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A certain group of Brec-MUT cells expresses low levels of protein A, unlike the high expression levels of most Brec-MUT cells. Researchers determine that the cells have an excess of ATP and that there are no mutations in the gene encoding protein A. Describe a change in the Brec signaling pathway that would lead to the decreased expression of protein A even in the presence of Brec-MUT. Explain why B is able to bind to Brec but not to A.

A certain group of Brec-MUT cells expresses low levels of protein A, unlike the high expression levels of most Brec-MUT cells. Researchers determine that the cells have an excess of ATP and that there are no mutations in the gene encoding protein A. Describe a change in the Brec signaling pathway that would lead to the decreased expression of protein A even in the presence of Brec-MUT. Explain why B is able to bind to Brec but not to A.

Human Anatomy & Physiology (11th Edition)
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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A certain group of Brec-MUT cells expresses low levels of protein A, unlike the high expression levels of most Brec-MUT cells. Researchers determine that the cells have an excess of ATP and that there are no mutations in the gene encoding protein A. Describe a change in the Brec signaling pathway that would lead to the decreased expression of protein A even in the presence of Brec-MUT. Explain why B is able to bind to Brec but not to A.

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 Phosphate group Figure 1. A simplified model of the normal signaling pathway hypothesized to play a role in certain cancer cells expressing A and stimulating blood vessel growth into solid tumors
Transcribed Image Text: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 Phosphate group Figure 1. A simplified model of the normal signaling pathway hypothesized to play a role in certain cancer cells expressing A and stimulating blood vessel growth into solid tumors
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