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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 ]
Embryoid body: hESCs in culture spontaneously form ball-like embryo-like structures termed "embryoid bodies", which consist of a core of mitotically active and differentiating hESCs and a periphery of fully differentiated cells from all three germ layers. iPSCs also form embryoid bodies and have peripheral differentiated cells.
At the intracellular level, hECTs exhibit several essential structural features of cardiomyocytes, including organized sarcomeres, gap-junctions, and sarcoplasmic reticulum structures; [1] however, the distribution and organization of many of these structures is characteristic of neonatal heart tissue rather than adult human heart muscle.
P53, p63, and p73 have similar features in their gene structures and functions but have also diverged evolutionarily. The p53 family evolved from an ancestor gene in unicellular life. [ 4 ] The ancestor gene functioned in germ line DNA protection early invertebrates. [ 5 ]
[88] p53 prevents the cell from replicating by stopping the cell cycle at G1, or interphase, to give the cell time to repair; however, it will induce apoptosis if damage is extensive and repair efforts fail. [89] Any disruption to the regulation of the p53 or interferon genes will result in impaired apoptosis and the possible formation of tumors.
AST-OPC1 is a population of cells derived from human embryonic stem cells (hESCs) that contains oligodendrocyte progenitor cells (OPCs). OPCs and their mature derivatives called oligodendrocytes provide critical functional support for nerve cells in the spinal cord and brain.
It was shown that, although p53 arrests the numbers of cells to different extents in different phases, the measured level of survivin mRNA and protein levels were the same across all the samples transfected with the wild-type p53. This shows that p53 acts in a cell-cycle independent manner to inhibit survivin expression. [17]
In short, p53 is a tumor-suppressor protein that arrests the cell cycle and prevents cell growth and survival when DNA damage occurs. [48] Thus, the degradation of p53, induced by E6, promotes unregulated cell division, cell growth and cell survival, all characteristics of cancer.