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.

Human Anatomy & Physiology (11th Edition)
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Author:Elaine N. Marieb, Katja N. Hoehn
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Chapter1: The Human Body: An Orientation
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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.

Question 1
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.
Brec
(Active)
D (Inactive)
C-P
B
℗-D (Active)
Kinase
(Inactive)
Brec (Inactive)
P-Kinase
(Active)
Plasma Membrane
A
Stimulate
growth of
blood vessels
into tumors
P Phosphate group
Transcribed Image Text:Question 1 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. Brec (Active) D (Inactive) C-P B ℗-D (Active) Kinase (Inactive) Brec (Inactive) P-Kinase (Active) Plasma Membrane A Stimulate growth of blood vessels into tumors P Phosphate group
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