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  • Bernard Straile

TP53 gene – tumor protein p53

“The guardian of the genome”


P53 is essential for regulating DNA repair and cell division. The TP53 gene provides instructions for making a protein called tumor protein p53 (or p53). This protein acts as a tumor suppressor, which means that it regulates cell division by keeping cells from growing and dividing (proliferating) too fast or in an uncontrolled way.

The p53 protein is located in the nucleus of cells throughout the body, where it attaches (binds) directly to DNA. When the DNA in a cell becomes damaged by agents such as toxic chemicals, radiation, or ultraviolet (UV) rays from sunlight, this protein plays a critical role in determining whether the DNA will be repaired or the damaged cell will self-destruct (undergo apoptosis). If the DNA can be repaired, p53 activates other genes to fix the damage. If the DNA cannot be repaired, this protein prevents the cell from dividing and signals it to undergo apoptosis. By stopping cells with mutated or damaged DNA from dividing, p53 helps prevent the development of tumors. (NIH, Genetics Home Reference)


So, should p53 or TP53 go into an IMAET Biofeedback treatment? Yes, whole-heartedly. Whether it’s to re-activate a mutant TP53 gene or just to upregulate it’s expression, it appears to be a good idea to include it into certain feedback sessions.

For a list of conditions caused by genetic changes in TP53, click here.

IMAET software search function: TP53


There are 2 varieties of TP53 in the IMAET software, neither is superior to the other. You may put both varieties in the feedback, or the one which became apparent in the scan result.

Note:

The RPL5 and RPL11 genes provide instructions for making one of approximately 80 different ribosomal proteins, which are components of cellular structures called ribosomes. Ribosomes process the cell's genetic instructions to create proteins such as TP53.


MDM2 proto-oncogene encodes a nuclear-localized E3 ubiquitin ligase. The encoded protein can promote tumor formation by targeting tumor suppressor proteins, such as p53, for proteasomal degradation. This gene is itself transcriptionally-regulated by p53. (NIH, Genetics Home Reference)



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