cancer

Few, if any, molecules can attest to being more important to life on earth than deoxyribonucleic acid (DNA). Life is based upon this critical molecule, as it defines the structure and function of each individual organism in which it is found. DNA comprises genes, which are responsible for the similarities between closely related organisms, as well as the unique and distinct differences that define individuals in these closely related groups. Such powerful and important responsibilities suggest that DNA must be greatly protected and preserved, and that changes in these critical DNA sequences could have devastating results. DNA sequences do, however, undergo changes and although the consequences of such changes in the genetic code can lead to disaster, there are mechanisms existing within the cell that may properly correct them. Such mechanisms are known collectively as DNA repair and they exist in several different forms (Setlow, 1998). Nucleotide excision repair (NER) is!

one such mechanism of preserving the DNA sequence and may be considered as not only the frontline of defense for a DNA molecule against sequence-damaging agents, but a possible defense mechanism against many forms of cancer as well.

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DNA ligase I is likely responsible for th!

is process. When in the presence of an ATP-regenerating system, the CAK-containing TFIIH performed repair at a significantly slower rate than the TFIIH lacking the CAK. Such additional examples further emphasize the critical importance of DNA repair mechanisms in the cell to ensure that potentially disasterous DNA damage can be fixed and normal cell functioning can continue. Additional experiments involving the CAK kinase inhibitor H-8 further supported the inhibitory activity of CAK.

Despite the differences observed between GG-NER and TC-NER in detecting damage in the DNA sequences, both modes of DNA repair rely on rather similar mechanisms for the execution of the remainder of their repair processes. With a functional NER pathway, they would be able to repair DNA damage caused by UV light with relative ease. Much knowledge has been gained on this subject through molecular epidemiology studies that analyze carcinogenesis and the risk of cancer at the molecular level. Individuals suffering from this disease are extremely sensitive to ultraviolet light.

Although both mismatch repair and nucleotide excision repair are both capable of fixing improper DNA sequences, they perform their duties in two rather unique and different ways. The NER reaction was followed in the presence of two different types of TFIIH complexes. This suggests that CAK kinase may inhibit NER activity by phosphorylating some component of the reaction, specifically the carboxy-terminal domain of RNAPII (Araujo et al 2000). Not only is cancer a serious problem resulting from such unrepaired mutations, but other disorders, such as Cocayne syndrome and trichothiodystrophy may result as well when defects in the genes producing essential!

components in the NER pathway are observed (Araujo et al 2000). In the case of XP, there is often a defect in a common component found in both GG-NER and TC-NER. These agents may damage the DNA, disrupting its function and altering its sequence by a much different process than in replication errors. Under normal conditions, this pathway can repair most any sequence damage caused by ultraviolet light.

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