Previous studies have identified several host proteins (p53, p107, and p193), which form prominent complexes with SV40 T antigen in transformed cardiomyocytes. Expression of p53 and p107 was monitored during normal and pathologic growth in nontransformed murine myocardium. Both genes were expressed at relatively high levels in embryonic cardiomyocytes. Transcript levels decreased markedly during the process of cardiomyocyte terminal differentiation and were very low or undetectable in adult animals. In contrast, retinoblastoma transcripts were observed at low levels throughout myocardial development. None of the tumor suppressor genes examined were transcriptionally activated during acute myocardial overload or isoproterenol-induced myocardial hypertrophy. The potential role of tumor suppressor gene product expression in myocardial development and pathology is discussed.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Biological Chemistry|
|State||Published - Jan 1 1994|
ASJC Scopus subject areas
- Molecular Biology
- Cell Biology