1.Substituents exhibit strong steric repulsion at the GABAA receptor ？what does it means？？2. Substitutions at C-6, C-8, and C-9 lower the activity？where is C-6, C-8, and C-9 ？can anyone help to lable out？ General Structure-Function Association for Different BenzodiazepineModifications.e.g. CH,Methyl substituent shows the highest increase in activity andbulky substituents such as a phenyl group lead to loss of activityTriazolo analogs tend to show a significantly higher activitye.g. CH,Decisive effect on the activitye.g. OH CH,Substituent leads to ane.g. NO, CI Brdecrease in activityActivityincreasewithe.g. F CIelectronwithdrawingHalogen substituents in ortho-position lead to significantlyenhanced activitysubstituent* Substitutions at C-6, C-8, and C-9lower the activitySubstituentsexhibitstericstrongrepulsion at the GABA, receptor" Phenyl ring at C-5 position seemsto be the best option with onlypyridylremarkable activityderivativesshowing

Benzodiazepines are the class of compounds that are used as muscle relaxants, hypnotics,…

1.Substituents exhibit strong steric repulsion at the GABAA receptor ？what does it means？？ 2. Substitutions at C-6, C-8, and C-9 lower the activity？where is C-6, C-8, and C-9 ？can anyone help to lable out？

1.Substituents exhibit strong steric repulsion at the GABAA receptor ？what does it means？？ 2. Substitutions at C-6, C-8, and C-9 lower the activity？where is C-6, C-8, and C-9 ？can anyone help to lable out？

Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

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please answer 25,26
9. Fill in the table below, outlining different aspects of neuronal signalling in sino atrial node of the mammalian heart. A legend of possible entries is provided below the table, specifically for the columns "marker genes", "associated G proteins" and "ionotropic targets" Marker gene Ionotropic receptors Possible associated G proteins Gs Gq Gi/Go Possible marker genes: Solute carrier family 17 Glutamate decarboxylase Dopamine ß hydroxylase Choline acetyltransferase Possible ionotropic targets: Cayl channels Ca 2 channels GIRK channels Metabotropic receptors M2,4 B1,2 Associated G protein Ionotropic target(s) Effects on heart Tryptophan hydroxylase 2 Tyrosine hydroxylase Histidine decarboxylase M-type K+ channels HCN channels BK and SK channels
Conotoxin is produced by marine cone snails. Among its effects is to block voltage-gated Ca2+ channels in n eurons. A. What anatomical part of a neuron would be affected by conotoxin? B. How would the neuron's action potential be affected by conotoxin? Explain, using at least TWO of the following terms: threshold, depolarization, repolarization, hyperpolarization, summation, IPSP, EPSP, exocytosis C. If conotoxin affected a somatic motor neuron, would this toxin cause muscle weakness or increased muscle tension? Explain why.
6. Define a receptor tyrosine kinase and distinguish it from a serine/threonine kinase. (As we discuss ANY kinase in signalling pathways, pay close attention to what type of kinase it is...does it phosphorylate serene/threonine resides or tyrosine residues?)
5.Myasthenia (muscle weakness)is characterized by damage in the transmission of neurotic impuise and decreased amount of acetylcholine due to autoimmune mechanisms. Prozerine is used for treatment of this disease.Specify the mechanism of this drug action. For this: 1)Write the reaction of acetylcholine degradation at neuromuscular junction. 2)What enzyme will be inhibited with prozerine? Name the class of this enzyme. 3)What is the mechanism of this enzyme inhibition?
1. List the specific steps of beta-adrenergic receptor signaling through PKA activation. 2. What is the chromophore in rhodopsin? How does light absorption activate rhodopsin signaling? 3. How does the rhodopsin signaling pathway effector enzyme PDE affect levels of cGMP? At the molecular level, what is the result of the changed levels of cGMP and what response does this trigger? 4. What class of receptor is the insulin receptor (INSR)? When IRS1 is phosphorylated by the insulin receptor, what are the two signaling pathway branches that are activated? What physiological responses do these two branches regulate? 5. Both insulin and epinephrine regulate levels of D-glucose in the blood. How?
9. Describe the steps in the G-protein coupled receptor/adenylyl cyclase/CAMP - signaling pathway. What are examples of physiological processes in the body that use this pathway? What are two toxins that activate this pathway and prevent it from being turned off?
7. The following happens when a G-protein-coupled receptor activates a G protein? A. The B subunit exchanges its bound GDP for GTP. B. The GDP bound to the a subunit is phosphorylated to form bound GTP. C. The a subunit exchanges its bound GDP for GTP. D. It activates the a subunit and inactivates the By complex. 8. Which of the following statements is true? A. MAP kinase is important for phosphorylating MAP kinase kinase. B. PI 3-kinase phosphorylates a lipid in the plasma membrane C. Ras becomes activated when an RTK phosphorylates its bound GDP to create GTP D. STAT proteins phosphorylate JAK proteins, which then enter the nucleus and activate gene transcription 9. A cell can crawl through a tissue because of the proteins that can transmembrane bind to fibronectin outside of the cell. A. Integrin B. Collagen C. Gap junction D. Claudin 10. Which of the following genetic changes cannot convert a proto-oncogene into an oncogene A. A mutation that introduces a stop codon immediately…