Phosphofructokinase (PFK-1) is ____ when ATP levels are low, and ____ when ATP levels are high. a Inhibited; inhibited b Activated; activated c Inhibited; activated d Activated; inhibited
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Phosphofructokinase (PFK-1) is ____ when ATP levels are low, and ____ when ATP levels are high.
| a |
Inhibited; inhibited |
|
| b |
Activated; activated |
|
| c |
Inhibited; activated |
|
| d |
Activated; inhibited |
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- After it has been activated a G-protein _______. moves along the inside of the cell's membrane and activates enzymes binds to its receptor in the cell's nucleus and initiates translation travels in the bloodstream to its target cell and then binds to its receptor binds to a receptor on a nearby cell and then activates multiple proteinsAn active Gai ultimately prevents production of its pathways second messengers, which means those second messengers are unable to activate the enzyme O phospholipase C O protein kinase A O adenylyl cyclase phosphodiesterase protein kinase Cthe MTOR kinase activity is stimulated by O all answers listed O cardiac mechanical stress O skeletal muscle stress O insulin
- . Melittin is a protein in bee venom that activates phospholipase Az. How might this effect contribute to the local inflammation that is caused by bee stings?Compound C is a pharmaceutical agent that blocks AMPK activity. How might compound C influence adaptation following resistance exercise? How might compound C influence adaptation following endurance exercise? Be specific and remember this section is Molecular SignalingThe figure below shows a signaling pathway activated by the bindiıng of adrehalMNe LU the beta-adrenergic receptor. Binding of adrenaline to the receptor causes GTP-binding and activation of G proteins. Active GTP-bound G protein activates adenylate cyclase to initiate a signaling cascade that affects cellular responses, and includes cellular changes to mediate increased heart rate and accounts for the flight-or-fight response. activated adenylate cyclase adrenaline activated B-adrenergic receptor adenylate cyclase G protein subunit 22 GTP SDP conformational ATP CAMP change in receptor heterotrimeric G protein ACAMP inactive protein kinase A active protein kinase A 4 cellular responses Consider the homozygous mutation in which a cell produces a variant of adenylate cyclase that can no longer be activated Which of the following are true in this cell? Select all that apply. Heart rate increases Protein Kinase A is not activated CAMP levels are lower than normal Heart rate decreases
- Match the G-protein with the action it causes: OPTIONS ARE (Gi , Gq, Gs) 1.Activates phospholipase C (PLC) 2.Activates Ca2+ channels 3.Inhibits Ca2+ channels PreviousNextnicotine from cigarette smoke acts as a lignad and associated with specific proteins on the surface of cells in the brain, causing felings of pleasure nad well being. What is the appropriate event in the cellular response to nicotine Rapid elimination of nicotine from the body is an example of: 1. receptor binding 2. signal termination 3. recepto activation 4. signal transduction 5. cellular responsethế hucleus When CAMP is formed, it will activate: O Protein Kinase C O Protein Kinase A O G-protein O Adenylyl cyclase Macrophages engulf bacteria through
- Put the steps of the process of G-protein signal transduction in the order (1-4) in which they occur. Second messenger molecules are activated and amplify the signal A signal molecule binds to a receptor on the outside of the cell The alpha (a) subunit of the G-protein inside the cell moves and binds to a nearby enzyme The receptor changes shape, transducing the signal into the cellIn the transduction pathway, protein kinase C (select all that apply): O Is activated by the second messenger IP3. Phosphorylates the Gq protein. Cleaves PIP2 into two different second messengers. Adds a phosphate group to the effector protein. O Is activated by the second messenger CAMP. Save for LaterWhich of the following is true of signal transduction mediated by protein tyrosine kinases production of cAMP phosphoinositides are activated arrestins compete with G-proteins phosphorylation of tyrosine residues