Induction of apoptosis by the Bcl-2 homologue Bak

Article Abstract:

The apoptosis suppression by the bcl-2 oncogene is counteracted by a newly discovered Bcl-2 homologue, Bak, which stimulates serum-deprived fibroblasts' cell death extensively and quickly. Apoptosis is regulated by the cells to prevent malignancies such as tumors developing and so the cell death mechanism is important. It is possible that Bak works through direct physical interaction with proteins while the apoptosis inhibitors work through suppressing Bak, though the exact molecular mechanisms are unknown. A function analysis and complementary DNA cloning of Bak is included.

Physiological aspects, Cell death

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Transcriptional activation by the human c-Myc oncoprotein in yeast requires interaction with Max

Article Abstract:

The c-myc protein (Myc) is a sequence-specific transcriptional activator that relies on the dimerization of the closely related Max protein to achieve DNA binding. The Max homodimers attach to the same DNA sequence as Myc+Max but cannot transactivate and so can prevent Myc+Max expression. Furthermore, the Max helix-loop-helix-leucine zipper (HLH-Z) domain has a stronger affinity for Myc HLH-Z than for itself, indicating that heterodimeric Myc+Max activator comes together optimally at equilibrium.

Genetic aspects, Genetic regulation, Genetic transcription, Transcription (Genetics)

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Cooperative interaction between c-myc and bcl-2 proto-oncogenes

Article Abstract:

The genetic expression of the protein Bcl-2, encoded by the proto-oncogene bcl-2, stops apoptosis or cell death caused by the proto-oncogene c-myc without altering the mitogenic role of c-myc. This finding illuminates the mechanism of synergy between the bcl-2 and c-myc proto-oncogenes. Moreover, the new insight into oncogene interrelations may improve understanding of carcinogenesis and the development of tumors that resist drugs.

Carcinogenesis, Proto-oncogenes

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