Jumonji is a potential regulatory factor mediating nitric oxide-induced modulation of cardiac hypertrophy.
BACKGROUND AND OBJECTIVES: Jumonji (jmj) is the prototypical member of the jmj domain-containing protein family. It regulates the expression of several genes, in particular genes involved in cardiac cell growth in the embryonic heart. The function of jmj in the mature or developed heart, however, is unclear. RESULTS: We propose that JMJ domain 2A family may be involved in modulating the development of cardiac hypertrophy through interactions with cell cycle-regulatory proteins, specifically retinoblastoma protein, cyclin D and transcription factor E2F, that lead to cell growth. Because nitric oxide can block the development of cardiac hypertrophy and upregulate both jmj gene and protein expression, we propose that jmj is a novel regulatory factor mediating nitric oxide-induced modulation of cardiac hypertrophy. CONCLUSION: Jmj may be a critical, previously unrecognized factor that 'counteracts' the development of cardiac hypertrophy. Biotechnology approaches to increase its expression may be a potential therapeutic strategy to mitigate the increased cardiovascular morbidity and mortality associated with cardiac hypertrophy.[1]References
- Jumonji is a potential regulatory factor mediating nitric oxide-induced modulation of cardiac hypertrophy. Rabkin, S.W., Klassen, S.S. J. Cardiovasc. Med. (Hagerstown) (2009) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg









