P53

organization. Cytochalasin-D can also have clinical applications because the treatment of cells with cytochalasin-D activate the p53 protein (Rubtsova et al., 1998). This p53 protein plays a major role in the control of cell growth and in the cell’s response to various stress signals. More importantly, p53 is a gene that functions as a tumor suppressor, and if cytochalasin-D activates the p53 protein then there are possible cancer treatments that can be found. Moreover, phalloidin was used to prevent depolymerization

Gene editing is one of the most researched fields of molecular biology, as manipulated genes deem possible studying the specific genes and their effects. In the past, there were several attempts to manipulate gene function, including homologous recombination, RNA interference (RNAi), zinc-finger nucleases (ZFNs) and transcription-activator like effector nucleases (TALENs). These past approaches are expensive and time-consuming to engineer as opposed to Crispr Cas9, limiting their widespread use

Discussion From the image is can been seen that some bands are lightly stained and some are darkly stained it might be of two reasons: 1 G banding techniques enhances the basic structures of chromosomes. The chromosomes consists of 8 histones proteins molecules , each of which is wrapped around by DNA of 146bp long to form a repeating units called nucleosomes, then successive nucleosomes are arranged to form a structure similar to that of beads of a string which again coil themselves to form chromatin

purpose of the G1 phase is so the cell can grow, increase size, and create proteins and organelles, being able to take up to a total of 11 hours. During the G1 phase of a normal cell, the p53 gene monitors and destroys any cells with damaged DNA. In a cancer cell, the p53 is most likely to have a mutation in the p53 gene which results in the having damaged DNA not being destroyed. Even with those differences, some similarities is that both type of cells grow and increase size in the G1 phase. In the

Decreased expression of ARF in human cancer Consistent with the findings in mice, frequent mutation or deletion of the ARF/INK4a in numerous human cancers was discovered (Refs. 41, 68, 69; Table 1). It is difficult, however, to assess the relative importance of p16INK4a and p14ARF individually in humans since mutation or deletion at the ARF/INK4a locus frequently affects both proteins (Ref. 8). Generally, exon 2 is the site of mutation, affecting either p16INK4a, p14ARF, or both proteins. Some

that would be replaced is the mutated p53 gene. If functioning correctly, the p53 gene should stop the formation of tumors.It works by binding to DNA in the cell and stimulates the production of p21, which when combined with a cell division- stimulating protein, stops cell division. When the p53 is mutated, it fails to stimulate the production of p21 and the cell begins to divide uncontrollably. The gene therapy would replace the faulty p53 gene with a normal p53 gene. Another treatment is gene inhibition

utilizes. The most commonly inactivated tumor suppressor gene, is the human p53 protein. Despite this, the protein has a short half-life and undergoes continual proteolytic degradation in healthy cells, regulated by the E3 ligase MDM2 [31]. MDM2 works by physically up taking the trans activation domain of the p53 and will thereby prevent its transcriptional production [32]. However, the feedback loop of the MDM2- p53 complex can be disturbed by stress due to DNA damage or lack of oxygen leading

How would you like your life being in danger right after you’re born because you can’t breathe? Treacher Collins syndrome (TCS) causes underdevelopment of facial bones that could threaten an infant’s life by making it difficult to breathe. If the baby lives past this point they will have many facial deformities. Treacher Collins syndrome happens because of a mutation in TCOF1, POLR1C, or the POLR1D genes. TCS causes an underdeveloped facial bone, a small jaw and chin, an opening in the top of the

isolated from emphysema patients have higher ROS levels (Figs. 1a, b), they don’t show a significant increase in γH2AX phosphorylation. This may suggest the impairment of DSBs repair signaling leading to lack of the DNA damage repair in these cells. P53 is involved in several pathways including apoptosis and cell cycle

CDKN1A encodes a potential cyclin-dependent kinase (CDK) inhibitor which then prevents the phosphorylation of critical CDK substrates and blocks cell cycle progression, thus functioning as a cell cycle regulator at the G1 checkpoint. CDKN1A, along with p53, are both involved