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NEIL Gene Knockouts: Correlation with mutation frequency. Illustrate your essay with specific examples.

Review of literature

Endogenous and exogenous ROS (reactive oxygen species) are responsible for causing damage to different cellular components especially DNA at the rate of 104 molecular lesions per cell per day. A number of disease etiology mechanisms are tied to mutations in mitochondrial or nuclear DNA (Bandaru et al, 2002). The Base Excision Repair mechanism is the first line of defense and consists of enzymes like NEIL1, NEIL2 and NEIL3 (nei endonuclease VIII-like 1, 2 and 3 respectively) that facilitate DNA damage repair (Conlon et al, 2005; Hazra et al, 2002; Morland et al, 2002). Studies have shown that deletion or mutation of genes coding these enzymes leads to a greater incidence of tumours. These enzymes function as DNA glycosylase and apyrimidinic/apurinic lyase catalyse beta and delta-elimination reaction steps in the DNA around the damaged base, generate 3' terminal phosphate and interact with DNA ligase III alpha, BER and DNMA Polymerase beta. Additional function include repair of bubble DNA/single-strand DNA for oxidised bases, stimulate production of another vital repair enzyme OGG1 by carrying our beta/delta elimination similar to APE1 at the AP site and excision of excises 5-hydroxyuracil and 3' end proximal 8-hydroxyguanine lesions.

Sources and data acquisition

Data for the present proposal was collected from PUBMED, Medline, Biomednet, and other medical databases.

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