DNA Damage Response Proteins

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DNA Damage Response Proteins

DNA Damage Response Proteins Background

DNA damage is a phenomenon in which DNA nucleotide sequences that occur during replication are permanently altered and cause changes in genetic characteristics. The situation is divided into: substituent, deletion and insertion exon skipping. DNA damage response (DDR) is a signal transduction pathway that detects DNA damage and replication stress and initiates an organized response to protect cells. Inducing DNA damage activates complex protein networks. Broadly speaking, sensor proteins recognize lesions and localize to DNA damage sites. These in turn activate and recruit transducer proteins to this site, thereby phosphorylating effector or mediator proteins that affect cellular activity. There are a variety of cellular responses to DDR activation. One of these is cell cycle arrest, allowing time for DNA repair to prevent genomic duplication or cell division in the presence of damaged DNA. In addition, DNA damage responses may induce cell death or cause cellular senescence through apoptosis.

Reasons about DNA damage

DNA stores the genetic information on which organisms depend for survival and reproduction, so maintaining the integrity of DNA molecules is critical to the cell. The external environment and the factors inside the organism often lead to damage or change of DNA molecules, and it is different from RNA and protein synthesis in cells. Generally, there is only one DNA in a prokaryotic cell, in eukaryotic diploid cells. There is only one pair of the same DNA. If the damage of DNA or the change of genetic information cannot be corrected, the body cells may affect their function or survival, and the germ cells may affect the offspring. Therefore, the ability of biological cells to repair DNA damage during evolution is important, and it is also where biological energy maintains genetic stability. The biological macromolecules that can be repaired in cells are only DNA, reflecting the importance of DNA to life. On the other hand, in biological evolution, mutations are a phenomenon that is ubiquitous and unified with heredity. Not all changes in DNA molecules can be repaired as they are, because they are mutated and evolved.

Factors affecting dna damage response

Every day, the DNA in our cells goes through tens of thousands of destruction events. If left unrepaired, this can damage the genome and even cause cell death. DDR contains at least 450 proteins that collectively recognize DNA damage, initiate repair where possible, or indicate that cells stop growing or even die in the event of severe DNA damage. There are two factors that affect DDR - the type of DNA damage and when it occurs in the cell cycle. There are multiple repair pathways to deal with specific types of DNA damage. Although some types of damage repair are relatively fast, complex DNA damage (such as two strand breaks in DNA double helices or damage that occurs during DNA replication) requires longer repair times. In this case, the pathway is activated to pause the cells to allow time for repair. These "cell cycle checkpoints that rely on DNA damage" ensure that cells do not enter the entire cell cycle due to damaged DNA. They also ensure that the most appropriate repair route is used. Thus, DNA repair and cell cycle checkpoint modulators are inherently interrelated in DDR processes. Human cells have evolved multiple ways to try and deal with all the different types of damage that DNA in our cells suffers. These are the DDR pathways. Under normal circumstances, there may be an optimal DDR path to deal with a particular type of damage. However, if this pathway is lost during cancer development, another DDR pathway may compensate to allow cancer cells to survive. This can represent the dependencies that can be exploited to provide potential new treatment opportunities.

DNA damage signaling - RNF168 ubiquitin ligase

The cellular DNA double-strand break repair pathway has evolved to protect the integrity of the genome from the continuing threat of potentially harmful damage. Genetic mutations in genes that control this process result in failure to properly repair DNA damage, ultimately leading to developmental defects and cancer susceptibility. It has been reported that a patient with a previously undescribed syndrome, called RIDDLE syndrome (radio-sensitive, immunodeficiency, malformation and learning difficulties), lacks the ability to recruit 53BP1 to the DNA double-strand break site. As a result, cells derived from the patient exhibit hypersensitivity to ionizing radiation, abnormal cell cycle checkpoints, and impaired end junctions of the recombination switch region. Sequencing of TP53BP1 (Figure 1) and other genes known to modulate the formation of 53BP1 lesions induced by ionizing radiation in this patient failed to detect any mutations. Thus, these data indicate the presence of a DNA double-strand break repair protein that acts upstream of 53BP1 and contributes to the normal development of the human immune system.

Structure of the TP53BP1 protein. Figure 1. Structure of the TP53BP1 protein.

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