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Levels of p53 play an important role in the maintenance of stem cells throughout development and the rest of human life. [citation needed] In human embryonic stem cells (hESCs)s, p53 is maintained at low inactive levels. [31] This is because activation of p53 leads to rapid differentiation of hESCs. [32]
[4] [5] [6] It is found within the nucleolus that binds p53. [7] Nucleostemin regulates the cell cycle and affects cell differentiation, decreasing in amount as this differentiation progresses. [7] It is a marker for many stem cells and cancer cells. [8]
Most cancer cells have a mutated p53 and p16INK4a-pRb, which allows the cancer cells to escape a senescent fate. [41] The p16 protein is a cyclin dependent kinase (CDK) inhibitor and it activates Rb tumor suppressor.
Germline stem cells (GSCs) are found in organisms that continuously produce sperm and eggs until they are sterile. These specialized stem cells reside in the GSC niche, the initial site for gamete production, which is composed of the GSCs, somatic stem cells, and other somatic cells.
P53 diverged from p63/p73 with a gene duplication in the cartilaginous fish. [7] P63 and p73 differentiated from each other in bony fish. [ 7 ] In vertebrates, p53 began the role of protecting the somatic cells and acting as a tumor suppressor.
The p53 upregulated modulator of apoptosis (PUMA) also known as Bcl-2-binding component 3 (BBC3), is a pro-apoptotic protein, member of the Bcl-2 protein family. [5] [6] In humans, the Bcl-2-binding component 3 protein is encoded by the BBC3 gene. [5] [6] The expression of PUMA is regulated by the tumor suppressor p53.
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