Propose specific types of mutations in the gene forthe regulatory subunit of cyclic-AMP-dependent proteinkinase (PKA) that could lead to either a permanently activePKA or a permanently inactive PKA.
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Propose specific types of mutations in the gene for
the regulatory subunit of cyclic-AMP-dependent protein
kinase (PKA) that could lead to either a permanently active
PKA or a permanently inactive PKA.
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- Determine the specific types of mutations in the gene for the regulatory subunit of cyclic-AMP-dependent protein kinase (PKA) that could lead to either a permanently active PKA or a permanently inactive PKA.Describe the intracellular, biochemical downstream signal cascade that results from the binding of menthol to TRPM8Explain how the pKa for histidine 57 is important to its role in the mechanism of chymotrypsin action
- What would be the metabolic consequences and symptoms of having a mutated form of phosphofructokinase-1 in muscle that is no longer allosterically regulated by [H+]? Speculate on how a patient with this mutation could deal with this.In studies trying to understand the regulation of hormone-sensitive adenylatecyclase, it was discovered that non-hydrolyzable GTP analogs and cholera toxin (that inhibits theGTPase activity of Gs ) were able to activate the enzyme in a sustained (irreversible) profile, thereforeindicating that GTP hydrolysis represents a deactivation (turn-off) regulatory step.a) Will these analogs or toxin have any effect on adenylate cyclase activity in the absenceof any added hormone?b) If you add an factor that increases the rate of GTPase hydrolysis of the Gs protein, willthis activate or inhibit the observed downstream effect upon addition of the hormone (this is in theabsence of GTP analogs or toxin). Explain your answer.What would be the effect of adequate concentration of AMP andGMP?
- Describe two roles for polyubiquitinylation in the NF-κB signaling pathwayNeuraminidase (NA) catalyzes a hydrolysis of the glycosidic linkages of sialic acids using a mechanism shown in Fig. (a). and Fig. (b) shows competitive inhibitors of NA Considering the mechanism of NA, why do zanamivir and oseltamivir inhibit NA so potently?neurokinin-1 receptor antagonists known to inhibit the CYP3A4 enzyme. There is a potential drug drug interaction between lopinavir/ritonavir combination and aprepitant. Explain the potential pharmacokinetic consequences of the interaction on PK parameters of lopinavir and ritonavir following oral administration. AUC, apparent volume of distribution, clearance.
- TPCK and TLCK are irreversible inhibitors of serine proteases. One ofthese inhibits trypsin and the other chymotrypsin. Which is which? Explainyour reasoning. Suggest the effects of each of the following mutations on the physiologicalrole of chymotrypsinogen:(a) R15S(b) C1S(c) T147SExplain how can cAMP’s activation of a single molecule, cAMPdependent protein kinase, be common to the great variety of biochemical sequences and cell responses initiated by cAMP-generating first messengers?Functional and structural analysis indicates that Gleevec is an ATPcompetitive inhibitor of the Bcr-Abl kinase. In fact, many kinase inhibitors under investigation or currently marketed as drugs are ATP competitive. Can you suggest a potential drawback of drugs that utilize this particular mechanism of action?