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- Post-synaptic receptors located on the membrane of skeletal muscle cells allow the muscle cells/fibers to respond to the neural-stimulus. What is the name of the receptors located on the post-synaptic membrane of the muscle cells (you can't find the answer in the textbook; you have to do some research)? 22. 26. A. beta receptors muscle contr alon is actually called The B. alpha receptors C. muscarinic receptorsry D. nicotinic receptorsThe voltage-gated calcium channel is a protein that is imbedded and spans the lipid membrane to allow the movement of calcium into the axon terminal. What is theappropriate amino acid configuration of this channel that allows this movement to happen?Select one:O a. non-polar amino acids on the interior surface and polar on the exterior surfaceO b. polar amino acids on the interior surface and polar on the exterior surfaceO c. non-polar amino acids on the exterior surface and polar on the interior surfaceO d. non-polar amino acids on the interior surface and non-polar on the exterior surfaceDescribe the steps of neurotransmitter release involving the proteins v-snare and t-snare.
- If you wanted to design a drug that interfered specifically with skeletal muscle, without effecting cardiac or smooth muscle, which of the following would be the best target? a myosin kinase b troponin c actin d myosin phosphatase e DHP receptorsThe Structure of the acetylcholine receptor is shown below: A. Knowing the amino acid sequence of this protein, what tool would you use to identify the membrane-spanning region? Explain how it works.You are studying a Drosophila protein called FROZN that you think is a vesicle snare that plays a role in exocytosis of synaptic vesicles containing acetylcholine at the neuro-muscular junction. Because this protein has been isolated from neuromuscular junctions, you hypothesize that this snare is a Ca+2 sensor that mediates the final merging of vesicles with the membrane. To test this hypothesis you perform 2 experiments: 1. You make a mutant Drosophila that lacks FROZN and find that synaptic vesicle release at the neuromuscular junction is blocked. 2. You block Ca+2 entry into the presynaptic neuron terminal in a normal (wild type) fly and find that synaptic vesicle release is blocked. Do these experiments support your hypothesis that FROZN is a vesicle snare and is the Ca+2 sensor? Is there another possible explanation for the function of FROZN? Explain your answer.
- Which of the following intracellular or plasma membrane proteins requiresCa21 for full activity?a. calmodulinb. janus kinase (JAK)c. cAMP-dependent protein kinased. guanylyl cyclaseWhich of the following is NOT considered a secondary messenger? A. diacylglycerol B. inositol triphosphate C. CAMP D.calcium ions E . GTP asapThis is a tyrosine kinase receptor. a. Briefly describe the action of the receptor upon binding to the logand. b. There are several intracellular pathway possibilities for downstream responses. How might this receptor be able to selectively activate one particular pathway over another?
- A mutation in p21 that destroys its binding site will Select one: a. inhibit sarcomere contraction b. inhibit sarcomere relaxation c. inhibit cell division d. inhibit transcription of p21 e. promote cell divisionIon channels are composed of different protein subunits. a. What features of an ion channel determine that ions are able to pass through the channel? Where is this found? b. Potassium channels are selective for potassium ions only. Sodium is a smaller ion than potassium yet is unable to pass through. Explain this behavior. What is the significance of an auxiliary subunit and why is this important? C.In relation to Cushing’s Syndrome, a method that some scientists have used to treat the disease is to use small molecules that bind to, but do not activate, MC2R. This type of molecule is considered an antagonist. How can an antagonist bind to the same receptor as ACTH but not activate it ? a. The antagonist binds covalently while ACTH binds non covalently b. The antagonist is only partially complimentary to the binding pocket of MC2R c. The antagonist binds to ACTH and blocks it from binding to the receptor properly d. The antagonist is the exact same structure as ACTH but since it is synthetic it doesn’t work