Cells repair

Cell Cycle Control. Figure 3 The DNA damage checkpoint. In response to DNA damage cells activate p53 dependent and independent checkpoint pathways leading to cell cycle arrest at G1/S and G2/M allowing DNA repair. If the cellular damage cannot be repaired, cells can initiate apoptosis. 

Hofmann, R. M. and C. M. Pickart, Noncanonical MMS2-encoded ubiquitin-conjugating enzyme functions in assembly of novel polyubiquitin chains for DNA repair. Cell, 1999, 96(5), 645-53. 

How does PARP-Fs role as a nucleosome-binding protein and modulator of chromatin structure, which is evident under normal physiological conditions, impact PARP-1-dependent DNA repair, cell death, and inflammatory response pathways, which occur under pathophysiological conditions A number of different scenarios are possible. For example, PARP-l s chromatin-dependent activities may be critical for its function as a DNA repair protein, since the repair of genomic DNA must occur in the context of chromatin. In addition, nucleosome-stimulated autoPARylation may play a role in depleting cellular NAD+ pools in response to cellular stresses. Furthermore, PARP-Fs chromatin-dependent activities may help to regulate the expression of immune and inflammatory response genes. These possibilities will need to be examined in the future. 

Huang SM, Harari PM. Modulation of radiation response after epidermal growth factor receptor blockade in squamous cell carcinomas inhibition of damage repair, cell cycle kinetics, and tumor angiogenesis. Clin Cancer Res 2000 6 2166-2174. 

Phosphorus, vitamin D, and calcium are all needed for bone health (Huth et al., 2006) and selenium has a role in the immune and antioxidant systems and in DNA synthesis and repair. Zinc is necessary for DNA repair, cell growth, gene expression, and is an essential part of some enzymes and metalloproteins. Magnesium has been implicated in the prevention of CVDs (Haug et al., 2007). For example, it is known that calcium, phosphorus, and magnesium may mediate beneficial effects on... 

Zyrek, A. A., Cichon, C., Helms, S., Enders, C., Sonnenborn, U., and Schmidt, M. A. (2007). Molecular mechanisms underlying the probiotic effects of Escherichia coli Nissle 1917 involve ZO-2 and PKCzeta redistribution resulting in tight junction and epithelial barrier repair. Cell Microbiol. 9(3), 804-816. 

Fig. 3. The cell-cycle perturbations that occur as a consequence ofDNA damage induced by cisplatin. The dark box represents the time period during which cells arrest at various phases of the cell cycle with the intent to repair the damage. Once the DNA is repaired, cells may recover and continue to grow. The dotted arrows imply that caffeine and UCN-01 can overcome S- and G2-phase arrest and drive the cells into a lethal mitosis.

Kadyrov, F. A., Dzantiev, L., Constantin, N., and Modrich, P. Endonucleolytic function of MutLalpha in human mismatch repair. Cell 126, 297-308, 2006. 

Hanakahi, L.A., Bartlet-Jones, M., Chappell, C., and West, S.C., 2000, Binding of inositol phosphate to DNA-PK and stimulation of double-strand break repair. Cell 102 721-729... 

---