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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2

ISSN Imprimir: 0893-9675
ISSN On-line: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.v5.i1.30
pages 59-68

Myc Protein: Partners and Antagonists

Imre Vastrik
Molecular/Cancer Biology Laboratory, Department of Pathology, University of Helsinki, P.O. Box 21 (Haartmaninkatu 3), Helsinki
Tomi P. Makela
Molecular/Cancer Biology Laboratory, Department of Pathology, University of Helsinki, P.O. Box 21 (Haartmaninkatu 3), Helsinki
Paivi J. Koskinen
Molecular/Cancer Biology Laboratory, Department of Pathology, University of Helsinki, P.O. Box 21 (Haartmaninkatu 3), Helsinki
Juha Klefstrom
Molecular/Cancer Biology Laboratory, Department of Pathology, University of Helsinki, P.O. Box 21 (Haartmaninkatu 3), Helsinki
Kari Alitalo
Molecular/Cancer Biology Laboratory, Department of Pathology, University of Helsinki, P.O. Box 21 (Haartmaninkatu 3), Helsinki

RESUMO

One of the first oncogenes identified from human tumors was c-myc, which is frequently activated in Burkitt's lymphomas due to chromosomal translocations. Subsequently, members of the myc oncogene family were found to be amplified in neuroblastoma and small-cell lung cancer. In normal cells, Myc activity has been shown to be both necessary and sufficient for resting cells to enter the cell cycle. Interestingly, it appears that Myc not only drives the cell cycle, but also induces cell death by apoptosis in certain situations. Myc contains a transcriptional activation domain and a basic helix-loop-helix-leucine zipper DNA-binding and dimerization domain. As a heterodimer with a structurally related protein, Max, Myc can bind DNA in a sequence-specific manner. These results suggest that the Myc/Max heterodimer functions as a transcriptional activator of genes that are critical for the regulation of cell growth.