Induction of Apoptosis via Intrinsic Pathways If the DNA damage is irreparable, p53 shifts its role from protector to executioner. Loss-of-function mutations often disable the G1 checkpoint, allowing cells with genomic instability to proliferate unchecked.
P53 Gene Work Apoptosis Mechanism Explained: How Intrinsic Pathways Trigger Cell Death
Challenges in Gene Therapy Applications Despite the promise of p53-based treatments, clinical applications face significant hurdles. The result is the activation of caspases and the systematic dismantling of the cell to prevent oncogenic transformation.
The delivery of functional p53 genes into tumor cells requires efficient vectors, and immune responses to viral vectors can limit efficacy. Depending on the severity of the stress, it can pause the cell cycle to allow repair, trigger programmed cell death, or maintain a state of permanent dormancy to prevent the propagation of mutations.
P53 Gene Work Apoptosis Mechanism Explained: Intrinsic Pathways and Caspase Activation
It transactivates pro-apoptotic genes such as BAX, PUMA, and NOXA while repressing anti-apoptotic genes like BCL-2. The Molecular Mechanism of Activation Under normal conditions, the p53 protein is kept at low levels by MDM2, an E3 ubiquitin ligase that tags it for destruction.
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