Select from the drop-down menu which type of regulation is occurring in each case. The Ixb12 gene sequence is in a region of condensed chromatin in fetal heart cells, but in adult heart cells, this region is uncondensed. This is an example of choose your answer. regulation. The Ixb12 protein is activated by a kinase, which is an example of choose your answer. regulation. Trx25 MRNA is targeted for degradation by a protein that is present in liver cells but not in heart cells, which is an example of choose your answer. regulation. The Trx25 protein is inactivated by a protein that removes its phosphorylated residues, which is an example of choose your answer. regulat

Select from the drop-down menu which type of regulation is occurring in each case. The Ixb12 gene sequence is in a region of condensed chromatin in fetal heart cells, but in adult heart cells, this region is uncondensed. This is an example of choose your answer. regulation. The Ixb12 protein is activated by a kinase, which is an example of choose your answer. regulation. Trx25 MRNA is targeted for degradation by a protein that is present in liver cells but not in heart cells, which is an example of choose your answer. regulation. The Trx25 protein is inactivated by a protein that removes its phosphorylated residues, which is an example of choose your answer. regulat

Name: 17. options are: transcriptional, post-transcriptional, post-transatio
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Description: 17. options are: transcriptional, post-transcriptional, post-transational Select from the drop-down menu which type of regulation is occurring in each case.The Ixb12 gene sequence is in a region of condensed chromatin in fetal heart cells, but in adu

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 1VCQ: Figure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is...

