The Rad51 Protein Paper Example

The Rad51 is a gene that contains a set of instructions for synthesizing a protein that is necessary for repairing damaged DNA. This damaged DNA is a result of either environmental or medical radiation or may also occur during cell division in the chromosomes when the chromosomes are exchanging genetic material. This protein binds to the DNA strand of the cell at the breaking point and covers all round in a protein sheath which is essentially the beginning of the repair process through homologous recommendation. This process is made possible because the Rad51 protein shows characteristics of ATPase activity. This exhibition acts as a catalyst to recognize the homology and DNA strand exchange between homologous DNA partners to form a jointed molecule between the broken DNA and the template repair. This process binds the single-stranded DNA in an ATP-dependent way forming nucleoprotein filaments which are vital for the strand exchange and the homology search.

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The Rad51 protein has been researched to show how it is involved in the development of the nervous system to see its function in controlling movement. Although this function of the Rad51 has not been researched it is an ongoing study. This protein plays a role in regulating the mitochondrial DNA copy

Instruments hidden mitochondrial genome upkeep have as of late increased wide consideration, as transformations in mitochondrial DNA (mtDNA) lead to acquired strong and neurological infections, which are connected to maturing and disease. It was recently announced that human RAD51, RAD51C, and XRCC3 restrict to mitochondria upon oxidative pressure and are required for the support of mtDNA dependability. Since RAD51 and RAD51 prologs are precipitously brought into mitochondria, their exact job in mtDNA upkeep under unperturbed conditions stays slippery. Here, we demonstrate that RAD51C/XRCC3 is an extra part of the mitochondrial nucleoid having core autonomous jobs in mtDNA support. RAD51C/XRCC3 restricts to the mtDNA administrative locales in the D-circle alongside the mitochondrial polymerase POLG, and this enrollment is needy upon Twinkle helicase. Besides, upon replication stress, RAD51C and XRCC3 are additionally enhanced at the mtDNA transformation problem area locale D310. Strikingly, the nonappearance of RAD51C/XRCC3 influences the steadiness of POLG on mtDNA. As a result, RAD51C/XRCC3-inadequate cells show diminished mtDNA union and expanded injuries in the mitochondrial genome, prompting generally undesirable mitochondria. Together, these discoveries lead to the proposition of an instrument for an immediate job of RAD51C/XRCC3 in keeping up mtDNA honesty under replication stress conditions

The mutation of the Rad51 protein can result in congenital mirror disorder which is characterized by unintended, no suppressible, homologous mirroring activity contralateral to the movement on the intended side of the body. In healthy controls, unilateral movements are accompanied with predominantly contralateral cortical activity, whereas in CMMD, in line with the abnormal behavior, bilateral cortical activity is observed for unilateral motor tasks. However, task-related activities in subcortical structures, which are known to play critical roles in motor actions, have not been investigated in CMMD previously.

Future studies for the protein are ongoing and there has been a remarkable stride in achieving a wide understanding of its function. It has been found that the Glioma Stem cells (GSCs) can play a role in gliobastoma recurrence which is an issue related to growth of tumors in the brain. If the homologous recombination is defective, there is an occurrence of radioresistance of GSCs. In this case the inhibition of Homologous recombination is essential for sensitization of GSCs to radiation.

Also there have been proposed researches to investigate the association of Rad51 protein mutation with gynecological tumor growths. It was evidently found out that the polymorphism of Rad51 cells resulted to an increase in the risk for growth of three common gynecological tumors. One such tumor is the endometrium cancer and breast cancer. The cancerous cells arise from the damaged cells which have mutated and started growing uncontrollably. Several studies have shown that the mutations of the genes responsible for repair mechanism are susceptible to the various cancer syndromes.

Conclusion

In conclusion, this article has discussed the Rad51 protein, its function in the cell and the studies that have occurred about it. It has been found out that it is the most essential protein in the process of DNA repair and the hazardous consequences of its mutation has been discussed. Cancer cells arising from the damaged genes grow as tumors and they result in the three common gynecological cancer that is endometrium cancer, ovarian cancer and breast cancer. It is important to learn about Rad51 and its association with cancer as this will give a wide understanding on the type of cancer, the cause and the preventive measures that can be taken.

Works Cited

Dufloth, Rozany Mucha, et al. "DNA repair gene polymorphisms and susceptibility to familial breast cancer in a group of patients from Campinas, Brazil." Genet Mol Res 4.4 (2005): 771-82.

Fan, X. J., et al. "The study of esophageal cancer risk associated with polymorphisms of DNA damage repair genes XRCC4 and RAD51." Sichuan da xue xue bao. Yi xue ban= Journal of Sichuan University. Medical science edition 44.4 (2013): 568-572.

Arnaudeau, Catherine, Cecilia Lundin, and Thomas Helleday. "DNA double-strand breaks associated with replication forks are predominantly repaired by homologous recombination involving an exchange mechanism in mammalian cells." Journal of molecular biology 307.5 (2001): 1235-1245.

Hu, Zhibin, et al. "XRCC1 polymorphisms and cancer risk: a meta-analysis of 38 case-control studies." Cancer Epidemiology and Prevention Biomarkers 14.7 (2005): 1810-1818.

Romanowicz, Hanna, et al. "Genetics polymorphism in DNA repair genes by base excision repair pathway (XRCC1) and homologous recombination (XRCC2 and RAD51) and the risk of breast carcinoma in the Polish population."

Polish Journal of Pathology 61.4 (2010).Smolarz, Beata, et al. "Association between polymorphisms of the DNA repair gene RAD51 and ovarian cancer." Polish Journal of Pathology 64.4 (2013): 290-295.