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Nowadays, cancer and infectious diseases are leading targets for the design of effective drugs, in which the primary mechanism of action relies on the modulation of programmed cell death (PCD).
In mammals various intracellular pathogens have evolved strategies, including the modulation of programmed cell death (PCD), which favours their survival.
Present results allow us to speculate on the possible implications of deamidation and methylation in the modulation of programmed cell death, under conditions in which this process is altered, such as in cancer.
To date, three major developmental pathways were shown to be involved with gonad differentiation through the modulation of programmed cell death.
In general, modulation of programmed cell death (PCD) can be achieved by the dynamic expression of pro- and anti-apoptotic BCL-2 protein family members and apoptosis inhibitor proteins, such as survivin.
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Our work demonstrates engineering of fully functional HSCs via modulation of genetic programs that govern self-renewal and lineage priming.
Metabolic and immune programming are also under epigenetic regulation, and there is increasing evidence now that nutrition can influence long-term health outcomes by modulation of epigenetic programming [78].
In addition, we suggest a widespread role for Math6 in the modulation of differentiation programs in various cell types during embryogenesis.
Collectively, these trends demonstrate the contribution of targeted mRNA degradation to the transcriptional bottleneck and the modulation of genetic programs subsequently deployed.
In light of incomplete characterization of proteins involved in the mitochondrial permeability transition (MPT) the genetic modulation of this program to prevent cardiomyopathy has to my knowledge not being explored.
Mechanisms being exploited by these agents include the modulation of cellular signaling, programmed cell death, the cell cycle, and angiogenesis.
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