P53

apoptosis and the cell divides uncontrollably. Eventually the cells become a tumor and reach the bloodstream spreading through metastasis. In response to this many organisms have a defense to help control and destroy these cells through a protein called p53. This protein is coded for by the gene Tumor Protein 53 or TP53 and helps to control the cells ability to divide rapidly. This gene can be found in small organisms like mice to large mammals like elephants and whales. Cancer’s success is dependent on

3.7.1 Familial melanoma Familial melanoma is a genetic or inherited condition. This means that the risk of having a melanoma can be passed from generation to generation in a family. Ordinarily, each cell has two copies of each gene: one inherited from the mother and one inherited from the father. Familial melanoma follows a dominant inheritance pattern, in which case a mutation happens in only one copy of the gene. As every cell has two copies of each gene, it means that a parent can potentially

tumor tissues exerts different clinical behavior in different tumor types. YY1 The loss of YY1 results in a significant increase in p53 levels. YY1, MDM-2 and p53 can form a ternary complex and YY1 is essential for optimal MDM2-p53 physical interactions in vivo, which is a prerequisite for MDM2 to be able to ubiquinate p53. Ubiquitination induces the translocation of p53 to the proteasome which leads to its

Squamous cell carcinoma is a form of cancer that occurs in the squamous cells, which are located on the surface layer of many organs and is most commonly associated with the epidermis of our skin. However, squamous cells are not only in the tissue that we see on the exterior of the body, but many of the surface tissues on the interior of our body like the oral cavity, lungs, and digestive tract. (Where Skin Cancer Develops, Mayo Foundation for Medical Education and Research, n.d.) Squamous cell

since it tends to metastasize and spread easily through the lymphatic system (Mayo Clinic, 2016a).. The root cause of malignant melanoma is due to mutations in the p53 gene protein which invariably leads to further mutations. The P53 Function The p53 negative regulator, is a tumor

Observing Bacteria and Blood Cynthia Alonzo, M.S. Version 42-0249-00-01 Lab Report Assistant This document is not meant to be a substitute for a formal laboratory report. The Lab Report Assistant is simply a summary of the experiment’s questions, diagrams if needed, and data tables that should be addressed in a formal lab report. The intent is to facilitate students’ writing of lab reports by providing

translocation. Scientific literature and empirical evidence regarding the relationships between SRSF1, p53/OIS, and MALAT1 have led us to our central hypothesis that MALAT1 overexpression disrupts the interaction between the RRM2 and RS domain in SRSF1, subsequently impairing its phosphorylation and thus its nuclear translocation. This change in subcellular localization, in turn, destabilizes p53, leading to loss of OIS in cervical cancer cells. We will address this hypothesis in the following Specific

from growing, this drug might have extra strength attacking the gene mutation p53. What is p53? This gene in its normal state is what prevents our healthy cells from constantly dividing and growing. When p53 is lost due to mutation, it can lift the sanctions on cell division and growth. Because cancer causes most of its damage through uncontrolled growth, it makes sense that many of them have a mutated p53. The p53 mutation is known to fuel some of the most aggressive solid tumors we know today

Trypanosomatidas, the entire set of centromere and kinetochore proteins differ from other eukaryotes[33, 34]. In Trypanosoma brucei, nineteen different centromere/kinetochore proteins without any similarity to other eukaryotes of which KKT2 and KKT3 are constitutively present at the centromere were identified. KKT2 and KKT3 have DNA binding motifs. Similar protein was also identified in Leishmania[34]. However, it is not yet clear whether a functional conservation of CENP-A exists in these centromeres

cyclin-dependent kinase inhibitor which stops cells in the G1 phase from dividing. The cylcin-dependent kinase inhibitor p16 is also thought to regulate contact inhibition but its levels do not change in mice or human samples. Tumor-suppressor genes Rb and p53 are present in high concentration during contact inhibition to help control cell proliferation and apoptosis respectively. It was hypothesized that the naked mole-rats' cancer resistivity