P53 is a gene that makes a protein found inside the nucleus of cells. It controls cell division and cell death. Its molecular mass is in the 53 kilodaltons. It's found on the seventh chromosome, 17p.
A mutated p53 gene causes cancer cells to grow in the body. A mutation is an alteration in the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA.
The p53 gene is a tumor suppressor gene. This tumor suppressor gene is also called TP53 gene and tumor protein p53 gene.
All cells have a nucleus, therefore p53 is found throughout the body. It has an important duty. In the immune system, lymph nodes defend against contaminations of our cellular processes. P53 is the backup. It destroys cancers and precancers.
Cellular stress activated p53 can implement DNA repair, stop cell division, and start apoptosis. Cellular stressors include extreme temperatures, toxic exposure, mechanism damage, and some viral infections. P53 has a full schedule. There are major problems when p53 isn't working.
Mutations are pushed into action in the absence of p53. Cancers proliferate. Cancer cells can spread through the bloodstream or lymphatic system.
This tumor suppressor is a very popular research topic. P53 related cancers are difficult to treat. Chemotherapy uses chemical agents to stop cancer cells from growing. Chemotherapy won't destroy them. Immunotherapy uses the power of the body’s own immune system to prevent, control, and eliminate cancer. Immunotherapy won't destroy them. (cancer.org)
MDM2 is a regulatory protein that binds inactive p53. MDM2 is a transcriptional target. p53 binds the first intron of the MDM2 gene to transcriptionally induce the expression of MDM2. This is an auto-regulatory negative feedback loop with MDM2. When cellular stress is present, MDM2 releases p53. The tumor suppressor places the nucleus under siege.
The tetramer binds the required DNA sequences. P53 is a phosphoprotein. It is 393 amino acids. Each domain has a job. It can either: activate transcription, find the recognizable sequences, start protein tetramerization, or sort the damaged base pairs. (nature.com)
P53 could pause cell division. Repair insues. Cell death can take place, also. 50% of all human tumors contain p53 mutants. Mutant p53 proteins not only lose their tumor suppressive activities but often gain additional oncogenic functions that endow cells with growth and survival advantages.
Unchecked cells give rise to tumor growth. TP53 gene mutation leads to misfolded proteins. An overpopulated presence of MDM2 deactivates p53.
Research is finding ways to overcome, though. There are therapies that reactivate p53. There are drugs looking to take part in the war on cancer.
Chemotherapy added to immunotherapy makes up combination therapy. This is powerful. It's not a permanent solution, yet.
P53 is a tumor suppressor.
All cells have a nucleus, therefore p53 is found throughout the body. It has an important duty. In the immune system, lymph nodes defend against contaminations of our cellular processes. P53 is the backup. It destroys cancers and precancers.
Cellular stress activated p53 can implement DNA repair, stop cell division, and start apoptosis. Cellular stressors include extreme temperatures, toxic exposure, mechanism damage, and some viral infections. P53 has a full schedule. There are major problems when p53 isn't working.
Mutations are pushed into action in the absence of p53. Cancers proliferate. Cancer cells can spread through the bloodstream or lymphatic system.
This tumor suppressor is a very popular research topic. P53 related cancers are difficult to treat. Chemotherapy uses chemical agents to stop cancer cells from growing. Chemotherapy won't destroy them. Immunotherapy uses the power of the body’s own immune system to prevent, control, and eliminate cancer. Immunotherapy won't destroy them. (cancer.org)
MDM2 is a regulatory protein that binds inactive p53. MDM2 is a transcriptional target. p53 binds the first intron of the MDM2 gene to transcriptionally induce the expression of MDM2. This is an auto-regulatory negative feedback loop with MDM2. When cellular stress is present, MDM2 releases p53. The tumor suppressor places the nucleus under siege.
The tetramer binds the required DNA sequences. P53 is a phosphoprotein. It is 393 amino acids. Each domain has a job. It can either: activate transcription, find the recognizable sequences, start protein tetramerization, or sort the damaged base pairs. (nature.com)
P53 could pause cell division. Repair insues. Cell death can take place, also. 50% of all human tumors contain p53 mutants. Mutant p53 proteins not only lose their tumor suppressive activities but often gain additional oncogenic functions that endow cells with growth and survival advantages.
Unchecked cells give rise to tumor growth. TP53 gene mutation leads to misfolded proteins. An overpopulated presence of MDM2 deactivates p53.
Research is finding ways to overcome, though. There are therapies that reactivate p53. There are drugs looking to take part in the war on cancer.
Chemotherapy added to immunotherapy makes up combination therapy. This is powerful. It's not a permanent solution, yet.
P53 is a tumor suppressor.
"A tumor suppressor gene directs the production of a protein that is part of the system that regulates cell division. The tumor suppressor protein plays a role in keeping cell division in check." (Genome)
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