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Compare and contrast oncogenes and tumor suppressor genes
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Introduction
TP53, more commonly known as the Tumor Suppressor Gene is what protects a gene from over developing into cancerous cell. TP53 is responsible for regulating nuclear processes within the chromosome ultimately maintaining the cell's cycle and making sure it stays on its correct course, even assisting in apoptosis. The TP53 gene sends signals to make a protein called tumor protein p53 (or p53). This protein is the tumor suppressor itself, it regulates cell division by keeping cells from proliferating too fast or uncontrollably. The p53 protein is located at the nucleus of all cells in the body, and it binds directly with DNA. Human protein p53 is a phosphoprotein; it has a very specific structure closely related to its function. The
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P53 is very significant to apoptosis, DNA damage, and gene stability through complex mechanisms. P53 can respond to DNA damage through DNA repair protein. An example of this would be when DNA damage occurs, p53 gets started and begins the transcription of repair protein XPC and DDB2. The domain p53-XPC-DDB2 can repair the DNA damages(Adimoolam and Ford, 2003). As Well, p53 put a halt to the cell cycle at S, G1, and G2 phase (Agarwal et al., 1995), which can provide time for proteins repair to fix the damaged DNA.
The beginning of apoptosis,, is the most significant anti-cancer function of p53. If DNA damage is not repairable, p53 can activate pro-apoptosis genes such as p21, DNA-damage-inducible protein 45, Bcl-2 family, and growth arrest, etc. Furthermore, p53 can interact with hundreds of proteins to maintain the cells processes and apoptosis. P53 can also keep the cell cycle in check by repressing the expression of genes like bcl-2, bcl-X, cyclin B1, MAP4 and survivin (Bai and Zhu, 2006). The physiological responsibilities of p53 are keeping the genetic stability and regulating the normal cell cycle through a regulatory network system. A mutation of Tp53 gene would cause a loss of function in the p53 protein, ultimately resulting in a cellular canceration. The function of p53 is preventing cancerization of cells by repairing genes or activating apoptosis. To achieve these functions, p53 interacts
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A tumor suppressor may have several mechanisms to suppress cancer cell growth. The most important tumor suppressor p53, as it’s associated with about 50% of human cancer cases, can trigger DNA repair processes, induce the transcription of other tumor suppressors, such as p21 and p16, and initiate cell apoptosis. Besides extreme growth in cancer research and discovering of many tumor suppressors, the underlying mechanisms that allow tumor suppressors function are not clear. Only four major mechanisms of tumor suppressors have been discovered: induction of apoptosis, suppression of cell division, inhibition of metastasis and DNA damage repair. Generally, p53 can lead to nucleotide excision repair which removes damaged DNA portions and facilitates synthesis from other
The unknown bacterium that was handed out by the professor labeled “E19” was an irregular and raised shaped bacteria with a smooth texture and it had a white creamy color. The slant growth pattern was filiform and there was a turbid growth in the broth. After all the tests were complete and the results were compared the unknown bacterium was defined as Shigella sonnei. The results that narrowed it down the most were the gram stain, the lactose fermentation test, the citrate utilization test and the indole test. The results for each of the tests performed are listed in Table 1.1 below.
The affects of pH, temperature, and salt concentration on the enzyme lactase were all expected to have an effect on enzymatic activity, compared to an untreated 25oC control. The reactions incubated at 37oC were hypothesized to increase the enzymatic activity, because it is normal human body temperature. This hypothesis was supported by the results. The reaction incubated to 60oC was expected to decrease the enzymatic activity, because it is much higher than normal body temperature, however this hypothesis was not supported. When incubated to 0oC, the reaction rate was hypothesized to decrease, and according to the results the hypothesis was supported. Both in low and high pH, the reaction rate was hypothesized to decrease, which was also supported by the results. Lastly, the reaction rate was hypothesized to decrease in a higher salt concentration, which was also supported by the results.
As the solution pH can influence the stability of NaClO-NH3 blend and the elimination of SO2, NOx, the impact of the pH of NaClO-NH3 blend solution on the instantaneous removal as well as the duration time was investigated, and the final pH after reaction was also detected and shown in Fig. 5. It can be seen that the variation of solution pH has a negligible effect on the desulfurization, but the elevated pH has a great promotion on the NOx removal, the efficiencies are significantly increased from 36% to 99% for NO2 in the pH range of 5–12 and from 19% to 65% for NO when the pH is between 5 and 10, after where, both of them are constant. Hence, the optimal pH of the NaClO-NH3 solution for the
Specifically “TP53, p16INK4A, and SMAD4. The p53 nuclear protein activates transcription of a cyclin kinase inhibitor p21WAF1/CIP1. Following genomic stress, inappropriate growth factor stimulation or expression of oncogenic ras increased expression of p53, and thus p21WAF1/CIP1 resulted in inactivation of specific CDK/cyclin complexes” (MedScape). If this transformed cell can escape internal and external fail-safe mechanisms, receive nutrients, and activate its proliferative program, it can form a mass of cancerous cells. Tumor growth can cause the loss of pancreatic functions. Another characteristic of pancreatic cancer is metastasis happens early in tumor growth, which is most likely responsible for pancreatic cancer’s aggressive
Alkaline Phosphatase (APase) is an important enzyme in pre-diagnostic treatments making it an intensely studied enzyme. In order to fully understand the biochemical properties of enzymes, a kinetic explanation is essential. The kinetic assessment allows for a mechanism on how the enzyme functions. The experiment performed outlines the kinetic assessment for the purification of APase, which was purified in latter experiments through the lysis of E.coli’s bacterial cell wall. This kinetic experiment exploits the catalytic process of APase; APase catalyzes a hydrolysis reaction to produce an inorganic phosphate and alcohol via an intermediate complex.1 Using the Michaelis-Menton model for kinetic characteristics, the kinetic values of APase were found by evaluating the enzymatic rate using a paranitrophenyl phosphate (PNPP) substrate. This model uses an equation to describe enzymatic rates, by relating the
In biology class, we were learning about enzymes. Enzymes are proteins that help catalyze chemical reactions in our bodies. In the lab, we were testing the relationship between the enzyme catalase and the rate of a chemical reaction. We predicted that if there was a higher percentage of enzyme concentration, then the rate of chemical reaction would increase or it would take less time. We placed 1 ml of hydrogen peroxide into four depressions. Underneath the first depression, we place 1 ml of 100% catalase and make 50% dilution with 0.5 ml of water. We take 50% of that solution and dilute with 0.5 ml of water and we repeat it two more times. there were four depressions filled with catalase: 100%, 50%, 25% , 12.5 % with the last three diluted
Chemotherapy is the treatment of a tumor with chemical agents to reduce mass or eradicate a tumor completely. There are certain mechanisms by which chemotherapy inhibits cancer. The first mechanism is cell death by cytotoxicity. Some chemical agents in certain amounts are toxic to cells. The cells die due to the toxic...
