P53

cells and cellular debris and recruits immune cells to form new blood vessels. The main constituents of this repair process are fibroblasts. Fibroblasts are able to convert into cardiac endothelial cells through the activity of transcription factor p53. The human heart consists of myocytes and non-myocytes. The non-myocytes include cardiac fibroblasts and endothelial cells which generate growth factors and extracellular matrix (ECM) proteins which are responsible for sustaining the…

this week. This research lead scientists to believe that Elephants have 20 imitates of a gene called p53, or called TP53 in their genome. How cool is that; because humans only have one. So why do Elephants have a smaller risk at obtaining cancer? Well, the p53 gene that they have is commonly known for playing a protective role when the DNA begins to suffer. This gene begins to then stir up copies of p53 which start to mend the infliction. After discovering this paradox Joshua Schiffman, a…

compare samples of Valerie’s blood and normal breast tissue to her tumor tissue and to a wild type DNA fragment to see whether or not her cancer has metastasized; it did not appear that this was the case. Lastly, her children’s p53 gene was sequenced and compared to the wild type p53 sequence to determine whether any of them carried the mutation. Two of her children do have the mutation at two points…

p53 plays a critical role in regulating cell-cycle progression and in maintaining genomic integrity when cells sustain DNA damage. The p53 protein functions as a nuclear transcription factor that regulates expression of various genes encoding proteins involved in cell-cycle checkpoints (e.g., p21WAF1/CIP1), apoptosis, and DNA repair .Since its important role in many cellular processes, p53 is prone to mutations and is mutated in 80–90% of NSCLCs…

substance affects our bodies in many contrasting ways. Examples are, our organs, DNA, our tissue, bones, and TP53 gene. In this paper, we will focus most on how Uranium affects TP53 to affect our body. The official name of the gene is tumor protein p53. It’s nicknamed the “guardian of the genome.” TP53 is what protects our cells from growing and dividing too fast, or uncontrollably. The gene has a very important location in the nucleus of our cells, where it binds directly to DNA. When DNA is…

limit the growth of tumors. A type of tumor suppressor gene, known as the p53 gene, is known for its role in repairing damaged DNA. It will often activate other genes that help to slow down the cell cycle and buy some time to repair damaged DNA. If the damage caused to DNA is deemed irreparable, the p53 gene can activate genes responsible for apoptosis, which is programmed cell suicide. If tumor suppressor genes like the p53 gene are unable to serve their function and prevent mutations from…

The activation of the pathway RAS and JAK pathway also results in the decrease p53 production. o P53 is a tumor protein that regulates the cell cycle. Suppression of this protein causes abnormalities in the cell cycle and thus abnormal growth. Decreased p53 is a hallmark of any cancer which results in the formation of tumors and abnormal growth. Treatment of CML varies from phase to phase. There is a variety of medication…

automatically activates the p53 gene. p53 or usually known as a tumor protein, attaches to miR-34a promoter in order to normalize the expression of microRNAs. p53 eliminates the opportunity for a tumor to occur in correlation with transcriptional targets and having miR-34a to the side in order to avoid any inappropriate cell propagation. Likewise, any damage in the DNA signaling could affect the evolutionary biogenetics process from the p53 gene activation. MicroRNA-34a together with p53,…

Senescence is a robust tumor suppressive mechanism that inhibits the proliferation of damaged as well as initiated cells in response to a diverse range of stresses. The observations that human benign cancer precursor lesions are comprised of senescent cells further provide evidence that senescence is a physiological mechanism that prevents cancer progression in humans, possibly at an early stage. Senescence is clearly not fail-safe, since cells in pre-cursor lesions occasionally progress towards…

The naked mole rat and the blind mole rat have developed unique anti-cancer mechanisms compared to other mammals. Mammals typically have several methods, such as inducing apoptosis, releasing cyclin-dependent kinase inhibitors (bound to CDK complexes) which signal cells to stop within a stage of the cell cycle, and contact inhibition in which cells stop growing once they make contact with each other. These mole rats’ distinct mechanisms modify contact inhibition and apoptosis to achieve the…