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Induced cell cycle arrest is the use of a chemical or genetic manipulation to artificially halt progression through the cell cycle. Cellular processes like genome duplication and cell division stop. [1] It can be temporary or permanent. [1]
The degradation has an inhibitory effect on the formation of cyclin-dependent kinase complexes, which are key drivers of the cell cycle. [14] Through targeting Cdc25, cell cycle arrest can occur at multiple time points including the G1/S transition, S phase and G2/M transition. [8] Furthermore, Chk1 can target Cdc25 indirectly through ...
Indefinite cell cycle arrest is another potential outcome. For this reason, it is considered to be a tumor suppressor gene. [3] Identification of this gene's repression via methylation to its upstream promoter region [2] [4] within various types of cancerous tissue have been used to suggest a connection to the formation of said cancer.
Studies of p53 dependent cell cycle arrest in response to DNA damage identified p21 as the primary mediator of downstream cell cycle arrest. Notably, El-Deiry et al. identified a protein p21 (WAF1) which was present in cells expressing wild type p53 but not those with mutant p53, moreover constitutive expression of p21 led to cell cycle arrest ...
p53 pathway: In a normal cell, p53 is inactivated by its negative regulator, mdm2. Upon DNA damage or other stresses, various pathways will lead to the dissociation of the p53 and mdm2 complex. Once activated, p53 will induce a cell cycle arrest to allow either repair and survival of the cell or apoptosis to discard the damaged cell.
The cell cycle checkpoints play an important role in the control system by sensing defects that occur during essential processes such as DNA replication or chromosome segregation, and inducing a cell cycle arrest in response until the defects are repaired. [8]
Under low nitrogen conditions, Rim15 is activated to promote cell cycle arrest through inactivation of the protein kinases TORC1 and Sch9. While TORC1 and Sch9 belong to two separate pathways, namely the TOR and Fermentable Growth Medium induced pathways respectively, both protein kinases act to promote cytoplasmic retention of Rim15.
The cytoplasmic distension is a direct result of the G2/M cell cycle arrest. The cell enlarges in preparation for mitosis, but cannot divide to restore its normal size. Aside from classical apoptosis, signs of cellular senescence has also been observed in normal and cancer cell lines (fibroblasts, HeLa and U2-OS) after CDT intoxication [9]