p53 is a cell cycle regulating gene which plays a role in tumor suppression. The gene is known to behave as both a transcription factor and an inhibitor depending on cell conditions.
In this article we describe the different cell response to p53 and tools to analyze the proteins involved in p53 mechanisms. These include:
- DNA repair
- Cell cycle arrest
Figure 1: Shows cellular responses mediated by p53 and the protein targets involved. Adapted from doi.org/10.3389/fonc.2014.00285.
In the presence of low stress conditions p53 can activate p53R2 and Gadd45 to help maintain gene stability.
The below table shows tools Abcam provide to research the role p53 responsive proteins play in DNA repair and increasing genomic stability.
By inhibiting the production of some genes, and promoting the production of others, p53 can inhibit the formation of new blood vessels (angiogenesis). p53 is known to inhibit the production of VEGF, which promotes angiogenesis, and to promote the production of the anti-angiogenic factors BAI1 and Tsp1.
The below table shows tools Abcam provide to research the role p53 responsive proteins play in angiogenesis suppression.
Cell Cycle Arrest
The progression of the cell cycle can be held back, i.e. arrested, via multiple p53 pathways. These include regulating the transcriptional expression of 14-3-3σ and Gadd45, and upregulating p21 an inhibitor of cyclin dependent kinases.
The below table shows tools Abcam provide to research the role p53 responsive proteins play in cell cycle arrest.
When exposed to high stress levels p53 can promote senescence (biological aging) rather than apoptosis. This pathway is believed to involve plasminogen activator inhibitor (PAI-1) and p21.
The below table shows tools Abcam provide to research the role p53 responsive proteins play in senescence.
The intrinsic and extrinsic apoptosis (cell death) pathways are both stimulated by p53 via several different signals.
The intrinsic pathway is mostly mediated by the Bcl-2 protein family which initiates cell death using an ‘execution cascade’ involving caspase. The extrinsic pathway also uses a caspase cascade, though in this instance the cascade is initiated by interactions with ‘death receptors’.
The below table shows tools Abcam provide to research the role p53 responsive proteins play in apoptosis.
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