BIM-46187 is a protein inhibitor that binds to the a-subunit of the G. protein. It prevents the GDP/GTP exchange and prevents activity of the G protein. Which of the following would you expect to see lower levels of as a result? You can select more than or answer. S-S NH2 Mol. M: 795.11 Image: https://aobious.com/aobious/protein-inhibitors/1086-bim-46187.html Select one or more: O a. Cyclic AMP (CAMP) O b. Tyrosine kinase O . HSP O d. Adenylyl Cyclase (AC) O e. DAG O f. JAK O g. IP3
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- BIM-46187 is a protein inhibitor that binds to the a-subunit of the G, protein. It prevents the GDP/GTP exchange and prevents activity of the G protein. Which of the following would you expect to see lower levels of as a result? You can select more than one answer. S-S Mol. W: 795.11 Image: https://aobious.com/aobious/protein-inhibitors/1086-bim-46187.html Select one or more: O a. Cyclic AMP (CAMP) O b. Tyrosine kinase HSP O d. Adenylyl Cyclase (AC) O e. DAG O f. JAK O g. IP3Cholera is an acute, diarrheal disease caused by infection of the intestine with the gram-negative, motile bacterium Vibrio cholerae. After colonizing the small intestine, V. cholerae secretes cholera toxin (CTX), a protein that ribosylates the Gsa subunit of a G protein, thereby inhibiting its GTPase activity. This causes the dysregulation of a cellular chloride ion channel, resulting in efflux of ions and water from the infected enterocytes into the intestinal lumen. Studies have implicated sodium bioenergetics in the pathogenesis of V. cholerae in humans. An electrochemical gradient of Na+ known as the "sodium motive force" provides V. cholerae with the energy for key functions. The gradient is predominantly established by the Nat-pumping NADH:quinone oxidoreductase (Na-NQR) enzyme. Na+-NQR is a multi-substrate enzyme comprised of six distinct subunits designated A-F (Table 1) that are encoded within the same operon. In a process similar to proton pumping by Complex I of the…The Table below shows the names of proteins whose functions are regulated through the binding of their ligands. Complete this Table by filling in the correct ligands for each of the proteins, the corresponding K, value, the affinity of this protein for its ligand and the source where the protein is found. Example Protein Avidin 1 Insulin receptor 2 Anti-HIV immunoglobulin 3 Nickel binding protein 4 Myoglobin 5 Myosin 6 Acetyl-CoA carboxylase 7 Cannabinoid receptor 1 (CB1) 8 Guanylyl cyclase Ligand Biotin Kd (M) 1 x 10-15 Affinity high Source/Organism Egg white
- In Alzheimer’s disease, nerve cell death is associated with the accumulation of aggregates of misfolded protein. Compare this process with the onset of diabetes mellitus.Some strains of bacteria or microorganisms have developed toxins that can modify the activity of the alpha subunit of G proteins which results in disease. For ex. cholera toxin, produced by Vibrio cholerae, causes ADP ribosylation of the stimulatory Gαs subunit of G proteins. This modification abolishes the GTPase of Gαs, and results in an αs subunit that is always in the “on” or active state. It results in continuous stimulation of adenylyl cyclase (AC). The main cells affected by this are the epithelial cell in gastrointestinal tract. Knowing this altered activity of AC, explain why patients affected by this toxin experience severe diarrhea and dehydration that may result in death.Give the normal value of CRP (C-Reactive Protein). Why is CRP significant? Is CRP specific to one disease?
- Diisopropylphosphofluoridate (DIPF) inactivates chymotrypsin by covalently modifying serine 195. Which statement is true of DIPF's inhibitory mechanism? DIPF randomly modifies all serine residues on the protein, and if enough is added, the serine in the active site will eventually be modified. DIPF approaches serine 195 more closely than other substrates. DIPF looks like the substrate for chymotrypsin and binds in the active site as a competitive inhibitor. Serine 195 is in an environment that gives it a higher than normal reactivity with respect to DIPF.One form of anemia results when individuals have a deficiency in the enzyme phosphatidylinositol glycan A (PIGA). This enzyme is required for the membrane attachment of proteins anchored by glycolipids to the plasma membrane, using what is called a ‘GPI-linkage.’ Included in the group of GPI-linked cell surface proteins is DAF/CD55. These individuals become anemic because: DAF/CD55 prevents the lysis of red blood cells by infecting pathogens. DAF/CD55 normally prevents the spleen from clearing healthy red blood cells from the circulation. In the absence of PIGA, the red blood cell membrane is bare of proteins allowing increased access of complement activating proteins to attach to the cell membrane. DAF/CD55 is a complement inhibitory protein that inactivates any C3 convertase that may form on host cell surfaces. In the absence of PIGA, red blood cells are unable to synthesize high levels of hemoglobin.One of the causes of morbidity for the Zika Virus is Guillain-Barré Syndrome, an immune attack of nerve cells. One possible mechanism for this is the virus's interference with normal immune function. In HIV the virus uses the CD4 receptor to enter T-cells. To assess if this might be a possibility in Zika infections BLAST the CD4 Reference Sequence (NG 027688.1) against the Zika Virus (taxid:64320) choosing "blastn" under Program Selection (select all that apply): O None of the recovered sequences have identities of greater than 80%. O Multiple Zika virus isolates are observed to have E-values of less than 0.02. O High scoring BLAST hits are observed in Zika virus isolates from humans, mosquitoes, and monkeys. O The BLAST hits return a partial cds collected in Uganda in 1947 - isolate Uganda1947.
- Place the following events in the proper order to describe the production of a second messenger from a G-protein. 1. Dissociation of G alpha from the beta and gamma subunits in the G protein complex 2. Ligand interaction with the G protein-coupled receptor (GPCR) 3. Recruitment of a G protein to the GPCR and replacement of GDP with GTP on the G alpha subunit 4. Conformational change in the G alpha a subunit causing a decreased affinity for the beta and gamma subunits 5. Activation of an effector, such as adenylyl cyclase to make CAMP, by the active G alpha subunit OA. 4, 5, 1, 2, 3 OB. 4, 3, 2, 1, 5 OC-3, 2, 1, 5, 4 OD. 1, 2, 3, 4, 5 OE. 2, 3, 4, 1,5 QUESTION 17 Kinases are essential in the cell because they directly OA. destroy IP3, turning off that signaling pathway. OB. phosphorylate proteins to cause conformational changes that change their activity. OC. directly activate translation. O D bind hydrophobic hormones in the cytoplasm to activate them. O E. bind and release calcium…Describe the general function and structural features of G-protein-coupled receptors (GPCRs). Be sure to include an explanation of GTPase activating proteins (GAPs) and GDP exchange factors (GEFs) in the context of the GTPase cycle. How are different classes of heterotrimeric G-proteins defined?The ABO blood group antigens are the terminal sugars covalently linked to the end of the glycolipid in the red blood cellmembrane. The H antigen is the precursor of the A and Bantigens. Individuals with type A blood produce a gene thatcodes for an enzyme that adds N-acetylgalactosamine in ana(1,3) linkage to the Gal* residue in the H antigen. Type Bblood requires that an enzyme add a d-a galactose in an a(1,3) linkage to the Gal*. Draw the structures of the A andB antigens.