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The p53 p63 p73 family is a family of tumor suppressor genes. [1] [2] This gene family codes the proteins: p53; TP73L (also known as "p63") p73; They are sometimes considered part of a "p53 family." When overexpressed, these proteins are known to be involved in tumor pathogenesis. [3]
p53, also known as Tumor protein P53, cellular tumor antigen p53 (UniProt name), or transformation-related protein 53 (TRP53) is a regulatory protein that is often mutated in human cancers. The p53 proteins (originally thought to be, and often spoken of as, a single protein) are crucial in vertebrates , where they prevent cancer formation. [ 5 ]
For example ESCs have been differentiated into insulin-producing cells, [26] and researchers at Harvard University were able to produce large quantities of pancreatic beta cells from ESCs. [ 27 ] An article published in the European Heart Journal describes a translational process of generating human embryonic stem cell-derived cardiac ...
However unlike mESCs, hESCs have a functional G1 phase. hESCs show that the activities of Cyclin E/Cdk2 and Cyclin A/Cdk2 complexes are cell cycle-dependent and the Rb checkpoint in G1 is functional. [39] ESCs are also characterized by G1 checkpoint non-functionality, even though the G1 checkpoint is crucial for maintaining genomic stability.
Low efficiency: in general, the conversion to iPS cells has been incredibly low. For example, the rate at which somatic cells were reprogrammed into iPS cells in Yamanaka's original mouse study was 0.01–0.1%. [1] The low efficiency rate may reflect the need for precise timing, balance, and absolute levels of expression of the reprogramming genes.
The fact that the blastocyst is destroyed during the process has raised controversy and ethical concerns. Embryonic stem cells are pluripotent, meaning they can differentiate to form all cell types in the body. In vitro, embryonic stem cells can be cultured under defined conditions to keep them in their pluripotent state, or they can be ...
Mutated p53 is involved in many human cancers, of the 6.5 million cancer diagnoses each year about 37% are connected to p53 mutations. [30] This makes it a popular target for new cancer therapies. Homozygous loss of p53 is found in 65% of colon cancers, 30–50% of breast cancers, and 50% of lung cancers.
[9] [13] One site is found within the first intron, and binds p53 with high affinity. [9] [13] The second is found just prior to the first exon, binds p53 with low affinity, [9] [13] and is conserved between mice and humans. [9] TIGAR expression can be regulated by other non-p53 mechanisms in tumour cell lines. [9]