Transformation-Related Protein 53 Essay

When cancer forms, your body has ways of trying to stop it from further developing. The four regulators are known as proto-oncogenes (which when mutated are known as oncogenes), tumor suppressor genes, apoptosis, and telomerase genes. When there is a mutation in each of the genes, cancer can develop. Once cancer develops it continues to grow and divide and turn into a tumor. For a tumor to develop it essentially needs something supplying it with blood and nutrients so that it can continue to grow. One player in the game of supplying the tumor with blood is a protein kinase known as Protein kinase C. A protein kinase is simply a molecule that regulates numerous cellular responses including gene expression, protein secretion, cell proliferation, and the inflammatory response. According to researchers at Harvard University, EBC-46 has the ability to target protein kinase C and inhibit it, which in turn causes the tumor to die because it is no longer has the ability to synthesize proteins it needs to survive. According to the Queensland Institute, the inhibition of  protein kinase C helps destroy the blood vessels that supply the tumor with the oxygen and the nutrients it would need for survival. Pretty exciting stuff

Its locus is particularly amplified in these noted tumours leading to the progression of these cancers, it can be suppressed by p53 (tumour/ proliferation suppressor) which represses the EZH2 promoter, resulting inhibition of cell proliferation and invasion (Bracken, 2003; Xiao, 2011).

Besides inducing apoptosis and controlling the cell cycle, p53 has been demonstrated to be a central component and key regulator of the metabolic stress machinery. The metabolic balance between glycolysis and oxidative phosphorylation is heavily coordinated by p53 activity, which is activated by

Human life starts from a fertilized cell which breaks down, again and again, an adult human body is composed of the abundance of cells and each one have their own specific function to perform. During adulthood, most of the cell does not duplicate except some cells continue to divide to replace the old or damaged cell in blood, skin and intestine. This growth is very controlled and no excessive cell growth takes place. But sometimes when a mutation occurs in one or more genes which causes unnecessary cell reproduction and as a conclusion, there is no control over the growth of cells. It is called malignant transformation and this is the starting of cancer (Hosick et al., 2015). There are many different types of cancer but the early stage diagnosis

There are twelve major types of cancer that affect most Americans and they can be related by the mutation of genes. Cancer is not just one disease, but a massive group with over 100 diseases by unrestrained and vicarious growth of the cells in the body and have the ability of the cells to propagate. One out of every four Americans will die from cancer. It is the second leading cause of death in this country, surpassed only by heart disease. Five to ten percent of cancer are genetic and hereditary. 1.2 million new cases are found in every year the United States, “Men have a one in two lifetime risk of developing cancer, and for women the risk is one in three” (Freivogel 201).

The article states that the importance of the research is to gain“insights into human physiology and pathophysiology, including tumor biology” through research of evolutionary medicine. The objective of the research as stated by the article is to “identify mechanisms for cancer resistance in elephants and compare cellular response to DNA damage among elephants, healthy human controls, and cancer-prone patients with Li-Fraumeni syndrome.” Persons with Li-Fraumeni syndrome have a 90% risk of cancer in their lifetime. Li-Fraumeni syndrome is an inherited autosomal dominant disorder in which the TP53 gene on one of the homologs of chromosome 17 is mutated usually passed on from a mutation in germ line cells. TP53 is a tumor suppressor gene which codes for p53, a nucleophosphoprotein that is able to bind to

Transactive response DNA binding protein 43 (TDP-43) has a molecular mass of 43 kDa and a multidomain structure that is composed of 414 amino acids, which is encoded by TARDBP (Bozzo et al., 2016; Chang et al., 2012; Igaz et al., 2011; Koyama et al., 2016). TDP-43 is a highly conserved DNA binding protein located in the nucleus for gene transcription (Chang et al., Igaz et al., 2011; 2012; Koyama et al., 2016; Neumann et al., 2006; Xu et al., 2012). However, a large number of RNA binding sites have been identified for TDP-43 that allow for pre-mRNA splicing and translational regulation including its own 3’ untranslated region 3’UTR (Ayala et al., 2011; Chang et al., 2012; Koyama et al., 2016; Xu et al., 2012). Similar to SOD1, TDP-43 is

The proteins are E1-E7 and L1-L2. E stands for early, while L stands for late. E6 and E7 are the two most studied proteins. They have important roles as p53 tumor suppressor and inhibitor of differentiation, respectively(3). Although both E6 and E7 have garnered much attention as potential therapeutic targets, E5 is largely unrecognized.

