As discussed in Lipids 3, SREBPs are a type of transcription factorinvolved in lipid homeostasis. SREBPs regulate the expression of genesthat encode for anabolic enzymes.Normally SREBPs are degraded within 3 hours. Pancreatic cancer cellsprevent this from happening, which increases cholesterol productionwithin the tumor.If maintaining SREBPs for a longer period of time increases lipidsynthesis, then these transcription factors are:O introducing a point mutation within the mRNA, causing the ribosome tosynthesize a better proteinbinding to the promoter and preventing RNA polymerase from accessing thetranscription start siteintroducing a premature stop codon within the mRNA, causing the ribosometo terminate translationbinding upstream of the promoter and recruiting RNA polymerase to thetranscription start sitebinding to the origin of replication and recruiting DNA polymerase forbidirectional synthesis

The full form of SREBPs is Sterol regulatory element binding proteinsSREBPsare composed of two…

Answered: As discussed in Lipids 3, SREBPs are a…

Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

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The p53 gene is a tumor-suppressor gene while p634 gene is an oncogene. Mutation in either one can result in the transformation of a normal cell into a cancer cell. Explain the difference between the functions of the two proteins and how their mutation can lead to cancer development.
Of 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 protein
1). Tumor suppressor proteins monitor DNA and detect damage. Some cancers evade this detection by removing tumor suppressor proteins from the nucleus. An overproduction of what transport molecule could cause this? What is one example of how this overproduction might be targeted for cancer treatment (suggest a hypothetical treatment that would prevent the cancer)? 2) :) Based on the course content thus far, would mRNA vaccines pose a risk to the genomic DNA in a cell? Explain.
LysR regulators like llvY repress transcription from their own promoters. This is called a negative feedback loop. Why might negative feedback be a good way to control expression of a transcriptional repressor? This type of negative feedback loop ensures that ilvC transcription will always be repressed when llvY levels are low, and ilvC will be transcribed highly when llvY levels are high. This type of negative feedback regulation ensures that ilvY is never transcribed. Since llvY is a transcriptional repressor, it will slow down cell growth by blocking transcription. So, llvY represses it's own transcription so that no llvY can ever be made, and the cell can grow. This type of negative feedback loop ensures that there is always a moderate amount of llvY. When IlvY levels fall too low, transcription from the promoter will increase since IlvY won't be able to repress it's own promoter. This negative feedback also ensures that IlVY levels don't rise too high - when llvY levels are high,…
Isothiocyanates arè compounds found in vegetables such as broccoli. Such compounds have been shown to induce the expression of proteins called caspases in cervical cancer cells. Outside of Cell Toxins DNA Damage p53 Apoptosis Inside of Cell Based on the above diagram, would you expect ingestion of broccoli to promote, suppress or have no effect on the progression or survival of cervical cancer cells? Promote progression of cervical cancer cells Suppress progression of cervical cancer cells O Have no effect on progression of cervical cancer cells
You are studying a new type of cancer and you discover that there is a mutation in a gene that encodes a histone acetylase. You hypothesize that the mechanism by which this mutation causes cancer is by altering the expression of a gene involved in the control of cell proliferation by introducing a mutation in a gene involved in the control of cell proliferation mutating DNA repair genes introducing random mutations
Long non-coding RNAs (lncRNA) can act as a scaffold to form protein/RNA complexes that regulate gene expression? True False Wnt is a regulatory factor that regulate myogenic stem cell proliferation? True False
The deregulation of several signal transduction pathways is integral to the onset of cancer. These pathways involve both tumor promoters (the "gas pedals") and tumor suppressors (the "brake pedals"). Which would be a more effective treatment for cancer: A small molecule inhibitor that targets a tumor suppressor or one that targets a tumor promoter? Briefly explain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND MINIMALLY IN ABOUT EIGHT WORDS.) Edit View. Insert Format Tools Table 12pt v Paragraph BI UAV 2VT² V| :
Mutations to SRP72 (the RNA component of the signal recognition particle) are known to cause some forms of familial bone marrow failure. Which of the following protein(s) is/are potentially affected by such deleterious mutations? Choose all that apply Epidermal growth factor receptor (EGFR) Cytochrome c Insulin (a secreted protein) uS7 (a small ribosamal subunit protein from all dornains of life) DO00
The G-protein Ras is involved in proliferative signaling, and is mutated is a large fraction of human cancers. Almost all mutations in Ras mutate the glycine at codon 12. These mutations lock Ras in an active conformation. How will the GTPase activity of a Ras protein with a G12 mutation compare to a normal Ras protein without the mutation? (10 words maximum)
You have developed an activator of a non-receptor tyrosine kinase. In three different cell types that all contain this receptor your drug has different effects. In cell type A you see activation of gene X and gene Y; in cell type B you note activation of Gene X, but no change in the mRNA levels for Gene Y. In cell type C your drug has no effect on either Gene X or Y. Describe how could each choice (A-D) be a possibility to suit the scenario? a. Genes X & Y are controlled by two separate STATs (STAT X & STAT Y). Cell type A contains both STATs; cell type B contains STAT X only; cell type C has neither STAT. b. Genes X & Y are controlled by two separate STATs (STAT X & STAT Y) and two separate JAKs (JAK X & JAK Y). Cell type A contains both STATs and JAKs; cell type B contains both STATs but JAK X only; cell type C has both STATs but neither JAK. c. Genes X & Y are controlled by two separate STATs (STAT X & STAT Y), two separate JAKs (JAK X & JAK Y) and…
Cellular levels of tumor suppressor protein p53 is maintained by a ubiquitin ligase protein, called Mdm2. Over expression of Mdm2 destabilizes p53. Another protein p19ARF inhibits the activity of Mdm2, thus stabilizing p53. Loss of p19ARF function converts normal cells into cancer cells With the above information, which of the following statements are true? Mdm2 is a tumor suppressor gene but p19ARF is an oncogene Both Mdm2 & P19ARF are oncogenes Both Mdm2 & P19ARF are tumor suppressor genes O Mdm2 is an oncogene but p19ARF is a tumor suppressor gene

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