Biochemistry
9th Edition
ISBN: 9781319114671
Author: Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Publisher: W. H. Freeman
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- Need the following questions answered please, thank you!arrow_forwardQuestion 2: lon channels are the key to cell signaling in the body. The voltage gated calcium channels discussed in question one are a part of that. These systems are in delicate balance, keeping ion concentrations around the cell at a specific level so that an electrical signal can travel, in this case, down a skeletal muscle, and cause a contraction. Both hypokalemic (too few ions) periodic paralysis and hyperkalemic (too many ions) periodic paralysis are caused by mutations to the CACNA1S gene. If a mutation created a hyperkalemic periodic paralysis phenotype, that mutation could be characterized as for the CACNA1s gene A. Gain of Function B. Loss of Function C. Null D. Silent If a mutation created a hypokalemic periodic paralysis phenotype, that mutation could be characterized as for the CACNA1s gene A. Gain of Function B. Loss of Function C. Null D. Silentarrow_forwardQUESTION 14 What switches off an activated G protein? A molecule of GDP replaces the GTP. There is an enzyme that reassembles the trimeric G protein. Ca2+ ions activate CAMKII, which inactivates the protein. The protein contains intrinsic GTPase activity which converts GTP to GDP. A phosphorylase enzyme removes the phosphate from the GTP.arrow_forward
- QUESTION 41 Which of the following statements is mismatched with the neurotransmitter? binds to muscarinic receptors - norepinephrine binds to ligand-gated ion channels - acetylcholine synthesized from tyrosine - epinephrine O released via exocytosis - dopaminearrow_forwardQUESTION 23 Which type of enzyme phosphorylates a protein? G protein protein kinase adenylyl cyclase guanosine triphosphatasearrow_forwardDear Expert. Thank you for your advice, which is good and helpful. I note that your answer is "when 3 binding sites have been occupied the activity of these receptors is maximum." However, I also note that for a similar question (see below) on α7 nicotinic Acetylcholine Receptor (nAChR) also gives the same answer, ie. at least 3 agonist binding sites should be occupied. Another Question - "To maximize the activity of an α7 nAChR, how many agonist binding sites should be occupied." I understand that in α7 nAChR, binding to two sites is more effective and binding to three sites is most effective for activation. On the other hand, binding to four or five sites in the nAChRs of chromosome 7 speeds up desensitization more than activation. Therefore, to maximize the activity of an α7 nicotinic Acetylcholine Receptor (nAChR) is also "3 sites". Am I right?arrow_forward
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