Biochemistry
6th Edition
ISBN: 9781305577206
Author: Reginald H. Garrett, Charles M. Grisham
Publisher: Cengage Learning
expand_more
expand_more
format_list_bulleted
Concept explainers
Question
Chapter 27, Problem 16P
Interpretation Introduction
Interpretation:
The reason for the T172D mutation of the AMPK to be locked in a permanently active state should be explained.
Concept introduction:
T172D shows that the mutation happens at position 172 in AMPK substitution from an essential amino acid to an aspartic resulting in charged aminoalkanoic acid (aspartic acid) in place of a polar neutral among acid (threonine).
Expert Solution & Answer
Trending nowThis is a popular solution!
Students have asked these similar questions
Which arrestin is required for activation of phosphorylation of MDM2 during chronic Iso stimulation?
use the following Figures 1and 2 respectively to explain please
The EC50 of an agonist for a GPCR is almost always (greater than, equal to, or less than) the KD of the same agonist at the same GPCR. Why?
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.
Knowledge Booster
Learn more about
Need a deep-dive on the concept behind this application? Look no further. Learn more about this topic, biochemistry and related others by exploring similar questions and additional content below.Similar questions
- If intracellular [ATP] = 5 mM, [ADP] = 0.5 mM, and [Pi] = 1.0 mM, calculate the concentration of AMP at pH 7 and 25°C under the condition that the adenylate kinase reaction is at equilibrium.arrow_forwardTrue or false 1. Cytochrome p450 is considered to be the “universal oxygenase” 2. In alzheimer’s and Parkinson’s diseases, there is hyperphosphorylation of tau that leads to the intracellular accumulation of tau in the form of neurofibrillary tangles.arrow_forwardA strain of mice has been developed that lack the enzyme phosphorylase kinase. Yet, after strenuous exercise, the glycogen stores of a mouse of this strain are depleted. Explain how this depletion is possible.arrow_forward
- The NMDA receptor I/V curve is nonlinear, why? What about the GluA2-containing AMPA receptor I/V curve? Draw both under normal physiological conditions. In addition, explain what happens for the NMDA receptor I/V curve when you lower the magnesium concentration.arrow_forwardThe mitochondrial form of carbamoyl phosphate synthetase is allosterically activated by N-acetylglutamate. Briefly describe a rationale for this effect.arrow_forwardPropose 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.arrow_forward
- The serine residues in acetyl CoA carboxylase that are the target of the AMP-activated protein kinase are mutated to alanine. What is a likely consequence of this mutation?arrow_forwardFunctional 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?arrow_forwardHydroxyurea has been shown to increase the expression of fetal hemoglobin in adult red blood cells, by a mechanism that remains unclear. Explain why hydroxyurea can be a useful therapy for patients with sickle-cell anemia.arrow_forward
- The interconversion of DHAP and GAP greatly favors the formation of DHAP at equilibrium. Yet the conversion of DHAP by triose phosphate isomerase proceeds readily. Whyarrow_forwardExplain the indirect effect that allosteric effectors have on pyruvate dehydrogenase activity through phosphorylation/dephosphorylation of components within the PDH-complex.arrow_forwardWhat 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.arrow_forward
arrow_back_ios
SEE MORE QUESTIONS
arrow_forward_ios
Recommended textbooks for you
- BiochemistryBiochemistryISBN:9781305577206Author:Reginald H. Garrett, Charles M. GrishamPublisher:Cengage Learning
Biochemistry
Biochemistry
ISBN:9781305577206
Author:Reginald H. Garrett, Charles M. Grisham
Publisher:Cengage Learning