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Therefore, cancer cells may be more susceptible to ALT activation due to the binding of epitalon to the already reduced levels of histone H1, whereas normal cells may be more resilient as they naturally express higher levels of H1

The mechanisms underlying this ability may involve interactions with receptor proteins, suppression of efflux protein activity, and regulation of tight junction protein expression [22]

Mechanisms of dendritic spine remodeling in a rat model of traumatic brain injury

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Cathepsin B facilitates autophagy-mediated apoptosis in SPARC overexpressed primitive neuroectodermal tumor cells