1/Vo 0.07 0.06 0.05 0.04 0.03 0.02 0.01 0 0 1 2 3 1/[S] (MM-¹) 4 y = 0.005x + 0.0337 R² = 0.95 y = 0.0044x + 0.0253 R² = 0.885 LO 5 01 6 T
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can you explain what is happening in the attached graph?
Figure 3: Lineweaver-Burke plot of alkaline phosphatase activity without inhibitor
![1/Vo
0.07
0.06
0.05
0.04
0.03
0.02
0.01
0
0
1
Effect on ALP activity with Inhibition
2
3
1/[S] (mM-¹)
Uninhibited
4
Inhibited
y = 0.005x + 0.0337
R² = 0.95
y = 0.0044x + 0.0253
R² = 0.885
5
6
7](/v2/_next/image?url=https%3A%2F%2Fcontent.bartleby.com%2Fqna-images%2Fquestion%2F11f0539d-c0c0-441d-9095-f5e5bd2f566a%2Fe329a484-cabb-4b90-addd-6e948a139129%2Fshxivbm_processed.png&w=3840&q=75)
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- PTP1B Substrate kcat Km kcat/Km UM 10-7 x (s-1 M) DADEPYLIPQQG DADAPYLIPQQG DAAEPYLIPQQG AAAAPYLIPQQG 44.6 + 1.8 39.8 + 0.32 3.9 + 0.9 13.7 + 0.46 1.1 + 0.25 0.29 + 0.01 35.3 + 0.22 6.6 ± 0.22 0.53 + 0.02 34.7 + 0.25 52.7 ± 0.7 0.066 + 0.001 (d) (. ) The units for kcat/KM in the above are given according to standard scientific notation. On this basis what is the value of this kinetic parameter for the DADEPYLIPQQG substrate?Below is a figure showing possible trajectories to maximum resistance to cefotaxime. Numbers indicate cefotaxime resistance in micrograms per ml. What is the most likely pathway to max resistance? a. G238S→ g4205a →A42G→M182T→E104K b. G238S→ A42G →E406F→M182T→g4205a c. E104K→A42G→G238S→M182T→g4205a d. G238S→E104K→A42G→M182T→g4205aHow was thermal stability measured in this paper and describe how GRL-1720 and 5h affect the thermal stability of Mpro and which drug has the larger effect? https://www.nature.com/articles/s41467-021-20900-6
- what are the effects of PSTMB shown and why is it important to show effects of PSTMB in vitro effects of PSTMB on LDHA? https://www.nature.com/articles/s41598-019-40617-3PTP1B Substrate kcat Km. kcat/Km UM 10-7 x (s-1 M) DADEPYLIPQQG DADAPYLIPQQG DAAEP YLIPQQG AAAAPYLIPQQG 44.6 + 1.8 39.8 + 0.32 3.9 + 0.9 13.7 + 0.46 1.1 + 0.25 0.29 + 0.01 35.3 + 0.22 6.6 + 0.22 0.53 + 0.02 34.7 + 0.25 52.7 + 0.7 0.066 + 0.001 ) The units for kcat/KM in the above are given according to standard scientific notation. On this (d) ( basis what is the value of this kinetic parameter for the DADEPYLIPQQG substrate?Using the information given, determine the Kd for the binding of HABA to BSA. B= y-intercept (E bound) 2457.6x (E unbound) Data for the binding of HABA to BSA y = 4E-06x + 5.2134 R² = 0.928
- The absolute bioavailability of clonazepam is about 90%. This sentence tells us that the value of ____ for clonazepam is 0.9. (A) F (B) FF (C) FG (D) FHWhy does the apparent KM decrease in the presence ofan uncompetitive inhibitor?Which arrestin is required for activation of phosphorylation of MDM2 during chronic Iso stimulation? use the following Figures 1and 2 respectively to explain please
- Ibuprofen and indomethacin are clinically important inhibitors of prostaglandin H₂ synthase-1. Cells expressing this enzyme were incubated under four different conditions, after which the activity of the enzyme was measured by adding radiolabeled arachidonic acid and detecting newly-produced prostaglandin H₂: 1. 40 min without inhibitor (control) 2. 40 min with inhibitor 3. 40 min with inhibitor, after which the cells were resuspended in medium without inhibitor 4. 40 min with inhibitor, after which the cells were resuspended in medium without inhibitor and incubated for an additional 30 min The bar graphs show the results of the experiments with ibuprofen and indomethacin. The bars in each graph correspond to the four different incubation conditions. Ibuprofen Prostaglandin H₂ synthesized (relative to control) 100 80 60 40 20 I I I (1) (2) ll (3) (4) Prostaglandin H₂ synthesized (relative to control) 100k 80 60 40 20 I (1) Indomethacin (2) (3) (4)The proline isomerase activity of FK506 is central to its mechanism of action as an inhibitor of the immune system response. * True * FalseAn experiment was carried out to measure the reaction rate of hydrolysis of acetylcholme (substrate) with serum enzymes (Eadie, 1949). In the experiment, two experiments were conducted, namely experiment 1 without using a prostigmine inhibitor and experiment 2 using a prostigmine inhibitor at 1.5 x 10^-7 mol/l. the data obtained are: a. Is prostigmine competitive or noncompetitive inhibitor? b. determine the value of km and rmax for the two experiments, compare