transcriptional cofactors such as TRRAP and GCN5, and interfaces with chromatin remodelers studied at Broad Institute, University of California, Berkeley, and Max Planck Institute for Molecular Genetics. Cross-talk with tumor suppressors and signaling nodes including TP53, RB1, PTEN, Wnt pathway, Notch signaling, and components explored by teams at University of Oxford, University of Cambridge, Yale School of Medicine, and Columbia University Irving Medical Center define context-dependent outcomes in proliferation, differentiation, and apoptosis.
Targeting c-Myc-driven tumors has been a major objective for biotechnology and pharmaceutical companies including Novartis, AstraZeneca, Bristol Myers Squibb, Eli Lilly and Company, and startups incubated at Biocon and Genentech. Strategies include small molecules disrupting Myc-Max dimerization (investigated at University of California, San Francisco and Stanford University), proteolysis-targeting chimeras informed by work at Kyoto University and ETH Zurich, and indirect approaches targeting epigenetic regulators and metabolic dependencies examined at Dana-Farber Cancer Institute, Memorial Sloan Kettering Cancer Center, Cold Spring Harbor Laboratory, and Broad Institute. Clinical trials at National Institutes of Health Clinical Center, MD Anderson Cancer Center, Mayo Clinic Cancer Center, and Royal Marsden Hospital are evaluating inhibitors of pathways that modulate c-Myc activity, with translational contributions from consortia such as International Cancer Genome Consortium and The Cancer Genome Atlas.
Category:Transcription factors Category:Oncogenes