You are studying the role of cAMP in cell signaling. You hypothesize that 2 intracellular signaling proteins, named GO and TIGERS, interact with each other when cells are treated with an extracellular source of CAMP. The two proteins were tagged with CFP or YFP (CFP = cyan fluorescent protein; YFP = yellow fluorescent protein). CFP is excited by 435 nm light and emits lights at 480 nm. YFP is excited by 480 nm light and emits light at 535 nm. H 400 Fluorescence 500 Wavelength of Emitted Light 400 500 Wavelength of Emitted Light 600 600 Fluorescence 400 400 500 Wavelength of Emitted Light 600 500 Wavelength of Emitted Light 600 Fluorescence Intensity 400 500 Wavelength of Emitted Light 600 Figure Legend. A. Cells expressing GO-CFP irradiate with 435 nm light. B. Cells expressing TIGERS-YFP and irradiated with 435 nm light. C. Cells expressing TIGERS- YFP and irradiated with 480 nm light. D. Cells expressing GO-CFP and TIGERS-YFP and irradiated with 435 nm light. E.Cells expressing GO-CFP and TIGERS-YFP treated with CAMP and irradiated with 435 nm

You are studying the role of cAMP in cell signaling. You hypothesize that 2 intracellular signaling proteins, named GO and TIGERS, interact with each other when cells are treated with an extracellular source of CAMP. The two proteins were tagged with CFP or YFP (CFP = cyan fluorescent protein; YFP = yellow fluorescent protein). CFP is excited by 435 nm light and emits lights at 480 nm. YFP is excited by 480 nm light and emits light at 535 nm. H 400 Fluorescence 500 Wavelength of Emitted Light 400 500 Wavelength of Emitted Light 600 600 Fluorescence 400 400 500 Wavelength of Emitted Light 600 500 Wavelength of Emitted Light 600 Fluorescence Intensity 400 500 Wavelength of Emitted Light 600 Figure Legend. A. Cells expressing GO-CFP irradiate with 435 nm light. B. Cells expressing TIGERS-YFP and irradiated with 435 nm light. C. Cells expressing TIGERS- YFP and irradiated with 480 nm light. D. Cells expressing GO-CFP and TIGERS-YFP and irradiated with 435 nm light. E.Cells expressing GO-CFP and TIGERS-YFP treated with CAMP and irradiated with 435 nm

Biology 2e

2nd Edition

ISBN:9781947172517

Author:Matthew Douglas, Jung Choi, Mary Ann Clark

Publisher:Matthew Douglas, Jung Choi, Mary Ann Clark

Chapter9: Cell Communication

Section: Chapter Questions

Problem 12RQ: Histamine binds to the H1 G-protein-linked receptor to initiate the itchiness and airway...

See similar textbooks

Similar questions

After establishing the importance of cGMP in the signaling pathway of the photoreceptor cells, the researchers wish to identify the exact target of cGMP. The researchers suspect that cGMP binds to an ion channel, causing the observed change in the membrane potential between the dark and the light conditions but they are not sure which one. The researchers determine the movement of three different ions (sodium, chloride and potassium) as a function of their respective electrochemical gradient across the plasma membrane: ● Sodium tends to enter the cell Chloride tends to enter the cell Potassium tends to leave the cell The researchers therefore propose three simple hypotheses for the effect of cGMP on the membrane potential of the rod photoreceptor cell: ● Hypothesis A: CGMP binds to a sodium-channel, that opens and lets sodium ions diffuse inside the cell. Hypothesis B: cGMP binds to a chloride-channel, that opens and lets loride ions diffuse inside the cell. Hypothesis C: cGMP binds to…
In Chapter 3, the Kd of calmodulin EF hands for binding Ca2+ is given as 10−6 M. Many proteins have much higher affinities for their respective ligands. Why is the specific affinity of calmodulin important for Ca2+ signaling pro- cesses such as that initiated by production of IP3?
Non-canonical Hedgehog signaling results in actin cytoskeleton rearrangements, leading to cellmovement and changes in cell shape. Describe how changes to the actin cytoskeleton lead to cellmovement and changes in cell shape.You do not need to draw out the signaling pathway again (#1b). Your answer should focus onthe changes to the actin cytoskeleton. Drawings will be helpful!
TGF-B Receptor I (RI) phosphorylation of Smad2/3 does all of the following EXCEPT: activate Smad2/3 binding to the Co-Smad Smad4 dissociate intramolecular binding of Smad2/3 MH1 and MH2 domains. RI phosphorylation of Smad2/3 does all of these things. release Smad2/3 from the nucleus into the cytoplasm unmask the Smad2/3 nuclear localization signal (NLS).
Why do we need to identify and determine the function of every single molecule involved in cell signalling? Provide one concrete example of an application of an elucidated cascade of events in cell signalling. (The answer should be no less than 300 words)
added ligand concentration of 10 µM is 5 × 10³ s¹. What is the value of the reverse rate constant k_1 = 1 ×10-4 Incorrect Macmillan Learning You have not correctly calculated the value of the reverse rate constant. To begin, calculate the value of k₁ by dividing the rate of receptor-ligand complex formation (the rate of the forward reaction) by the ligand concentration. k₁ = rate forward [L] Then, calculate the value of the reverse rate constant, k_₁, by multiplying the dissociation constant, Kd, and the forward rate constant, k₁. k_1 = Kak₁
Put the following steps for the outline of the growth factor signaling pathway in order: Map Kinase Kinase is Phosphorylated Proteins involved in gene transcription are activated Growth factor binds to its receptor in the cytoplasmic membrane Receptor recruits adaptor protein and GEF Autophosphorylation of tyrosine residues on the receptor Structural change of the receptor activates Tyrosine Kinase Map Kinase Kinase Kinase is phosphorylated Ras, a small GTPase, is activated by the exchange of GTP for GDP Map Kinase is Phosphorylated Map Kinase enters the nucleus
Much of what we know about cell signalling comes from biochemical studies of proteins isolated in test tubes. What is the precise quantitative behaviour of intracellular signalling networks in an intact cell where countless other signals and cellular components can influence the specificity and intensity of signalling?
i) For serotonin receptor associated with the G protein class of subtype Gs, list the various ways how cell signalling can be terminated at stage 0 and 2 shown in Figure 1. 1 Reception ExtracellularA Hama Membra ely Malecle 2 Transduction 3 Response At Select by putting an arrow at the end of the correct choice(s). 2 a) - ) Cytoplase
Histamine binds to the H1 G-protein-linked receptor to initiate the itchiness and airway constriction associated with an allergic response. If a mutation in the associated G-protein’s alpha subunit prevented the hydrolysis of GTP how would the allergic response change? More severe allergic response compared to normal G-protein signaling. Less severe allergic response compared to normal G-protein signaling. No allergic response. No change compared to normal G-protein signaling.
You perform a competition study on a GPCR. You have isolated the plasma membrane from cells which contains the GPCR of interest. If an agonist and an inverse agonist are at equal concentrations in your study but the inverse agonist has a 10 x higher affinity for the receptor than the agonist, what would you expect to be the overall outcome to be? More of the agonist is bound and so most of the receptor is in its active conformation and is stimulated More of the inverse agonist is bound and so most of the receptor is in its inactive conformation and is unstimulated.
List two ways that GPCR signaling transduction can be turned off (go back to inactive state)