P53

p53 gene, also known as tumor protein 53 (TP53), encodes for a tumor suppressor protein which regulates the cell cycle and apoptosis. The p53 protein has been described as the guardian of the genome (1) because of its role in preventing genetic mutation. It belongs to a protein family which includes p53, p63 and p73 and these are structurally and functionally related to each other. However, p53 seems to have evolved as a tumor suppressor in higher organisms, while p63 and p73 play a role in normal

Alteration of p53, p53 family proteins and their isoforms by H pyroli in gastric cancer p53 is the most studied tumor suppressor protein involved in the negative regulation of cell cycle and prevention of tumorigenesis . P53 induction usually occurs during cellular stresses like DNA damage or activation of other oncogenic proteins. P53 transcribes its target genes like p21,PUMA through p53 response element and halts the cell cycle until the stress is overcome, if not severely damaged cells

P53 is a tumor suppressor gene. In all kinds of malignant tumors, above 50% appears p53 gene mutation. The protein encoded by this gene is a transcriptional factor, which controls to start the cell cycle. Many signals of the cell health directly send to the p53 protein. It also decides when the cells begin the division. If the cells are damaged and cannot be repaired, the p53 protein would start the boot process and lead the cell go to apoptosis died. Some p53 deficient cells without this control

Introduction P53 tumor suppressor plays a vital role in the prevention of transformation of oncogene. However, stresses from area such as DNA damage, oncogenes, spindle damages etc. can cause a mutation in TP53 tumor suppressor gene which can alter and cause disturbance in the P53 pathway which involved certain protein and genes regulator dealing with growth arrest, apoptosis, DNA repair and angiogenesis. Mutation to TP53 genes has been seen with most cancers patient. The specific activation of P53 pathway

cancer is p53. The protein was discovered in the 1970s when research was focused on cancers that are caused by viruses and was later identified as being a tumor suppressor (1). One of the most studied areas of cancer is how p53 functions and its role in the cell cycle which has led to studies that target p53 as a therapeutic agent for cancer (1). In the year 2001, it was found that the protein product of the gene hSIR2SIRT1, which is a homolog of S. cerevisiae Sir2 protein, deacetylates the p53 protein

1001/jama.2015.13134 Questions 1. Why were elephants considered for cancer research? 2. Why might elephants have evolved to be more resistant to cancers than other mammals? 3. Are there other mammals possessing multiple copies of p53 genes? 4. How is p53 expressed when there are multiple copies? 5. What are the implications of this research for medicine? The article states that the importance of the research is to gain“insights into human physiology and pathophysiology, including

protein 53 is a tumor suppressor gene that encodes p53 and acts as a control center for the cell to act on when stressed (Brachova). Human p53 is a nuclear phsophoprotein of molecular weight 53kDa located on chromosome 17 containing 11 exons and 10 introns (Ling). One of its primary roles is as a transcription factor and in its active state is a homotetramer comprised of four 393 amino acid residues (Joerger , The tumor suppressor p53). Another main role p53 plays is as a tumor suppressor and once activated

Skin, the largest organ in the human body covers the whole body. It has many function such as protecting as barrier against radiations, pathogens etc. Skin mainly consists of 3 layers, epidermis, dermis and hypodermis. Epidermis is the outer layer of the skin which is comparatively thin and tough. Epidermis does not have blood vessels and comprised of epithelial cells. Most of the cells in the epidermis are keratinocytes. Epidermis is originated from the deepest layer of the epidermis called basal

Shh-pathway such as E2F1, CCND1, CDC2 and epidermal differential genes. Over-expression of Gli2 causes the up-regulation of such cell cycle regulation genes in developing hair follicles. Shh-activation most specifically promotes degradation of the p53 tumor suppressor gene (2), thus repressing transcription of p21, a key suppressor of cyclin E in cell-cycle regulation. Thus, G1 arrest is overrode, and the inability to control cell cycle is promoted: a key feature of cancer. Sufu and Kif7 have overlapping

CUL5 was also reported to be involved in regulating apoptosis by modulating the phosphorylation of mitogen-activated protein kinase (MAPK) and induce p53 mRNA and protein expression. The substantial increase in the expression of CUL5, due to the inhibition of a miRNA-145 expression by HBx, results in less phosphorylation of MAPK and therefore less p53 mRNA and protein expression. This study confirmed a significant decrease in the expression of miRNA-145 and a substantial increase in the mRNA and protein