The gene most associated with HCC is the TP53 gene, which is a tumor suppressor gene universal among many cancers. The p53 protein, when turned off, can mistakenly cause cancer since they are normally turned on (Rhine 4). When normal, the TP53 gene assures that cells do not grow beyond where the should, meaning they have anchorage dependence and density dependent inhibition. When damaged, abnormal cells and the formation of HCC can occur since the P53 protein is involved in cell cycle functions and apoptosis, because it does not stop the cells from accumulating mutations over time if its function is degraded (¨“Do We Know [...]?¨, Debuire and Lemoine). This tumor suppressor gene follows Mendelian rules, meaning they are recessive and must

One of these genes is p53 which helps to control apoptosis and the cell cycle.3 In sarcomas p53 complexes with MDM2 which causes p53 to lose its normal function.3 In neurofibrosarcomas, a mutation of the NF-1 gene can inhibit tumor suppression.3 In almost all forms of sarcomas the lack of expression of FUS1 occurs.4 Another common tumor suppressor gene that is down regulated in various sarcomas is

Cancer is a disease caused by an uncontrollable increase in rate of cell division often leading to abnormal cell sizes and cell counts ultimately causing detrimental effects on cellular function especially if it has the ability to evade many treatments, as cancer has been proven to be quite adaptable. The path to curing cancer has been a long and expensive one, and while the discovery of a universal cure is currently being pursued, several treatments have been discovered and designed to treat the various subtypes of cancer .

The human genome is the complete set of nucleic acid sequence including the coding DNA regions (called genes which make proteins), the non-coding DNA regions and the mitochondrial DNA. However, Tumor suppressor genes (TSGs), or anti-oncogenes are proteins that play a vital role in regulating and controlling the cell proliferation through different mechanisms including suppress the cell division, promote apoptosis or programmed cell death, and repair DNA damages. Without which the cell can divide out of control and progress to cancer.

. The TP53 gene is located on the short (p) arm of chromosome 17 at position 13.1. [7]. TP53 has many important mechanisms of anticancer function and plays a role in apoptosis, genomic stability, and inhibition of angiogenesis. In its anti-cancer role, p53 works through several mechanisms: p53 can activate DNA, and repair proteins when DNA has sustained damage. Thus, it may be an important factor in aging. The gene has a very important location in the nucleus of our cells, where it binds directly to DNA. TP53 can arrest growth by holding the cell cycle at the G1/S regulation point on DNA damage recognition. If it holds the cell here for long enough, the DNA repair proteins will have time to fix the damage and the cell will be allowed to

This includes covalent modifications of the p53 gene (altering positive and negative feedback loops in the signaling pathway). P53 gene can be modified at twenty sites, which can change the protein’s behavior in a number of ways. Phosphorylation can inhibit or stimulate protein activity. The attachment or removal of modifying groups controls the behavior of a protein changing it’s activity or stability, which could permit the production of large quantities of the desired protein. Through posttranslational modifications of the p53 gene, this could mediate the control of P53 gene expression through the wnt signaling pathway. The p53 circuit communicates with the Wnt-beta-catenin, IGF-1-AKT, Rb-E2F, p38 MAP kinase, cyclin-cdk, p14/19 ARF pathways. Wnt proteins bind to receptors on the surface of a cell, switching on an intracellular signaling pathway that ultimately leads to the activation of a set of genes that influence cell growth. Wnt transmits its signal by promoting accumulation of free beta-catenin proteins which migrate from the cytoplasm to the nucleus to bind to TCF transcription regulators, creating a complex that activates the transcription of various Wnt-responsive genes, including genes whose products stimulate cell

It may be possible to correct an abnormality in a tumor suppressor gene such as P53 by inserting a copy of the wild-type gene; in fact, insertion of the wild-type P53 gene into P53-deficient tumor cells has been shown to result in the death of tumor cells (3). This has significant implications, since P53 alterations are the most common genetic abnormalities in human cancers. The over expression of an oncogene such as K-RAS can be blocked at the genetic level by integration of an antisense gene whose transcript binds specifically to the oncogene RNA, disabling its capacity to produce protein. Experiments in vitro and in vivo have demonstrated that when an antisense K-RAS vector is integrated into lung cancer cells that over express K-RAS their tumorigenicity is decreased (4).