2) After plotting actin bound to cofilin versus the cofilin concentration, you generate thefigure below.v (cofilin binding density)10.80.60.40.202468[S. pombe cofilin] free (UM)10a) What is the Kd you measure for thisinteraction?b) What is the AG of the interaction?c) Based on the data, is there anything yoususpect about the binding of protein andligand?

Actin - Actin is a family of globular multi-functional proteins which form microfilaments in the…

Answered: 2) After plotting actin bound to…

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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From the Hill Plot below, the of the first binding event for the receptor-ligand system under study is: Q1 4 nM 10 μΜ -2 nM 2 nM Calculate the Hill Coefficient from the receptor-ligand binding data below: Q2 4 100 2 3 (077) log 10 8 6 4 2 0 -2 -4 -6 -6 -4 -2 0 2 4 log [L] (nM) 6 8 10
Answer the following step by step A) How many milliliters of 1:100 epinephrine are needed for a 5 mg dose? B) How many milligrams are there in a 1cc dose of 2% Xylocaine? C)You have 20% acetylcysteine; how many milliliters do you need of this to form 4 ml of 8% solution?
A tetrapeptide, glutamate-glycine-alanine-lysine, is prepared at at concentration of 1 mM (0.001 M) and is measured in the standard setup (pathlength of 1 cm). What is the approximate absorbance of this peptide at 280 nm? Hint: if the peptide contained a single tryptophan, the answer would be about 10. 10 280 1 0
a) What is the KDD for this myoglobin variant? b) What is the predicted fractional saturation for the last box in the table? (please show your work so I can better understand) c) What is unexpected about the binding curve above? (5 words or less) d) What must be structurally different about this new variant relative to other known Myoglobin variants to generate this graph?
The plasma profiles of codeine (COD) and metabolites for 2 individuals (labeled A and B) are shown below. The X-axis is time in hours after an oral dose of codeine. [M=morphine; C6G=COD-6-glucuronide; M3G = morphine-3-glucuronide; NM (ignore)]. Note the data is shown on a log scale on the Y-axis. (A) Which individual is the poor metabolizer? Explain how you know this from the profiles? (B) Is this a problem for cough suppression? Explain. -CH HO Codeine COD 10 000 1000 C6G COD 100 M3G M6G NM 10 M 10 20 30 0 10 20 30 Plasma concentration (nmol I-)
what possible outcome may be produced when the molecular weight of an alcohol antiseptic is increase to a C20, will it still be effective? Explain your answer
Estimate the binding affi nity of a ligand for its receptor from the followingdata:
A series of novel phenadoxone derivatives without mu2 receptor activity (mu2 activity is responsible for physical dependence) proposed to be developed as analgesics is shown below. Addition of which heterocyclic substituent R to phenadoxone is LIKELY to cause the MOST binding of the corresponding derivative to plasma proteins? Use the additivity of approximate estimates of logP to answer this question. phenadoxone derivatives A. Azetidine B. Thiophene C. Oxetane D. Furan E. Pyrrole ترف لي تي في R= -NH
A family eats homegrown vegetables daily which is irrigated with water from a river polluted with benzene having a concentration of 0.05 mg/L. The cancer potency factor for ingesting benzene is 2.9 x 10² mg/kg.day. a) Following the EPA exposure factors, determine the lifetime cancer risk assuming the receptor is an adult. State all assumptions. b) To reduce the lifetime cancer risk, it is proposed that the village replaces their homegrown produce with fish caught in the same river. Determine the percentage change in lifetime cancer risk from this potential solution and advise the community on the better food source of the two.
One such neurotoxin, Sarin (chemical name: propan-2-yl methylphosphonofluoridate) is considered a weapon of mass destruction by the United Nations by virtue of its ability to kill with great efficiency in very low concentrations. a. Where does Sarin have its effect (what is/are its target) and describe the mechanism of action of Sarin (how does it kill)? b. Describe the physical symptoms observed in those stricken with Sarin that are consistent with this mechanism of action. Include flaccid/tonic paralysis, as applicable.
Based on your Lineweaver-Burk plot, what is the mode of PaESBL-1 inhibition by NSAMB? What is the equation for the double-reciprocal plot at 20 nMnM NAMB?
Which arrestin is required for activation of phosphorylation of MDM2 during chronic Iso stimulation? use the following Figures 1and 2 respectively to explain please

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