An intimate alliance of DNA-damage response network with cell-cycle checkpoints amid events of uncontrolled cellular proliferation- a minireview

Author(s):  
Aroni Chatterjee ◽  
Keshav Rajarshi ◽  
Rajni Khan ◽  
Hiya Ghosh ◽  
Sonia Kapoor ◽  
...  

: There is close interdependence between cell survival, cell senescence, events of the cell cycle, apoptosis, malignancy development, and tumor responses to cancer treatment. Intensive studies and elaborate researches have been conducted on the functional aspects of oncogenes, tumor suppressor genes, apoptotic genes, and members guiding cell cycle regulation. These disquisitions have put forward the existence of a highly organized response pathway termed as a DNAdamage response network. The pathways detecting DNA damage and signaling are intensively linked to the events of cellcycle arrest, cell proliferation, apoptosis, and cell senescence. DNA damage responses are complex systems that incorporate specific "sensor" and "transducer" proteins, for assessment of damage and signal transmission, respectively. These signals are thereafter relayed upon various "effector" proteins involved in different cellular pathways. It may include those governing cell-cycle checkpoints, participating in DNA repair, cell senescence, and apoptosis. This review discusses about the role of tumour suppressor gene, oncogenes, cell cycle checkpoint regulators during DNA damage response and regulation.

2020 ◽  
Author(s):  
Rajni Khan

There is a close interdependence between the cell survival, cell senescence, events of cell cycle, apoptosis, malignancy development and tumor responses to cancer treatment. Intensive studies and elaborate researches have been conducted on the functional aspects of oncogenes, tumor suppressor genes, apoptotic genes and members guiding cell cycle regulation. These disquisitions have put forward the existence of a highly organized response pathway termed as DNA-damage response network. The pathways detecting DNA damage and signaling are intensively linked to the events of cell-cycle arrest, cell proliferation, apoptosis and cell senescence. DNA damage responses are complex systems that incorporate specific "sensor" and "transducer" proteins, for assessment of damage and signal transmission respectively. These signals are thereafter relayed upon various "effector" proteins involved in different cellular pathways. It may include those governing cell-cycle checkpoints, participating in DNA repair, cell senescence, and apoptosis.


2014 ◽  
Vol 322 (2) ◽  
pp. 324-334 ◽  
Author(s):  
Rumani Singh ◽  
Rajkumar S. Kalra ◽  
Kamrul Hasan ◽  
Zeenia Kaul ◽  
Caroline T. Cheung ◽  
...  

Author(s):  
Jessica M. Molkentine ◽  
David P. Molkentine ◽  
Kathleen A. Bridges ◽  
Tongxin Xie ◽  
Liangpeng Yang ◽  
...  

Stem Cells ◽  
2012 ◽  
Vol 30 (9) ◽  
pp. 1901-1910 ◽  
Author(s):  
Nevila Hyka-Nouspikel ◽  
Joëlle Desmarais ◽  
Paul J. Gokhale ◽  
Mark Jones ◽  
Mark Meuth ◽  
...  

2013 ◽  
Vol 41 (3) ◽  
pp. 777-782 ◽  
Author(s):  
Aoife O’Shaughnessy ◽  
Brian Hendrich

The CHD4 (chromodomain-helicase-DNA-binding 4) (or Mi-2β) protein is a founding component of the NuRD (nucleosome remodelling and deacetylation) complex. NuRD has long been known to function in transcriptional regulation, and is conserved throughout the animal and plant kingdoms. In recent years, evidence has steadily accumulated indicating that CHD4 can both function outside of the NuRD complex and also play important roles in cellular processes other than transcriptional regulation. A number of loss-of-function studies have identified important roles for CHD4 in the DNA-damage response and in cell cycle progression through S-phase and into G2. Furthermore, as part of NuRD, it participates in regulating acetylation levels of p53, thereby indirectly regulating the G1/S cell cycle checkpoint. Although CHD4 has a somewhat complicated relationship with the cell cycle, recent evidence indicates that CHD4 may exert some tumour-suppressor functions in human carcinogenesis. CHD4 is a defining member of the NuRD complex, but evidence is accumulating that CHD4 also plays important NuRD-independent roles in the DNA-damage response and cell cycle progression, as well as in transcriptional regulation.


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