negative regulation of intrinsic apoptotic signaling pathway in response to osmotic stress by p53 class mediator

Definition

Target type: biologicalprocess

Any process that stops, prevents or reduces the frequency, rate or extent of intrinsic apoptotic signaling pathway in response to osmotic stress by p53 class mediator. [GOC:krc, GOC:mtg_apoptosis, GOC:TermGenie, PMID:16571598]

The p53 class mediator plays a crucial role in negatively regulating the intrinsic apoptotic signaling pathway in response to osmotic stress. This process involves a complex interplay of molecular events that aim to protect cells from programmed cell death.

Upon encountering osmotic stress, cells experience changes in their intracellular water content and solute concentration. This triggers a cascade of events, including the activation of various stress sensors and signaling pathways. One of these pathways involves the tumor suppressor protein p53, a key player in cellular responses to stress.

The p53 class mediator acts as a downstream effector of p53 activation. It modulates the activity of pro-apoptotic proteins, particularly those involved in the mitochondrial apoptotic pathway. This pathway is a critical component of intrinsic apoptosis, where mitochondria release apoptotic factors like cytochrome c into the cytoplasm, triggering the activation of caspases and ultimately leading to cell death.

The p53 class mediator exerts its negative regulatory influence on the intrinsic apoptotic signaling pathway by several mechanisms:

1. **Inhibition of pro-apoptotic Bcl-2 family members:** The p53 class mediator can directly interact with and inhibit the activity of pro-apoptotic Bcl-2 family proteins such as Bax and Bak. These proteins promote the release of cytochrome c from mitochondria, and their inhibition prevents this process.
2. **Activation of anti-apoptotic Bcl-2 family members:** Conversely, the p53 class mediator can enhance the activity of anti-apoptotic Bcl-2 family proteins such as Bcl-2 and Bcl-xL. These proteins counteract the pro-apoptotic effects of Bax and Bak, preventing mitochondrial dysfunction and apoptosis.
3. **Regulation of mitochondrial permeability transition pore:** The p53 class mediator can also influence the opening of the mitochondrial permeability transition pore (mPTP). The mPTP is a channel in the mitochondrial membrane that allows the release of apoptotic factors. By regulating mPTP opening, the p53 class mediator can control the flow of these factors and prevent excessive apoptosis.

By modulating the activity of these key players in the intrinsic apoptotic signaling pathway, the p53 class mediator effectively dampens the apoptotic response to osmotic stress. This protective mechanism helps to maintain cell viability and prevent premature cell death under challenging environmental conditions.

However, the precise mechanisms and downstream targets of the p53 class mediator in this process may vary depending on the specific cell type and the nature of the osmotic stress. Further research is needed to fully elucidate the complex interplay of p53, the p53 class mediator, and other signaling pathways involved in the regulation of cellular fate during osmotic stress.'
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Proteins (1)

Compounds (13)