Madar, Sylvia S., & Windelspecht, Michael. (2014). Inquiry into Life, Metabolism: Energy & Enzymes (pp. 104-107). New York: McGraw Hill.
Thought to be an oncogene, a gene that has potential in transforming normal cells into tumor cells, p53 was regarded as the most prominent tumor suppressor gene [1]. P53 is a gene which signals apoptosis (programmed cell death) if a cell cannot be repaired due to an extensive amount of damage. As stated in the textbook, p53 regulation occurs by an E3 ubiquitin-protein ligase known as MDM2 [1]. "Controlling the controller" is a statement that describes the molecular interaction where the presence of MDM2 targets the p53 for proteosome via degradation. With three main checkpoints in cell cycle, the literature states p53 functioning from G1 into S phase in a chaotic cell [2]. The normal state of cells is to keep p53 levels low in order to prevent uncontrolled apoptosis and random cell cycle arrest from occurring. In a further note, although p53 promotes apoptosis and cell cycle arrest, cancer may result from p53 unable to recognize the problematic site. In turn, a mutation in p53 may result engaging in new activities. These activities include cellular transformation, tumor metastasis,...
Apoptosis is a distinct form of a programmed cell death ( PCD) or cell suicide , first described by Kerr et. al. in the 1970s(1, 2). It is a normal physiological phenomenon that plays an important role in embryonic development, maintenance of tissue homeostasis and pathology(3) . Apoptosis triggered by exogenous and endogenous stimuli as radiation, oxidative stress and genotoxic chemicals. It is defined by characteristic changes in the nuclear morphology including chromatin condensation and fragmentation , overall cell shrinkage and formation of apoptotic cell bodies. Among the many markers of apoptosis, DNA fragmentation is...
Throughout the years, apoptosis has been thoroughly studied and investigated by millions of scientists around the world. Throughout people’s knowledge of cells, the cell cycle, mitosis and meiosis, and viruses, there are still questions that we ask. These questions can range from why doesn’t a human continue to grow when we produce millions of cells, what happens to cells that fail the mitosis and meiosis checkpoints, and what happens to the cells that are infected by viruses. The answer to these common and educational questions is all in the process known as apoptosis. Apoptosis is the death of cells that occurs as a normal and controlled part of an organism's growth or development. The common questions that people ask about the cell process
Another preventative step is to understand how cancer functions. If people can educate themselves about how cancer survives and works, they can take necessary steps to change their lifestyle to prevent cancer. Cancer is a loss of mitosis, or cell division. Cells begin to divide at an uncontrollable rate, which eventually spreads and eats awa...
For years, people have been looking for a cure for the devastating disease of cancer. Cancer is the third highest killer in the US, with over 2,500,000 victims per year. Oncologists and scientists around the country are researching all forms of cancer in an effort to understand, treat, and ultimately defeat this disease. Already there have been numerous advances in the field, such as chemotherapy and gene therapy. One advance has been the use of a cell process known as apoptosis.
The Cell, the fundamental structural unit of all living organisms. Some cells are complete organisms, such as the unicellular bacteria and protozoa, others, such as nerve, liver, and muscle cells, are specialized components of multicellular organisms. In another words, without cells we wouldn’t be able to live or function correctly. There are Animal Cells and Plant Cells. In Biology class the other day we studied the Animal Cell. We were split into groups of our own and we each picked a different animal cell slide to observe. My group chose the slide,'; Smeared Frog Blood ';.
Tumors are formed by the alteration of the body’s own cells. This can be caused by environmental factors such as radiation, like UV exposure, chemicals or viruses 1. These can disrupt genes that control growth and cause an increase in cell division and proliferation. Proto-oncogenes are those genes that control normal but essential cell processes that keep cell growth and death in check. Two important categories are apoptosis genes, which regulate cell death, and tumor suppressor genes, which decrease cell propagation 1 . If these genes were mutated to the point where they cannot produce a functioning protein, cell division would continue far past what it was supposed to and unhealthy cells would be allowed to live and continue to multiply. This is what creates a malignant tumor. Certain conditions in the body can also promote the growth of cancer cells. One of these is a deficiency of natural killer (NK) cells, which are able to kill cancer cells by creating a pore in the cell membrane with perforin and releasing granzymes into the cell. Low levels of perforin allow for tumor growth 1. Chronic inflammation can also ...