Q10 ›Suppose that each ß-adrenergic receptor bound to epinephrine converts 100 molecules of the G₁ subunit to the GTP-boundform, Gas.If each molecule of activated adenylate cyclase produces 1000 molecules of cAMP per second, how many molecules of CAMPare produced in 10 seconds after the formation of a single complex between epinephrine and the ß-adrenergic receptor? Assumethe pathway is fully responsive.molecules of cAMP:x10

Biochemical signal transduction pathways taking place within lifeforms have the ability to amplify…

Answered: Suppose that each ß-adrenergic receptor…

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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GTPYS is a nonhydrolyzable analog of GTP. Suppose this compound were added to a cell-free system containing active components of an adrenergic signaling system. What consequences would you expect? What would be the effects on CAMP levels? || -0-P-o-P-0-P-o-CH, guanine он он GTPYS -
You are studying a cell line that expresses both GPCR-A and GPCR-B, each receptor binds the same ligand but activates different heterotrimeric G proteins that act on adenylyl cyclase. GPCR-A causes an increase in adenylyl cyclase activity, while GPCR-B causes an decrease in adenylyl cyclase activity. There is a basal level of adenylyl cyclase activity that produces a baseline CAMP concentration. Which of the following mutations would increase the intracellular levels of CAMP upon ligand addition? Select all that apply. A mutation in Gi that prevents GTP hydrolysis A mutation in GPCR-B that prevents G protein activation A mutation in GPCR-A that prevents G protein activation A mutation in Gs that prevents GTP hydrolysis
You are studying a cell line that expresses both GPCR-A and GPCR-B, each receptor binds the same ligand but activates different heterotrimeric G proteins that act on adenylyl cyclase. GPCR-A causes an increase in adenylyl cyclase activity, while GPCR-B causes an decrease in adenylyl cyclase activity. There is a basal level of adenylyl cyclase activity that produces a baseline CAMP concentration. Which of the following mutations would decrease the intracellular levels of cAMP upon ligand addition? Select all that apply. A mutation in Gi that prevents release of bound GDP A mutation in GPCR-B that prevents G protein activation A mutation in GPCR-A that prevents G protein activation A mutation in Gs that prevents release of bound GDP
Explain in detail the funcations and signalling and activation of ephrin receptor EPHB2. Give step by step explanation
Hormone H regulates these effects via its receptors which are found at both the cell surface (csRH) and within the cell (içRH). The signalling pathways that become activated in the presence of hormone H are depicted and described below. hormone H. H H extracellular fluid inactive GTP inactive RAS Lyn cell-surface receptor for H (csR») icR GDP RAS-GTP hexose metabolism cell survival H icR G, phase (resting) Raf HK GSK-3P MEK M G2 icR - hexose kinase ERK promoter HRE CDK1 Cyclin A nucleus cyclin A Fos A promoter Created in BioRender.com bio Signalling via the cell surface receptor Hormone H mediates its cell cycle stimulatory and pro-survival effects by binding to and activating the cell surface hormone H receptor (csRH). The activated CSRH activates Lyn, which activates RAS and ultimately the Raf/MEK/ERK kinase cascade. Active ERK: o phosphorylates and inactivates GSK-3B. Inhibition of GSK-3ß promotes cell survival. inhibits p27, preventing it from inhibiting cell cycle progression.…
You are studying a drug that affects a cAMP signalling pathway that is normally initiated when a signalling molecule binds to a G-protein coupled receptor. You determine that the drug prevents the hydrolysis of GTP bound to G-proteins in this pathway. Describe the impact, if any, that this drug would have on the G-protein coupled receptor (GPCR), assuming that the pathway has been activated by the presence of the signalling molecule (first messenger). Include an explanation for your response.
Epinephrine causes a liver cell to produce glucose from glycogen in a flight-or-fight response. In the signaling pathway triggered by the specific receptor binding, explain the mechanism for activation of Protein kinase A (PKA). indicate what mechanism/s for enzyme regulation is/are involved in the process (focus on the activation of PKA in response to epinephrine and draw what happens to the enzyme ie how it becomes activated).
Psilocybin is rapidly de-phosphorylated in the body into psilocin, which is anagonist For the 5-HT 2A Serotonin receptor, which binds the neurotransmitter serotonin as its natural ligand, and acts as a ligand-gated ion channel in the central nervous system. HO. Serotonin (a) Part of the sequence of the 5-HT 24 Receptor is NH₂ ...RQKACKVIGIVFFLFVVMWLAFFITNICDES... Identify the trans-membrane region within this sequence. Do you predict this sequence will Be transmembrane a-Helix or ß sheet? Why? (b) What is the distance spanned by this transmembrane region?
Compare the G protein Gs, which acts in transducing the signal from β-adrenergic receptors, and the G protein Ras. What properties do they share? How do they differ? What is the functional difference between Gs and Gi?
In a hypothetical cAMP-mediated signal transduction cascade, the GTP-αs/adenylate cyclase interaction following a single hormone–receptor binding event lasts for 2.3 seconds. The catalytic rate (turnover number) for the adenylate cyclase in question is 350 cAMP molecules produced per second. How many cAMP molecules would be produced if five hormone-receptor binding events were to occur before the hormone molecule dissipates in the bloodstream? What is the amplification effect of this step in the signaling pathway?
Three potential inhibitors for VEGF were discussed in the signal transduction simulation. Explain two possible steps that these drugs can be expected to interfere with VEGF signaling (Hint: think about the requirements for signaling to occur).
GTPγS is a nonhydrolyzable analog of GTP. Suppose this compound were added to a cell-free system containing active components of an adrenergic signaling system. What consequences would you expect? What would be the effects on cAMP levels?

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