Role of Cell Cycle Checkpoints In Cell Division Regulation

Authors

  • Shweta Pandey
  • BIT Gorakhpur

DOI:

https://doi.org/10.53555/rytgqf44

Keywords:

Cell cycle checkpoints, p53 gene, CDK proteins, MAPK, Non-small-cell lung carcinomas (NSCLC).

Abstract

- Cell cycle is the regulatory mechanism of regulated cell division process in the body. The cell cycle checkpoints such as regulatory protein and genes work together in different stages during interphase stage of the cell cycle that regulates the cell division in regulatory manner. Some of the regulatory proteins and gene such as p53, CDK family, cyclin family MAPK etc. responsible for proper functioning of the cell division processes such as unreplicated sections of DNA blocks progression in the cell cycle, DNA replication, cell growth, growth factors, cell proliferation, differentiation etc. in both the cells prokaryotic as well as eukaryotic cell. A proto-oncogene is a normal gene having the potential to become an oncogene by mutations, while oncogene is a gene that when mutated, gains a function or is over-expressed, abnormally resulting in the conversion of a normal cell into a cancer cell and the CDKIs are commonly mutated or suppressed in many human malignancies. For instance, germline mutations of p16 causes melanoma. At the single cell level, each cell either had entirely phosphorylated MAPK or no phosphorylated MAPK, confirming that it acts as a switch-like mechanism in each cell. While cyclins activate the CDKs, their inhibitors (CDKIs) suppress the CDKs, exerting negative control over the cell cycle. Somatically acquired inactivation or deletion of p16 causes carcinoma pancreas, glioblastomas, cancer of esophagus, acute lymphocytic leukemia (ALL), Non-small-cell lung carcinomas (NSCLC), soft-tissue sarcomas, and urinary bladder cancers.

Author Biographies

  • Shweta Pandey

    Department of Zoology, Marwar Business School, Gorakhpur.

  • BIT Gorakhpur

    Department of Zoology, Marwar Business School, Gorakhpur.

Downloads

Published

2022-10-16

Issue

Section

Articles