Yahoo Answers is shutting down on May 4th, 2021 (Eastern Time) and beginning April 20th, 2021 (Eastern Time) the Yahoo Answers website will be in read-only mode. There will be no changes to other Yahoo properties or services, or your Yahoo account. You can find more information about the Yahoo Answers shutdown and how to download your data on this help page.
Trending News
Cell Biology Problem help needed!!!?
I could really use some help answering these questions for my homework. Thanks.
A)
Succinylcholine is a chemical analog of acetylcholine. It is used by surgeons as a muscle relaxant. Care must be taken in the use of succinylcholine because some individuals have an adverse reaction, with life threatening consequences. Such individuals are deficient in an enzyme called pseudicholinesterase, which is normally present in the blood, where it slowly inactivates succinylcholine by hydrolysis to succinate and choline.
If succinylcholine is an analog of acetylcholine, why do you think it causes muscles to relax and not contract as acetylcholine does?
B)
A single amino acid change in Ras elimintaes its ability to hydrolyze GTP, even in the presence of a GTPase-activating protein (GAP). Roughly 30% of human cancers have this change in Ras. You have just identified aa small molecule that prevents the dimerization of a receptor tyrosine kinase that signals via Ras. Would you expect this molecule to be effective in the treatment of cancers that express this common, mutant form of Ras? Why or why not?
1 Answer
- 1 decade agoFavorite Answer
Succinylcholine is a noncompetitive nicotinic agonist. It means that it acts at a different site than Acetylcholine but on the same receptor. Initially, succinylcholine will cause depolorization and lead to contraction just as acetylcholine would. However, at the end of an action potential, acetylcholine will be broken up into choline and an acetyl group by acetylcholinesterase, and the choline will be taken back into pre-synaptic nerve terminal to be made into another acetylcholine molecule.
This does not happen to succinylcholine for a while. Succinylcholine maintains its depolarization. The muscle innervated by the nerve will relax because that is an independent mechanism. However, since succinylcholine is continuing to depolarize the cell, acetylcholine produced by the nerve can no longer produce a new action potential to contract the muscle, leading to flaccid paralysis (rather than spastic...because the muscle relaxes in this case, despite the fact that the nerve is still depolarized)
That's how succinylcholine stops acetylcholine from working.
I'm not sure about the relationship between the Ras proto-oncogene and Tyrosine Kinase. I do know that Tyrosine Kinase (and all kinases) cause phosphorylation of enzymes. Some enzymes are activated by phosphorylation. Others are inactivated.
Hope that helps