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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 ...
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.
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 ]
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]
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.
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.
An example of one such gene is p53. Patients with Li-Fraumeni syndrome , for example, have mutations in the p53 gene that suggest caretaker function. p53 has an identified role, however, in regulating the cell cycle as well, which is an essential gatekeeper function.
There is also debate on if there can be a defined distinction between therapeutic and non-therapeutic germline editing. An example would be if two embryos are predicted to grow up to be very short in height. Boy 1 will be short because of a mutation in his Human Growth Hormone gene, while boy 2 will be short because his parents are very short.