If a mutation is introduced into I-KBα that inhibits it phosphorylation by the IKK complex, this would prevent: O dimerization of the p50 and p65 subunits. translocation of NF-kB into the nucleus. O TAK1 phosphorylation of IKKB. recruitment of Nemo to the IKK complex.
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- Which of the following would be expected to inhibit PKC activation by a GPCR ligand? phospholipase C inhibitor cAMP phosphodiesterase inhibitor Ras inhibitor MAP kinase inhibitorAn SH2-containing protein contains a mutation that changes its binding pocket such that tyrosine and phosphotyrosine bind with equal affinity. As a result, MEK activity: does not change with receptor dimerization and transautophosphorylation decreases due to changes in Raf activation increases with ligand binding-induced dimerization decreases due to allosteric inhibition of SH2-domain bindingBinding of PGI2 to its protein binding receptor leads to
- The MARCH-1 E3-ubiquitin ligase is expressed in B cells, dendritic cells, and macrophages. The pathway regulated by MARCH-1 is targeted by some pathogens in an immune evasion strategy. In this strategy, the pathogens encode: A protein that induces degradation of MARCH-1 A protein that mimics MARCH-1 and functions similarly A protein that binds to MARCH-1 and inhibits its function A protein that is induced by IL-10 in macrophages and dendritic cells A protein that induces degradation of CD86TGF-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).The MARCH-1 E3-ubiquitin ligase is expressed in B cells, dendritic cells, and macrophages. The pathway regulated by MARCH-1 is targeted by some pathogens in an immune evasion strategy. In this strategy, the pathogens encode a protein that binds to MARCH-1 and inhibits its function. OOOO a protein that is induced by IL-10 in macrophages and dendritic cells. a protein that induces degradation of MARCH-1. a protein that mimics MARCH-1 and functions similarly.
- See figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. Cyclin Serine Lysine Aspartic "Acid Lysine -OH NH3t -Coo NH3+ NH3 + -OH Aspartic Aad Aspartic Acid /Lysine Serine сокSee figure 12.16b regarding the process by which cyclin regulates the Cdk. Suppose that the cyclin binding site in the Cdk contains these FOUR amino acids in this order from top to bottom: serine, lysine, aspartic acid acid and lysine and the Cdk binding site in the cyclin contains these FOUR amino acids in this order from top to bottom: aspartic acid, aspartic acid, lysine and serine. Use the schematics below to show the R groups and how they might interact to create the cyclin.cdk complex. Label both binding sites, show all charges that will be used to create any bonds, and label all bonds formed and add the ATP active site. A Explain what a kinase does and how the cyclin controls the activity of the Cdk.What is meant by intrinsic GTPase activity? Exchange of GDP for GTP on the a-subunit of the G protein Inhibition of GBCR receptor activity Activation of Adenylyl Cyclades Breakdown of cAMP by phosphodiesterase Spontaneous hydrolysis of GTP on the a-subunit of the G-protein
- If you wanted to engineer the initiator caspase from the Fas/FasL extrinsic apoptosis pathway to function in the intrinsic pathway (e.g. in response to DNA damage), which of the following would be the most likely approach to succeed? O Replace the extrinsic pathway's initiator caspase Death Effector Domain with a CARD domain O Replace the Fas Death Domain with a cytochrome C binding domain O Generate a version of the Fas receptor that localizes to the mitochondrial intermembrane space 80 O Replace the intrinsic pathway's initiator caspase CARD domain with a Death Effector Domain F3 0 $ 4 DOD DOO R F4 S % 5 T No new data to save. Last checked at 3:01pm Submit Qu B4 ♫ 8 tv A F5 < 6 MacBook Air F6 Y & 7 F7 * 8 X F8 ( 9Referring to Figure 18.5, predict what would happen if the SRPRNA was unable to stimulate the GTPase activities of the GTPbindingproteins within SRP and the SRP receptor.GTP binding proteins are molecular switches. How do GTP binding proteins work? Provide two examples of GTP binding proteins that function in intracellular protein transport. Make a drawing that illustrates the function of each of these proteins in their respective roles. Predict the direct outcome of a mutation that: Inhibits GTPase activity Inhibits interaction with the GEF