Solid tumors are clusters of cancer cells and often contain blood vessels. When molecule B binds to the wild-type Brec protein in the plasma membrane of certain solid tumor cancer cells (Figure 1), the cancer cells express the membrane protein A and sometimes stimulate increased growth of blood vessels into the tumors.
Cells with a particular mutation in the Brec gene (Brec-MUT cells) have much increased expression levels of A and stimulate greater growth of blood vessels than do cancer cells with the wild-type Brec (Brec-WT cells); the cells with the mutant Brec can trigger intracellular signaling in the absence of B.
Researchers proposed that the signaling pathway modeled in Figure 1 is triggered by activation of the wild-type Brec and is associated with phosphorylation and activation of kinase D, expression of A, and the ability of the cancer cells to stimulate blood vessel growth.
Part A: Based on the signaling model shown in Figure 1, describe the role of molecule C-P in the activation of D.
Part B: Explain how a molecule such as kinase D can amplify an extracellular signal. Explain how the mutant Brec protein is able to activate kinase D even in the absence of its ligand.
Part C: Based on the proposed signaling pathway, predict the relative activity of kinase D in the Brec-WT cells compared with kinase D in the Brec-MUT cells when both cell types are grown in nutrient broth lacking B. Justify your prediction.
Part D: The researchers claim that treatment with a compound that inhibits dephosphorylation of the intracellular domain of the Brec protein will inhibit expression of A in Brec-WT cells but not in Brec-MUT cells. Based on the information provided, provide reasoning to refute their claim.