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Wilms tumor 1, or nephroblastoma, is caused by mutations in the WT1 gene, which encodes a transcription factor. You have identified a novel variant in WT1: Arg422Pro. You have control cells and cells that have been engineered to carry the homozygous WT1 p.Arg422Pro mutation. You want to assess effects of this mutation on a variety of endpoints. For each endpoint listed below, choose the one technique is best suited to answer the question. Choose from: array CGH, qRT-PCR, qPCR, RNA-seq, FISH, in situ hybridization, western blot, immunostaining, WT1 ChIP-seq, WT1 ChIP-PCR, ATAC-seq, 3C Endpoint Technique? WT1 protein amount (quantitative) Western blot WT1 protein binding to all enhancers, genome-wide Chip-seq WT1 mRNA amount (quantitative) WT1 protein subcellular localization Quantitative assessment of all mRNAs in these cells (genome-wide) RNAseq Chromatin interactions between a specific WT1 chromatin binding site (identified above)…
Cancer can be defined as an abnormal proliferation of cells that defy the normal regulatory controls observed by normal cells. Recently, histone deacetylation therapies have been attempted in the treatment of certain cancers [reviewed by Delcuve et al. (2009)]. Specifically, the FDA has approved histone deacetylation (HDAC) inhibitors for the treatment of cutaneous T-cell lymphoma. Explain why histone acetylation might be associated with cancer and what the rationale is for the use of HDAC inhibitors in the treatment of certain forms of cancer.
You are researching the regulation of cell-size control and discover that a signaling pathway that acts through a particular enzyme-coupled receptor is important for the size growth (enlargement) of rat kidney cells. Receptor activation causes activation of adenylyl cyclase, which ultimately leads to the activation of PKA. PKA then phosphorylates a transcription factor called BTS on threonine 84. This phosphorylation is required to allow BTS to bind to specific regulatory DNA sequences, increasing the transcription of Zrt2, a gene encoding a protein vital for kidney cell growth. You find that kidney cells without this receptor are 25% smaller than normal cells. When you measure cells expressing a constitutively active version of PKA, you find they are 25% bigger than normal kidney cells. Based on these results, predict whether a kidney cell’s size would be bigger or smaller than normal kidney cells in each of the following circumstances. Explain why in 1-2 sentences for each. You add…
You are researching the regulation of cell-size control and discover that a signaling pathway that acts through a particular enzyme-coupled receptor is important for the size growth (enlargement) of rat kidney cells. Receptor activation causes activation of adenylyl cyclase, which ultimately leads to the activation of PKA. PKA then phosphorylates a transcription factor called BTS on threonine 84. This phosphorylation is required to allow BTS to bind to specific regulatory DNA sequences, increasing the transcription of Zrt2, a gene encoding a protein vital for kidney cell growth. You find that kidney cells without this receptor are 25% smaller than normal cells. When you measure cells expressing a constitutively active version of PKA, you find they are 25% bigger than normal kidney cells. Based on these results, predict whether a kidney cell’s size would be bigger or smaller than normal kidney cells in each of the following circumstances. Explain why in 1-2 sentences for each. You…
This is the full question.. "Both the cytokinin receptor encoded by CRE1 and the ethylene receptor encoded by ETR1 are examples of" Both the cytokinin receptor encoded by CRE1 and the ethylene receptor encoded by ETR1 are examples of O Leucine-rich repeat receptor kinase • The response regulator component of a two-component sensor histidine kinase (i.e., the component that directly activates transcription (type B ARRS, in the case of cytokinin) or directly mediates a response (type A ARRS)) O Regulatory molecules that bind calcium O The sensor histidine kinase component of a two-component sensor histidine kinase (i.e., the part that receives the signal and passes it to other components of the signal transduction cascade) O Proteins that shuttle from the cytoplasm to the nucleus to alter gene expression
6) The functioning of the "Ras/MAPK" signal transduction pathway is absolutely essential in order for cells to grow, divide, and migrate. One important protein that is part of this pathway is BRAF. This protein is a kind of enzyme called a "kinase" – an enzyme that transfers a phosphate group onto another protein. - In some melanomas, a mutated form of BRAF called BRAF Val600AGlu drives the progression of the cancer. The drug “vemurafenib" slows the progression of the cancer by slowing the production of the mutant BRAF protein. (National Cancer Institute. 2019. Types of Cancer Treatment. Retrieved from: https://www.cancer.gov/about-cancer/treatment/types/ Is this an example of a traditional cancer therapy or a targeted therapy? Briefly explain your reasoning in the space provided, using information provided in the text to support your answer. Type of therapy (traditional or targeted)?: Brief explanation: 19
Cancers are often caused by overactive growth factor receptor signaling (remember growth factor receptors are enzyme-linked receptor pathways). If you were able to use gene therapy to overexpress a particular protein in a cancer cell, which of the following might be useful to overexpress in order to combatt cancer? a GAP that acts on Ras a phosphatase that acts on GPCR a protein that enhances the activity of Akt a ubiqtuin ligase that acts on the MAPK phophatase
A temperature-sensitive mutant yeast strain stops dividing when shifted from 25°C to 37°C. These cells are analyzed at different temperatures by a machine that measures the amount of DNA they contain, and the following graphs are obtained. number of cells number of cells [ Select] [Select] [Select] 25°C [Select] مل Cells in G1 phase should have [Select] Which of the following would explain the behavior of your mutant? Mark yes or no for each of the following choices. 2 amount of DNA/cell (arbitrary units) 37°C 1 2 amount of DNA/cell (arbitrary units) unit(s) amount of DNA. ✓ Inability to initiate DNA replication Defect in chromosome condensation ✓Defect in centrosome duplication ✓Defect in cytokinesis
do 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…
The following diagram is from a paper investigating the role of β4 integrin in breast cancer. They examined the expression of miRNAs (rows) in ten β4 positive and ten β4 negative breast cancers. Each array was performed in triplicate (columns) (Gerson, 2012). B. β4 integrin is normally involved in attaching epithelial cells to the extracellular matrix and holding them in place, but in cancer, it can be involved in attaching cells to actin and increasing motility as well as in cell signaling. How is β-integrin expression related to miRNA expression? What do you think this means for these breast cancers?
As discussed in Lipids 3, SREBPs are a type of transcription factor involved in lipid homeostasis. SREBPs regulate the expression of genes that encode for anabolic enzymes. Normally SREBPs are degraded within 3 hours. Pancreatic cancer cells prevent this from happening, which increases cholesterol production within the tumor. If maintaining SREBPs for a longer period of time increases lipid synthesis, then these transcription factors are: O introducing a point mutation within the mRNA, causing the ribosome to synthesize a better protein binding to the promoter and preventing RNA polymerase from accessing the transcription start site introducing a premature stop codon within the mRNA, causing the ribosome to terminate translation binding upstream of the promoter and recruiting RNA polymerase to the transcription start site binding to the origin of replication and recruiting DNA polymerase for bidirectional synthesis
BCL2 binds to and inactivates BAX and other pro-apoptotic proteins, thereby inhibiting apoptosis. Venetoclax has been approved for marketing in patients with chronic lymphocytic leukemia (CLL) Venetoclax is a highly selective BCL2 inhibitor that disrupts the interaction of this protein with BH3 domain proteins thereby permitting apoptosis. Proapoptotic Proapoptotic proteins protein binds to BCL2 BCL2 Venetoclax Venetoclax displaces proapoptotic proteins BCL2 Venetoclax Proapoptotic proteins No venetoclax binding BCL2 Glys01Val mutation Which of the following can you conclude from this information? Select all that apply Bcl2- mutations that prevent Ventoclax binding promote cell survival Venetoclax binding to Bcl2 promotes cell survival . Venetoclax binding to Bcl2 promotes cell death Proapoptotic protein binding to Bcl2 promotes cell survival