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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 ]
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 ...
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]
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.
Tumor suppressor p53-binding protein 1 also known as p53-binding protein 1 or 53BP1 is a protein that in humans is encoded by the TP53BP1 gene. [ 5 ] [ 6 ] [ 7 ] Clinical significance
The most well-known example of a ubiquitin-independent proteasome substrate is the enzyme ornithine decarboxylase. [73] Ubiquitin-independent mechanisms targeting key cell cycle regulators such as p53 have also been reported, although p53 is also subject to ubiquitin-dependent degradation. [74]
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[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]