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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 ]
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.
P53 causes cells to enter apoptosis and disrupt further cell division therefore preventing that cell from becoming cancerous (16). In the majority of cancers it is the p53 pathway that has become mutated resulting in lack of ability to terminate dysfunctional cells.
Part of this pathway includes alpha-interferon and beta-interferon, which induce transcription of the p53 gene, resulting in the increase of p53 protein level and enhancement of cancer cell-apoptosis. [85] 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 ...
High-normal levels of the bile acid deoxycholic acid cause apoptosis in human colon cells, [56] but may also lead to colon cancer if repair and apoptotic defenses are insufficient. [57] Apoptosis serves as a safeguard mechanism against tumorigenesis. [58] It prevents the increased mutagenesis that excess DNA damage could cause, upon replication ...
P53, a transcription factor, can bind two sites within the human TIGAR gene to activate expression. [ 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 ]
The maintenance of such arrest in the G2 phase is further sustained by p53 and p21. In the absence of p53 or p21, it was demonstrated that radiated cells progressed into mitosis. [ 17 ] The absence of p21 or 14-3-3 cannot sufficiently inhibit the CyclinB-Cdc2 complex, thus exhibiting the regulatory control of p53 and p21 in the G2 checkpoint in ...
The cell cycle control system is biochemically based so that the proteins of the mitosis promoting factor (MPF) control the transition from one phase to the next based on a series of checkpoints. MPF is a protein dimer made up of cyclin and cyclin-dependent kinase (Cdk), a serine and threonine kinase , which come together at different points in ...