2. Transcription of gene X is controlled by transcription factor A (TFA). Gene X is only transcribed when factor A is phosphorylated. Data on the tissue distribution of TFA and the activities of a protein kinase and a protein phosphatase specific for TFA are presented on the table below. What tissue will gene X be expressed? Explain. Protein Protein Tissue Factor A kinase phosphatase activity activity Muscle + Heart

2. Transcription of gene X is controlled by transcription factor A (TFA). Gene X is only transcribed when factor A is phosphorylated. Data on the tissue distribution of TFA and the activities of a protein kinase and a protein phosphatase specific for TFA are presented on the table below. What tissue will gene X be expressed? Explain. Protein Protein Tissue Factor A kinase phosphatase activity activity Muscle + Heart

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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TNF-alpha treatment of prostate carcinoma, LNCAP cells decreases cell survival as shown in the graph below. Which of the following would you observe in these cells treated with TNF- alpha? Select all that apply TNF-a 120 100 80 - 60 40 20 0. 24 72 (hrs) Control + TNF-a 100 ng TNFA 10 ng O Activation of extrinsic pathway of apoptosis O Activation of intrinsic pathway of apoptosis Activation of executioner caspases Recruitment of adapter protein FADD to the TNF-alpha receptor LNCAP cell viability (% of control)
The PYK gene codes for the expression of pyruvate kinase, which is one of the enzymestargeted for anti-cancer drug design. You have identified an RNAi that targets the mRNAof PYK gene. To study the effect of the RNAi towards pyruvate kinase, the respected RNAiis expressed in Saccharomyces cerevisiae. The level of pyruvate kinase can be detectedwith a fluorescent antibody.(a). Predict the result that you will obtain in recombinant S. cerevisiae that expresses therespected RNAi.(b). Compare the result in Q3a(i) with the wild-type S. cerevisiae.
1 of 16 Data from an experiment is shown in the figure below. In the experiment, murine cells were treated with a specific a ligand that activates receptor R. In some cases, the cells were exposed to one of two drugs (X or Y) as well as the ligand or were left untreated (UT). After 30 minutes of treatment, the cells were lysed with a detergent-based buffer to release the soluble membrane, cyosolic and nuclear proteins. Samples from each cell extract were run (in duplicate) by SDS-PAGE (SDS-polyacrylamide gel electrophoresis) in order to separate the proteins by molecular mass (size). The separated proteins were then transferred to a nitrocellulose membrane which was then probed with different antibodies in a western blotting procedure to detect specific phosphorylated proteins or total proteins. If present in the cell extract, these proteins appear as a dark band in the relevant western blot image within the figure. Drug X Drug Y UT Ligand Ligand Ligand Western blotting antibodies…
5) Briefly explain why the formation of a tumour can pose a risk to a person's homeostasis. 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…
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
The progressive loss of cardiac myocytes due to cell death has been associated with cardiac dysfunction and heart failure. Which of the following would lead to a significant loss of cardiac myocytes? Select all that apply Treatment of rapamycin which results in inhibition of mTOR activity Prolonged or severe ER stress with increased accumulation of unfolded proteins Activation of AMPK and phosphorylation of the TSC1 complex mTOR activation and phosphorylation of Ulk1
1.Describe in detail the signal transduction pathway that leads to activation of either PKA, Kinase or PC. 2. Describe in detail the signal transduction pathway that leads to activation of MAPKinase or Akt/PKB. 3.Describe the similarities and differences in the structures of GPCRs specific for various ligands including the extracellular , transmembrane , and intracellular domains.
TGF-B Receptor I (RI) phosphorylation of Smad2/3 does all of the following EXCEPT: activate Smad2/3 binding to the Co-Smad Smad4 dissociate intramolecular binding of Smad2/3 MH1 and MH2 domains. RI phosphorylation of Smad2/3 does all of these things. release Smad2/3 from the nucleus into the cytoplasm unmask the Smad2/3 nuclear localization signal (NLS).
TNF-alpha treatment of prostate carcinoma, LNCAP cells decreases cell survival as shown in the graph below. Which of the following would you observe in these cells treated with TNF- alpha? Select all that apply TNF-a 120 100 80 - 60- 40- 20 - 24 72 (hrs) + Control - TNF-a 10ng + TNF-a 100 ng O Activation of extrinsic pathway of apoptosis O Activation of intrinsic pathway of apoptosis Activation of executioner caspases Recruitment of adapter protein FADD to the TNF-alpha receptor LNCAP cell viability (% of control)
Plasma PDGF levels can be a diagnostic marker for severity and progression of breast cancer. The assay data below shows the plasma levels of PDGF in normal individuals, Stage II and Stage IV (More severe). You are treating a patient with breast cancer and assay indicates that their plasma PDGF level 6 fmoles/ 100 uL.Based on this info, in which stages has this patient's cancer progressed? Explain what process this patient's tumor has likely undergone and which cell types you would expect to now be associated with this tumor.
which of hthe following would result in a persisting proliferation response to growth factor receptor activation after the ligand is no longer binding to its rceptor kinase? 1. Both a mutation that blocks the GTPas activity of Ras and a mutation that blocks the exchange of GDP with GTP would cause the response to persist. 2. a mutation that blocks the GTPas activity of Ras 3. neither a mutation that blocks the GTPas activity of Ras nor a mutation that blocks the exchange of GDP with GTP would cause the response to persist 4. a mutatiaon that blocks the exchange of GDP with GTP
Signaling pathways often require receptor dimers to become active. What would be an advantage of the extrinsic apoptosis pathway requiring a trimer? I note from the article "Nature Reviews, Cancer 16:539, 2016" the following: The extrinsic apoptotic pathway, upon binding to their cognate ligand, death receptors such as tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) receptor (TRAILR) and FAS can activate initiator caspases (caspase-8 and caspase-10) through dimerization mediated by adaptor proteins such as FAS-associated death domain protein (FADD). Active caspase-8 and caspase-10 then cleave and activate the effector caspase-3 and caspase-7, leading to apoptosis. I can't think of any other pathway that uses a trimer, so there must be a reason. Glad an exprt can help.