Table of contents

1. Introduction to Biochemistry4h 34m
2. Water3h 23m
3. Amino Acids8h 10m
4. Protein Structure10h 4m
5. Protein Techniques14h 5m
6. Enzymes and Enzyme Kinetics13h 38m
7. Enzyme Inhibition and Regulation 8h 42m
8. Protein Function 9h 41m
9. Carbohydrates7h 49m
10. Lipids5h 49m
11. Biological Membranes and Transport 6h 37m
12. Biosignaling9h 45m
Review 1: Nucleic Acids, Lipids, & Membranes2h 47m
Review 2: Biosignaling, Glycolysis, Gluconeogenesis, & PP-Pathway3h 12m
Review 3: Pyruvate & Fatty Acid Oxidation, Citric Acid Cycle, & Glycogen Metabolism2h 26m
Review 4: Amino Acid Oxidation, Oxidative Phosphorylation, & Photophosphorylation1h 48m

12. Biosignaling

Recap of Insulin Signaling As A Growth Factor

Biochemistry

12. Biosignaling

Recap of Insulin Signaling As A Growth Factor

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Multiple Choice

In a tumor cell line, Raf-1 is mutated such that it is constitutively activated by Ras even in the absence of insulin signaling. How can you inhibit the growth of this tumor cell line?

Blocking insulin receptor autophosphorylation.

Inhibiting the kinase activity of ERK.

Preventing the production of cAMP.

Blocking the recruitment of PI3K to the plasma membrane by IRS-1.

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Verified step by step guidance

Understand the signaling pathway: In normal cells, the Ras-Raf-MEK-ERK pathway is activated by growth factors like insulin. Ras activates Raf-1, which then activates MEK, leading to the activation of ERK, a kinase that promotes cell growth and division.

Identify the mutation effect: In the tumor cell line, Raf-1 is constitutively activated by Ras, meaning it is always active regardless of insulin signaling. This leads to continuous activation of the downstream pathway, promoting uncontrolled cell growth.

Consider the role of ERK: Since ERK is the final kinase in this pathway and is responsible for promoting cell growth, inhibiting its activity can potentially stop the growth of the tumor cells.

Evaluate the options: Blocking insulin receptor autophosphorylation or preventing cAMP production would not affect the constitutively active Raf-1. Blocking PI3K recruitment affects a different pathway (PI3K-Akt), not the Ras-Raf-MEK-ERK pathway.

Conclude with the best approach: Inhibiting the kinase activity of ERK directly targets the downstream effects of the constitutively active Raf-1, making it the most effective strategy to inhibit tumor cell growth in this scenario.