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 32, Problem 22P
Interpretation Introduction
To propose:
Using the Active Model for c-Abl kinase, explain how Gleevec functions as a therapy for chronic myelogenous patients.
Introduction:
Specific inherited mutations in BRCA1 and BRCA2 most notably increase the risk of female breast and ovarian cancers, but they have also been linked with increased risks of numerous additional kinds of cancer. A harmful BRCA1 or BRCA2 mutation can be inherited from a person's mother or father.
Expert Solution & Answer
Want to see the full answer?
Check out a sample textbook solutionStudents have asked these similar questions
describe the outcome of EGFR inhibition as well as the differences between erlotinib and panitumumab’s mechanisms of action. EGFR- driven cancer cells can become resistant to tyrosine kinase inhibitors. Explain the two types of EGFR blockade acquired resistance and propose a subsequent treatment option.
Which ONE of these statements is the most accurate definition of the mode of action of imatinib?
Select one:
A.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks phosphatase activity by competing with adenosine triphosphate (ATP) binding
B.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks tyrosine kinase activity by competing with adenosine triphosphate (ATP) binding
C.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks tyrosine kinase activity by interaction with the enzyme site
D.It is a specific inhibitor of the BCR‐ABL1 fusion protein and blocks phosphatase activity by interaction with the enzyme site
CTP inhibits ATCase; however, the inhibition is not complete. Can you suggest another molecule that might enhance the inhibition of ATCase?
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
- Need help 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)arrow_forwardThree potential inhibitors for VEGF were discussed in the signal transduction simulation. Explain two possible steps that these drugs can be expected to interfere with VEGF signaling (Hint: think about the requirements for signaling to occur).arrow_forwardBriefly present the mechanism of action of inhibitors of intracellular signaling used for antineoplastic therapy?arrow_forward
- Pathway 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_forwardVenurafenib Select one: a. Was developed as a treatment of Gleevec-resistant CML patients b. Inhibits MEK in some melanoma patients c. Melanoma patients with a V600E mutation became resistant to this treatment o d. Inhibits RASarrow_forwardFrom 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?arrow_forward
- During an SAR effort to identify tyrosine kinase inhibitors, it was found that compound 2 was significantly more potent and selective than compound 1. To what might you attribute this improvement in activity and selectivity? Explain. IC-5 micromolar IC-0.1 mromolararrow_forwardIn expressing therapeutic proteins (check all that apply): O Bacteria could be used if you want the protein's disulfide bonds formed before secretion from the bacterial cell. The N-terminal signal sequence and the C chain of insulin must be cleaved off in the rough ER before it's active. O Proteolytic protein maturation can be performed by mammalian cells. □ One of the required modifications to preproinsulin, before it's mature, is glycosylation. Both preproinsulin and proinsulin are inactive proteins.arrow_forward1J. Please help me in detail. for molecular Mechanism of ATP versus GTP selectivity of adenylate kinasearrow_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