Baez, Jaydon (2012) DNA repair. Research World, Delhi, India. ISBN 9788132332701
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Abstract
DNA repair refers to a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. In human cells, both normal metabolic activities and environmental factors such as UV light and radiation can cause DNA damage, resulting in as many as 1 million individual molecular lesions per cell per day. Many of these lesions cause structural damage to the DNA molecule and can alter or eliminate the cell's ability to transcribe the gene that the affected DNA encodes. Other lesions induce potentially harmful mutations in the cell's genome, which affect the survival of its daughter cells after it undergoes mitosis. As a consequence, the DNA repair process is constantly active as it responds to damage in the DNA structure. When normal repair processes fail, and when cellular apoptosis does not occur, irreparable DNA damage may occur, including double-strand breaks and DNA crosslinkages. The rate of DNA repair is dependent on many factors, including the cell type, the age of the cell, and the extracellular environment. A cell that has accumulated a large amount of DNA damage, or one that no longer effectively repairs damage incurred to its DNA, can enter one of three possible states: 1. an irreversible state of dormancy, known as senescence 2. cell suicide , also known as apoptosis or programmed cell death 3. unregulated cell division, which can lead to the formation of a tumor that is cancerous. The DNA repair ability of a cell is vital to the integrity of its genome and thus to its normal functioning and that of the organism. Many genes that were initially shown to influence life span have turned out to be involved in DNA damage repair and protection.
| Item Type: | Book |
|---|---|
| Subjects: | Q Science > QP Physiology |
| Divisions: | Electronic Books |
| Depositing User: | Esam @ Hisham Muhammad |
| Date Deposited: | 02 Jan 2023 02:10 |
| Last Modified: | 02 Jan 2023 02:10 |
| URI: | http://odlsystem2.utm.my/id/eprint/3889 |
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