Repair Essay

because they go through the same process but are also different because a cancer cell does some of those processes a little different. A normal cell in the G1 phase uses p53 which inhibits the cell cycle almost like a pause. It gives the body time to repair the dna cells or dispose of the ones that cannot be fixed. Once it is fixed then the P53 releases the repaired cell and continues on to the next phase. The G1 phase in a 150 minute cell cycle would be around 30 minutes. However in the mutated cancer

Transformation-Related Protein 53, also known as TP53, is a tumor suppressor gene. It is named after its molecular mass. The gene was discovered by Arnold Levine, David Lane, and William Old in 1979 and was voted molecule of the year by science magazine in 1993. Although, it was not until 1989 that it was revealed to be a tumor suppressor gene. It was previously thought of as an oncogene. TP53 encodes for a protein, called p53 protein, that helps to regulate the cell cycle and inhibits mutations

are seldom.1 The mutS gene in E.coli takes part in the repair and recombination of DNA.2 When mutS was deleted from E.coli in a previous study, the mutation rate increased when compared to the wild type strain.2 Rifampicin is known for its inhibition of RNA Polymerase production.3 Without RNA Polymerase, RNA is incapable of production and thus protein synthesis ceases within the cell, resulting in cell death. We hypothesize that since mutS repairs recombinant DNA within E. coli, the deletion of the

of cell death due to loss of two genes which fails in deletion of each individually). Due to mutation or inactivation of BRCA1 and BRCA2, tumor cells become susceptible to impaired homologous repair (HR) and thus rely on PARP to repair DNA damage via non-homologous end joining (NHEJ) and base excision repair (BER) [184-187]. Therefore to target PARP in BRCA deficient tumors is a good strategy, as inhibition of PARP will force cells to enter apoptosis upon DNA damage [188] (Figure 5.6). Veliparib and

and DNA ligase IV (hligIV). hligI plays an important role in DNA replication by joining Okazaki fragments on the lagging strand of DNA. Apart from this it also plays important roles in DNA damage repair pathways, single strand breaks are repaired by nucleotide excision repair (NER) and base excision repair (BER) pathways. Results of preclinical studies support that Human DNA ligases are an attractive target for the development of new anticancer agents for selective inhibition against rapidly proliferating

Abstract: Provided the demographic changes affecting America, it is increasingly important to identify the key factors in healthy aging and longevity. The prohibitive cost of health care for chronically ill individuals makes it important to pursue all avenues of study related to health in an aging population. Genetics is thought to comprise ~30% of the multi-faceted factors associated with longevity. It is important to summarize the current information available on the molecular basis of longevity

1.3 Defects in DNA replication Point mutation is a random SNP (single-nucleotide polymorphism) mutation in the deoxyribonucleic acid (DNA) that occurs at one point. Point mutations usually take place during DNA replication. DNA replication occurs when one double-stranded DNA molecule creates two single strands of DNA that is a template for the creation of the coinciding strand. A single point mutation can change the whole DNA sequence. Changing one purine or pyrimidine may change the amino acid

With modern technology comes the breakthrough of the decade by altering the human genes. This altering gene invention is called CRISPR/Cas9. However, this invention in the beginning stages of altering genes, began with rats until perfection. The process began early with the embryo stages to edit the genes. With the introduction of CRISPR surrounds a lot of controversy. Some people believe editing genes is playing with the hands of God and refuse to believe in CRISPR. With the article, “Let’s Hit

Duchenne Muscular Dystrophy (DMD) is a lethal genetic X-linked disease results from the mutation in the reading frame of the dystrophin protein, and it affects mostly boys in their muscle and cardiopulmonary function. Although there are no effective treatments to cure DMD patients right now, scientists consistently explore more methods to come up with the practical treatments. One of the most popular and valid approaches is a gene-editing therapeutic method – CRISPR/Cas9 Genome Editing. It adapts

The inability of the functionality of these genes disrupts apoptosis, programmed cell death and DNA repair which results in cancer, the regulation and dividing of cells out of