Recall that when we calculated the fraction of estrogen receptors occupied in the presence of 1 nM estradiol and 1 µM BPA, wefound that the fraction of receptors occupied with estradiol was 0.14 and the fraction of receptors occupied with BPA was 0.71.Calculate the concentration of free receptor in terms ofthe total concentration of receptor, Rtotal0.15R totalCalculate the concentration of free BPA in terms of thetotal concentration of receptor, R total.Confirm the approximate value for the dissociationconstant for the estrogen receptor-BPA complex.0.2 nM200 nM5 μ.1 μΜCalculate the concentration of free estradiol in terms ofthe total concentration of receptor, Rtotal1 nM - 0.14R,totalConfirm the approximate value for the dissociationconstant for the estrogen receptor-estradiol complex.

To calculate the concentration of free receptor (Rfree) in terms of the total concentration of…

Answered: Recall that when we calculated the…

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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distribution of Benzene in a 4-compartment PBK model after an exposure of 6h. Convert Berkeley Madonna code to Matlab. Note: The parameters in the table below are for a mouse model. 1a) What are the two type of products containing Benzene consumers were recently concerned about. Which of these two different type of products is likely more harmful? (hint: check news/reports and social media channels) 1b) Plot Jresp along with the concentrations of Benzene in blood, fat, non-fat and liver in a 24h window (pdf). Why is Jresp slightly decreasing within 6h of exposure? Here is the Berkeley Madonna code: {Top model} METHOD RK4 STARTTIME = 0 STOPTIME = 24 DT = 0.02 {Reservoirs Blood, Fat, NonFat and Liver} d/dt (NF) = + Jnf INIT NF = 0 d/dt (F) = + Jf INIT F = 0 d/dt (B) = - Jnf - Jf - Jl + Jresp INIT B = 0 d/dt (L) = + Jl - Jmetab INIT L = 0 {Flows} Jnf = Qnf*(Cb-Cnf) Jf = Qf*(Cb-Cfv) Jl = Ql*(Cb - Clv) Jmetab = vmax*Cl/(Km +…
Calculate KI' of the inhibitor from the information given. All information may not be needed to calculate. K'm = (29Ki+1.45x10^-10)/Ki Vmax = 11.7 µMs-1 Kcat = 130 s^-1 Vo = 3.0 μMs-1 S = 10 μM Et = 0.09 µM Inhibitor Concentration = 5x10^-12
Provide a diagram of the EPH RECEPTOR B2 (EPHB2) structure. Give bioinformatics structure
From experiments in which cells expressing normal myosin II heavy chain were altered to either lack (mhckA-) or overexpress (MHCKA ++) a myosin heavy chain kinase (MHCKA). For answering this question recall the earlier the variants on the myosin II heavy chain, in which three key threonines, normally subject to reversible phosphorylation, were altered in various ways: 3X Ser = Serines in place of Threonines 3X Ala = Alanines in place of Threonines 3X Asp = Aspartate in place of Threonines MHCKA is present at normal levels. Which of the two mutants (mhcp- or MHCP++) would be most likely to have a defect in cytokinesis?
Give typed explanation Which of the following effects is NOT true? If stripped Hb is treated with 2,3-BPG, the O2-binding curve for Hb will shift left. If stripped Hb is treated with 2,3-BPG and CO2, the O2-binding curve for Hb will mirror that of fully intact Hb. If stripped Hb is treated with CO2, the O2-binding curve for Hb will shift right. All of the listed effects are true.
Help me please
16
What is signal transduction? Illustrate and describe the molecular events in signal transduction pathways involving 1) G-protein-coupled receptors and 2) enzyme linked receptors.
Superfamily Give the superfamily to which the receptor belongs Accession Give the Uniprot accession number Name Give the molecule name Species Give the species Ligand What is the ligand, or class of ligands which bind to this receptor? What are the physiological processes involved? Is this autocrine, paracrine or endocrine or some combination of them? What is the Key physiological pathology of the receptor? process involved What are the downstream actions of the receptor? Which molecules does it interact with, how, and to what effect? How rapidly doe the effects appear? Mechanism of action Give one key journal reference in Vancouver format that describes the mode of action of the receptor Key reference Focus dom)
Explain, in detail, how tyrosine kinase proteins are involved in one signal transduction pathway of your choice. Make sure you describe the complete pathway in which it is involved. Then, describe how you would experimentally demonstrate the requirement of a tyrosine kinase protein in your chosen 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).
Dear 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?

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