Tumor Necrosis Factor Receptor Signaling Q8.2: What is the key activating signal in the TNF receptor signaling pathway that occurs downstream of TNF-alpha binding to the extracellular domain? What are the analogous activating signals downstream of receptor activation in the GPCR and RTK pathways.
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BIOC 384
Tumor Necrosis Factor Receptor Signaling
Q8.2: What is the key activating signal in the TNF receptor signaling pathway that occurs downstream of TNF-alpha binding to the extracellular domain? What are the analogous activating signals downstream of receptor activation in the GPCR and RTK pathways.
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- BIOC 384 Receptor Tyrosine Kinase Signaling Q8.1: Explain why a glycine residue at position 12 of the G protein Ras is only active in the presence of growth factors but Ras with an aspartate residue at the same position is oncogenic (can cause cancer).Which ONE of these statements is the most accurate definition of the mode of action of imatinib? Select one: A.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks phosphatase activity by competing with adenosine triphosphate (ATP) binding B.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks tyrosine kinase activity by competing with adenosine triphosphate (ATP) binding C.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks tyrosine kinase activity by interaction with the enzyme site D.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks phosphatase activity by interaction with the enzyme site1 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…
- BIOC 384 Nuclear Receptor Signaling Q8.3: Glucocorticoids are potent anti-inflammatory molecules that repress inflammation through transcriptional mechanisms. Beginning with inhalation of the asthma drug fluticasone, describe how this treatment reduces inflammation at the molecular level.Q1. Explain why GDP cannot dissociate from the alpha subunit of the Trimeric G-protein even though the receptor is activated by ligand binding and there is enough GTP for the exchange process.Can anyone suggest a way of increasing phosphorylation of IKK alpha (Ser176/180)? Any potent phosphatase inhibitor in combination with TNF alpha?
- PDGF 100 PI3K 740 751 PI3K 50 - GAP O771 O GAP PTP P 1009 O PTP protein P-site 1 12 4 5. 6. 7. PI3K 740, 751+ 1021 GAP 771 +] +] PTP 1009 PLC PLCy PLCT 1021 When activated by ligand binding, the PDGF (platelet-derived growth factor) receptor becomes phosphorylated on 5 tyrosine residues (left figure). These phosphorylated tyrosines serve as binding sites for proteins that contain SH2 domains (SH2 domains bind phosphorylated Y). These proteins include phospholipase C-gamma (PLC-gamma), a phosphotyrosine phosphatase (PTP), a Ras GTPase-Activating Protein (GAP), and a phosphotidylinositol 3-Kinase (PI3K). PDGF stimulates several changes in the target cell, one of which is DNA synthesis. To determine which effectors of the PDGF receptor is/are responsible for stimulating DNA synthesis, you construct several mutant forms of the receptor that retain individual or combinations of the phosphorylation sites. You express these in cells and monitor DNA synthesi The results are shown in the right…Which phenomenon is not readily explained by the 'induced-fit' hypothesis, that is readily explained by the 'fluctuation-fit hypothesis? Catalysis by optimal interaction with the transition state of substrates. O Specificity of enzymes for substrates. O Lower binding affinity for products, enabling their release once chemistry has happened. O Cooperativity of binding to the remaining 3 sites of hemoglobin when oxygen binds to the first of the four sites.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
- Describe the similarities and differences in the structures of GPCRs specific for various ligands including the extracellular , transmembrane , and intracellular domains.Which statements are true? Explain why or why not.1 All second messengers are water-soluble and dif-fuse freely through the cytosol.2 In the regulation of molecular switches, proteinkinases and guanine nucleotide exchange factors (GEFs)always turn proteins on, whereas protein phosphatasesand GTPase-activating proteins (GAPs) always turn pro-teins off.3 Most intracellular signaling pathways providenumerous opportunities for amplifying the responses toextracellular signals.4 Binding of extracellular ligands to receptor tyro-sine kinases (RTKs) activates the intracellular catalyticdomain by propagating a conformational change acrossthe lipid bilayer through a single transmembrane α helix.5 Protein tyrosine phosphatases display exquisitespecificity for their substrates, unlike most serine/thre-onine protein phosphatases, which have rather broadspecificity.6 Even though plants and animals independentlyevolved multicellularity, they use virtually all the same sig-naling proteins and second…Hedgehog - Cell signaling pathway 1) describe its normal function and mechanism, and 2) predict what may happen if certain proteins in the pathway become mutated to be constitutively active (activated even in the absence of the preceding step in the pathway) or inactivated. It will be clearest to include a drawing of the pathway.
