Biochemistry
6th Edition
ISBN: 9781305577206
Author: Reginald H. Garrett, Charles M. Grisham
Publisher: Cengage Learning
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Chapter 32, Problem 4P
Interpretation Introduction
Interpretation:
The effect of the given action of the antibiotic on the rat kidney cells transformed by the Rous sarcoma virus needs to be explained. The other expected effects should also be discussed.
Concept Introduction :
An antimicrobial element that is active against the bacteria is known as an antibiotic. It effectively fights against the bacterial infections.
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Intaractions of FAK kinase which directly depend on the tyrosine residue 397 (Y397) are inhibbited by a chemical compound in cancercells.
Intaraction of FAK kinase with what proteins are blocked by this inhibition? (please give a listt of them all, and that's it)
From experiments in which cells expressing normal myosin II heavy chain were altered to either lack (mhckA-) or overexpress (MHCKA ++) a myosin heavy chain kinase (MHCKA). For answering this question recall the earlier the variants on the myosin II heavy chain, in which three key threonines, normally subject to reversible phosphorylation, were altered in various ways:
3X Ser = Serines in place of Threonines
3X Ala = Alanines in place of Threonines
3X Asp = Aspartate in place of Threonines
MHCKA is present at normal levels.
Which of the two mutants (mhcp- or MHCP++) would be most likely to have a defect in cytokinesis?
Pay close attention to the information related to figure 3.14a and the structure of the PKA catalytic site in this figure.
In a few well-written sentences, propose the following:
A mutation that would result in PKA becoming a dead kinase*.
A mutation that would result in PKA becoming a constitutively active** kinase.
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- Helparrow_forwardSuppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: a. Which of the ligands, based on the table, has the highest specificity in binding to the target Protein J?arrow_forwardSuppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: Describe the relative binding affinities of Ligand A to Protein K and to the active and inactive forms of Protein J. Determine which will Ligand A bind with the highest, medium, and lowest affinity.arrow_forward
- Suppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: a. Which of the ligands, based on the table, may be expected to be the most potent or have the highest activity against cancer? Explain. b. Which of the ligands, based on the table, may be expected to be least toxic to normal cells? Explain.arrow_forwardSame question but two different sectionsarrow_forwardThe properties of two types of organization of kinases (held in a signaling complex by a scaffolding protein and the other kinases are freely diffusible) in terms of signal amplification, speed, and potential for cross-talk between signaling pathways.arrow_forward
- 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?arrow_forwardSame question but two different sectionsarrow_forwardPathway analysis: Link the protein names to the correct statements by interrogating the depicted pathway. Options: A. RTK Receptor Threonine Kinase B. GEF Guanidine Exchange Factor C. PLC Phospholipase C D. GAP GTPase Activating Protein E. Gαi F. Raf Rapidly Accelerated Fibrosarcoma G. PAK1 p21 Activated Kinase H. WASP Wiscott Aldrich syndrome protein I. RTK Receptor Tyrosine Kinase J. GPCR G-protein Coupled Receptor K. Steroid Receptor L. Phosphatase M. MEK1 (Mitogen-Activated Protein) Kinase/ERK (Extracellular Signal-Regulated Kinase) Kinase 1 N. AC Adenylyl cyclase O. IP3R IP3 Receptor P. ERK1/2 Extracellular Signal-Regulated Kinasearrow_forward
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