Explanation Imatinib is an inhibitor of some tyrosine kinase enzymes. It functions by occupying the TK active site, and act as a competitive inhibitor. Imatinib specifically blocks the TK domain in abl (the Abelson proto-oncogene), c-kit and PDGF-R (platelet-derived growth factor receptor). In the condition of chronic myelogenous leukemia, the chromosome Philadelphia leads to the attachment of the protein of abl with bcr (breakpoint cluster region), which is also termed as bcr-abl. This is how the imatinib is used to decrease bcr-abl activity. The active sites of the TK have binding sites for the molecule ATP. The enzymatic activity of tyrosine kinase is the transfer of the terminal phosphate from ATP molecule to the tyrosine residues on the substrates. This process is known as the protein tyrosine phosphorylation...

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.

Biochemistry

6th Edition

ISBN: 9781305577206

Author: Reginald H. Garrett, Charles M. Grisham

Publisher: Cengage Learning

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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.

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Chapter 32, Problem 21P

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Solution Summary: The author explains how Gleevec functions as a therapy for chronic myelogenous patients by using the Active Model for c-Abl kinase.

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