| First Author | Lee LA | Year | 1995 |
| Journal | J Clin Invest | Volume | 95 |
| Issue | 2 | Pages | 900-4 |
| PubMed ID | 7860774 | Mgi Jnum | J:22682 |
| Mgi Id | MGI:70540 | Doi | 10.1172/JCI117741 |
| Citation | Lee LA, et al. (1995) Cell density and paradoxical transcriptional properties of c-Myc and Max in cultured mouse fibroblasts. J Clin Invest 95(2):900-4 |
| abstractText | Deregulated expression of the c-Myc oncoprotein occurs in several human malignancies. The c-Myc protein behaves as a transcription factor, and undoubtedly its role in carcinogenesis involves its ability to affect the expression of genes involved in cell growth. c-Myc has been reported to both activate and repress transcription in transient transfection experiments using reporter constructs bearing multiple copies of the c-Myc binding site, CAC (G/A) TG. We investigated these apparently paradoxical effects of c-Myc by determining if they arose from differences in the cell proliferation states of transfected cells. We found that endogenous c-Myc protein levels vary inversely with the degree of cell confluency, such that at low cell confluency, where endogenous levels of c-Myc are high and presumably endogenous levels of Max are limiting, exogenous c-Myc fails to affect basal transcription. In cells at high cell confluency, in which endogenous c-Myc levels are low, exogenous c-Myc augments transactivation by titrating the relative excess endogenous Max. These observations suggest that the apparently paradoxical behavior of c-Myc in transfection experiments is partially dependent on ambient cellular levels of c-Myc. |
