Ink4A/ARF controls at least two pathways p16 and p53 to force the cell into senescence.
p16 seems to be inactive in mouse (probably because TERT is active). In humans p53 is more emphasized.
Image source
Is Ink4a/ARF controlled by the epigenetic clock?
Is the culture shock actually accelerated epigenetic aging?
Epithelial cells escaping the Ink4a/ARF related replicative senescene seems to go into a mesemchynal like state (they no longer need cell-cell adhesion). Mesemchymal cells are not restricted by the Ink4a/ARF checkpoint.
Maybe the epigenetic clock was originally the program from mesemchymal transformation?
p16 seems to be inactive in mouse (probably because TERT is active). In humans p53 is more emphasized.
Image source
Is Ink4a/ARF controlled by the epigenetic clock?
Is the culture shock actually accelerated epigenetic aging?
Epithelial cells escaping the Ink4a/ARF related replicative senescene seems to go into a mesemchynal like state (they no longer need cell-cell adhesion). Mesemchymal cells are not restricted by the Ink4a/ARF checkpoint.
Maybe the epigenetic clock was originally the program from mesemchymal transformation?
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