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Activation of the tumor suppressors encoded by this locus leads to an irreversible cell cycle exit.
Altogether, these findings are suggestive of reduced proliferation, premature cell cycle exit and induction of differentiation.
Conversely, overexpression of CBF slows cell cycle exit and delays muscle differentiation.
Thus, thyroid hormones regulate muscle development and function by inducing myoblast cell cycle exit [8].
We postulate that this role is to inhibit cell cycle progression and promote cell cycle exit.
Runx1 or CBFβ downregulation in myoblasts induced an accelerated cell cycle exit.
Our findings suggest that Ngn2 regulates amplification and cell cycle exit of DG granule progenitors.
NeuroD1, on the other hand, induces cell cycle exit and promotes rapid neuronal maturation.
We also saw that Ngn2 does not always efficiently induce cell cycle exit.
Cell cycle exit is also characterized by a decrease in the expression of cyclins [34].
This family of CKIs has been implicated in mediating cell cycle exit prior to terminal differentiation.
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