DNA repair

Impact toxicity of commercial Sodium Chlorid Salt on Kidney and DNA of male mice Part 1 1*Aly, H. M. 2Gamela S.M. El-Saeed, 3Rizka K.Ali. 1Department of Cell Biology, 2Department of Medical Biochemistry, 3Department of Water Pollution Research, Abstract: Sodium chloride is widely used in various industrial, medical and food applications that increasing human exposure to it by excessive amount. However, almost all studies focused on its nephrotoxicity and adaptation of kidney cells to high concentration

domains, also called units. Each one of these domains has a different responsibility. One domain, called the core domain, identifies specific DNA sequences. Another domain stimulates transcription factors. The third domain controls the tetramerization of the protein. The last domain is able to distinguish damaged DNA. This may include single-stranded DNA or base pairs that are misaligned (Vijayaraj). The gene also contains twenty

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

in cell cycle arrest, apoptosis, DNA repair,

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 mutS gene

this gene p53 which changes the biochemical and the biophysical properties is strongly associated with an increase to cancer as the article “p53 in health and disease” describes. (Vousden & Lane 2007). The mutated genes are called oncogenes, where the DNA is altered from its original form. These gene help in growth regulation and division of the cells and are often causes the cells to divide out of control causing cancer to develop from the mutations of the gene p53. The p53 protein has five highly

of longevity to provide the foundation for future therapies. Two of the most highly associated genes with longevity across populations are APOE and FOXO3A. Additionally, signaling cascades associated with inflammation, immunity, nitrous oxide, and DNA

Some individuals have a greater risk of developing cancer because they have inherited mutations in certain genes. Mutations are abnormal changes in the DNA of a gene. The building blocks of DNA are called bases, and the sequence of the bases determines the gene and its function. Mutations change the arrangement of the bases that make up a gene, and even a change in just one base can have a major effect. A gene mutation can affect the cell in many ways. Some mutations stop a protein from being made

Metaphase in M. The checkpoint G1 checks if the cell should go through the cell division cycle and whether it has appropriate growth factor. If a cell passes the checkpoint, it comes all the way to the G2 checkpoint, where it is checked on complete DNA replication. The M checkpoint is for making sure that chromosomes are properly attached to microtubules, and they get accurately divided without getting more chromosomes

the tissue induced by elevated NO• concentrations. The successive drop in blood pressure and reduced supply of tissues leads to systemic circulatory failure and death of the patient. Inhibitor studies have shown that PARP-1 is not only involved in DNA repair, but also in septic shock. Hauschildt and coworkers have shown that the induction of pro-inflammatory cytokines by LPS treatment of macrophages could be prevented by inhibiting PARP (Hauschildt et al., 1997). An anti-inflammatory effect of PARP