Cell Differentiation and Aging Lead To Up-Regulation of FTO, While the ALKBH5 Protein Level Was Stable During Aging but Up-Regulated During in vitro-Induced Cardiomyogenesis
Cell Development and Aging Increase FTO Levels, While ALKBH5 Stays Stable with Age but Rises During Lab-Induced Heart Cell Formation
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Abstract
Aging in male and female mice is associated with FTO up-regulation in multiple organs.
- FTO and ALKBH5 proteins are crucial for removing N6-adenosine methylation from RNA.
- FTO levels increased during aging in the hearts, brains, lungs, and kidneys of mice, while ALKBH5 levels remained stable.
- Both proteins were elevated during cardiomyogenesis, but ALKBH5 levels did not change during neuroectodermal differentiation.
- Depleting HDAC1 in mouse embryonic stem cells led to a decrease in FTO levels.
- In these stem cells, specific gene loci showed reduced N6-adenosine methylation that influences cell differentiation into neuroectoderm.
- FTO appears to have a more significant role than ALKBH5 in regulating m6A RNA demethylation during aging and neuronal differentiation.
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