How does GSK3β mechanistically regulate p16INK4A and p53 to drive senescence signaling?

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Description

While the abstract shows GSK3β physically interacts with p16INK4A and p53 as putative substrates, the specific phosphorylation sites and downstream signaling cascades remain undefined. Understanding these mechanisms is critical for developing targeted senostatic therapies.

Gap type: unexplained_observation Source paper: Age-related GSK3β overexpression drives podocyte senescence and glomerular aging. (None, None, PMID:35166234)

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