Chronic Myelogenous Leukemia (CML) is a type of cancer that is caused by a specific chromosomal alteration that leads to the inappropriate expression of a kinase called Abl. Kinases are enzymes that put phosphate groups onto macromolecules such as proteins. A drug used to treat CML, imatinib, binds to the active site of Abl kinase. Why does this drug work to treat this type of cancer?

A) By binding to the active site, the drug decreases the activation energy for the reaction driven by Abl kinase.

B) By binding to the active site, the drug prevents the ability of Abl kinase to bind to its substrate.

C) By binding to the active site, the drug allows for a better induced fit between Abl kinase and its substrate.

D) By binding to the active site, the drug increases the amount of free energy released from the reaction driven by Abl kinase.

Question

Gustavo Estes

Biology

Today, 02:28

Chronic Myelogenous Leukemia (CML) is a type of cancer that is caused by a specific chromosomal alteration that leads to the inappropriate expression of a kinase called Abl. Kinases are enzymes that put phosphate groups onto macromolecules such as proteins. A drug used to treat CML, imatinib, binds to the active site of Abl kinase. Why does this drug work to treat this type of cancer?

A) By binding to the active site, the drug decreases the activation energy for the reaction driven by Abl kinase.

B) By binding to the active site, the drug prevents the ability of Abl kinase to bind to its substrate.

C) By binding to the active site, the drug allows for a better induced fit between Abl kinase and its substrate.

D) By binding to the active site, the drug increases the amount of free energy released from the reaction driven by Abl kinase.

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Darion Dalton · Answer 1

A drug used to treat CML, imatinib, binds to the active site of Abl kinase. Why does this drug work to treat this type of cancer?

B) By binding to the active site, the drug prevents the ability of Abl kinase to bind to its substrate.

Imatinib works against CML by binding close to the ATP binding site of bcr-abl. The binding results to the locking in of the bcr-abl to a closed or self-inhibited conformation and inhibiting the enzyme activity of the protein semi-competitively.