Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN: 9780134580999
Author: Elaine N. Marieb, Katja N. Hoehn
Publisher: PEARSON
expand_more
expand_more
format_list_bulleted
Question
The P63 and P53 have similar functionalities in the cell, however, p53 is rarely associated directly with p63, suggesting that p63 may indirectly act as an oncogene by blocking p53 function. This hypothesis may also explain why p63 is associated with other indications of misinterpretation.
I do understand the above statement, however once piece not clear – why would p63 block p53 function? Have these genes been shown to have opposing functions? From the background information provided above, it seems like they would have seminar functions. Explain.
Expert Solution
This question has been solved!
Explore an expertly crafted, step-by-step solution for a thorough understanding of key concepts.
Step by stepSolved in 2 steps
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biology and related others by exploring similar questions and additional content below.Similar questions
- could you explain a bit more what this sentences mean: The information displayed demonstrates a significant increase in cell proliferation inside the dentate gyrus of mice that were locked in voluntary exercise compared to the control group. The use of 5-Bromo-2'-deoxyuridine (BrdU), a thymidine analog, permits the following of recently formed cells because it is incorporated into the DNA of dividing cells amid the S stage of the cell cycle. The immunocytochemical examination uncovered a 67% increase in BrdU-labeled cells within the running group, meaning upgraded neurogenesis, which is factually noteworthy as shown by the p-value of 0.0001. The observation that the runner group effectively utilized the running wheels given in their cages relates to the increment in BrdU-labeled cells.arrow_forwarddo you have any clues? GAP protein helps hydrolyze the GTP to GDP in RAS protein. Argenine 789 residue in GAP protein interacts with GTP in RAS protein. However, Arg 789 is mutated to Alanine. which are true or false? ____We expect Ala789 GAP to have no consequence for cell growth or survival signaling. ____Arg789 stabilizes the T-loop of GAP in the outward (active) position, so we expect Ala789 GAP to have no kinase activity. ___Arg789 participates in the GTP hydrolysis reaction carried out by RAS, so we expect RAS to be catalytically inactive when partnered with Ala789 GAP. ____Arg789 binds in the major groove of the DNA double helix, so we expect Ala789 GAP to be inactive as a transcriptional regulator. __Arg789 interacts with RAS switch 1 and switch 2 regions, so we expect the RAS switch to fail with Ala789 GAP. ____The RAS switch would be locked in the OFF position by Ala789 GAP, so we expect no constitutive RAS signaling and hence no risk of this tumor metastasizing. ____The…arrow_forwardThis TSG targets beta-catenin for degradation and inhibits the Wnt signaling pathway but when it is silenced, predisposes patients to Familial Adenomatous Polyposis and colorectal cancer. Group of answer choices APC WT1 p53 ARFarrow_forward
- Classify the following genes as proto-oncogenes or tumor-suppressor genes: p53, ras, Bcl-2, telomerase, jun, andarrow_forwardGive only typing answer with explanation and conclusion A healthy asymptomatic 27 year old female, Susan, presents to your clinic with known family history of Spastic Paraplegia 4 caused by pathogenic SPAST mutation identified in her mother. She wants to know the risk that she will develop symptoms eventually based on this information. the penetrance of SPAST mutation is approximately 85% for women and 96% for men.arrow_forwardOf the following choices a loss of function mutation would most lukely contribute to cancer onset if the mutant gene codes for a : telomerase tumor suppressor protein ATP synthesis enzyme RNS binding proteinarrow_forward
- Using your Western Blot data and your knowledge of nuclear receptors, discuss which type of drug you would recommend for a cancer therapy targeting c-Myc expression.arrow_forward1. Anaphase promoting complex is inactivated, s cycling cannot bind s cdk, m cycling cannot be produced ( chioces for all 3) 2.much higher; much lower, similararrow_forwardPlease answer all questions if possible. -B-Raf is not overexpressed in cancer though shows altered structure, why? -What is the specific structural change in B-Raf that causes oncogenic activation of this proto oncogene.arrow_forward
- You established two cell lines (Cell line X and Cell line Y) from colon cancer patients and both of them can proliferate without the Wnt ligand. When you analyze the tumor suppressor APC (Adenomatous Polyposis Coli) protein in these lines, X does not express functional APC but Y expresses functional APC. How can Y keep proliferating without Wnt? Which function (protein) within the Wnt signaling pathway might be defective in Y?arrow_forwardcan u help with this please thank you so mucharrow_forwardhe human phenotype is regulated by epigenetic control of gene expression. Discuss the three main types of epigenetic regulation, illustrating your answer with examples of diseases arising from impairment of each of these processesarrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
- Human Anatomy & Physiology (11th Edition)BiologyISBN:9780134580999Author:Elaine N. Marieb, Katja N. HoehnPublisher:PEARSONBiology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStaxAnatomy & PhysiologyBiologyISBN:9781259398629Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa StouterPublisher:Mcgraw Hill Education,
- Molecular Biology of the Cell (Sixth Edition)BiologyISBN:9780815344322Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter WalterPublisher:W. W. Norton & CompanyLaboratory Manual For Human Anatomy & PhysiologyBiologyISBN:9781260159363Author:Martin, Terry R., Prentice-craver, CynthiaPublisher:McGraw-Hill Publishing Co.Inquiry Into Life (16th Edition)BiologyISBN:9781260231700Author:Sylvia S. Mader, Michael WindelspechtPublisher:McGraw Hill Education
Human Anatomy & Physiology (11th Edition)
Biology
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:PEARSON
Biology 2e
Biology
ISBN:9781947172517
Author:Matthew Douglas, Jung Choi, Mary Ann Clark
Publisher:OpenStax
Anatomy & Physiology
Biology
ISBN:9781259398629
Author:McKinley, Michael P., O'loughlin, Valerie Dean, Bidle, Theresa Stouter
Publisher:Mcgraw Hill Education,
Molecular Biology of the Cell (Sixth Edition)
Biology
ISBN:9780815344322
Author:Bruce Alberts, Alexander D. Johnson, Julian Lewis, David Morgan, Martin Raff, Keith Roberts, Peter Walter
Publisher:W. W. Norton & Company
Laboratory Manual For Human Anatomy & Physiology
Biology
ISBN:9781260159363
Author:Martin, Terry R., Prentice-craver, Cynthia
Publisher:McGraw-Hill Publishing Co.
Inquiry Into Life (16th Edition)
Biology
ISBN:9781260231700
Author:Sylvia S. Mader, Michael Windelspecht
Publisher:McGraw Hill Education