There are many enzymes involved in HRR in humans. Several diseases have been linked to defects in individual enzymes. For many enzymes, however, there is no human disease identified. This is because most enzymes involved in HRR do not play an active role in the malignancy of cells.
Homologous Recombination Repair (HRR) is a cellular repair mechanism for mending spoiled DNA elements. Damage to DNA strands arises from errors in replication, contact with ionizing waves, chemical corrosion from bases, and harm from rash oxygen types. An intact chromatid is a requirement for HRR because it acts as a template (63). RAD51 is a crucial enzyme for this process. It supports exchanges between homologous DNA threads in the presence of replication protein A (RPA). Several proteins affect the functioning of RAD51 including p53, BRCA2, RAD54, and RAD52. RAD52, one of the proteins, promotes the pairing of similar strands of DNA during the pairing process, before the completion of repair. DNA polymerases and DNA ligases complete the HRR process. DNA polymerases synthesize the omitted sequences of DNA, whereas DNA ligases connect the newly made pieces. Resolvases (types of endonucleases) work out the Holliday junctions that result from the entire process.
The power of cells to divide determines the continuity of life. Cell division is the production of numerous, precise copies of cells. Inaccurate cell division cropping up from chromosomal and DNA transformation is the main feature of cancer (Hall and Giaccia 295). The cell cycle has two gaps (G1 and G2). A cell arrests when it fails to advance in the course of the cycle. According to Hall and Giaccia, cell arrest correlates with malignancy. Normal cells show arrest in G1 and G2 stages whereas malignant cells arrest in the G2 phase only. HRR happens in the delayed S or G2 stage of the cell cycle. This ensures that an intact sister chromatid is accessible for guidance. The unearthing of cyclins, cyclin-inhibitors, and cyclin-dependent kinases further enhances the comprehension of the cell cycle. Cyclins, therefore, are the critical components that affect the development of cancers in humans.
Moderation of the intricate processes which occur during the cell cycle result from “changes in the activity of intracellular enzymes known as cyclin-dependent kinases (cdks)” (Hall and Giaccia 295). Protein complexes containing cyclins have the active varieties of cyclin-dependent kinases. Changes from one stage of the cell cycle to the subsequent occur when the enzymatic action of a specified kinase activates the proteins needed for advancement. The ability of oncogenes to change cells relies on G1 cyclins and cyclin-dependent kinases. Reilly indicates that c-ABL kinase is the only kinase enzyme that takes part in HRR (428). The c-ABL kinase is not cyclin-dependent. All these findings explain why there are no human diseases identified for many enzymes in HRR.