Becker's World of the Cell (9th Edition)
9th Edition
ISBN: 9780321934925
Author: Jeff Hardin, Gregory Paul Bertoni
Publisher: PEARSON
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Textbook Question
Chapter 24, Problem 24.4CC
Both EGF (a mitogen) and TGFβ (when acting as an inhibitor) affect Cdk-cyclin complex function. Compare and contrast the ways in which EGF and TGFβ operate. What would happen if a cell were exposed to both at the same time?
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EGF
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100 nM ChB
P-Ak47
total Akt
GAPDH
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0
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0
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0
0 1h 24h
1h 24h
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Why do you think the researchers included GAPDH in the
figure?
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B.
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D.
Control for…
Describe the roles of p53 and NFAT and their nuclear import. How does the phosphorylation regulate the nuclear import/export of Pho4? Propose an experiment to test this mechanism
Chapter 24 Solutions
Becker's World of the Cell (9th Edition)
Ch. 24 - Prob. 1QCh. 24 - Which DNA sequences are more alike: a pair of...Ch. 24 - Suppose you treat rapidly dividing tissue culture...Ch. 24 - Cyclin D is part of the G1 Cdk-cyclin complex....Ch. 24 - Both EGF (a mitogen) and TGF (when acting as an...Ch. 24 - A knockout mouse has been produced using the...Ch. 24 - Cell Cycle Phases. Indicate whether each of the...Ch. 24 - QUANTITATIVE The Mitotic Index and the Cell Cycle....Ch. 24 - Chromosome Movement in Mitosis. It is possible to...Ch. 24 - Cytokinesis. Predict what will happen in each of...
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- Briefly describe how the cyclin D-cdk4/6 and cyclin E-cdk2 complexes regulate Retinoblastoma protein (pRb) functions?arrow_forwardThe progressive loss of cardiac myocytes due to cell death has been associated with cardiac dysfunction and heart failure. Which of the following would lead to a significant loss of cardiac myocytes? Select all that apply Treatment of rapamycin which results in inhibition of mTOR activity Prolonged or severe ER stress with increased accumulation of unfolded proteins Activation of AMPK and phosphorylation of the TSC1 complex mTOR activation and phosphorylation of Ulk1arrow_forwardThe destruction of the various cyclins is commonly used to inactivate the Cdk/cyclin complexes. Why is it advantageous to inactivate these complexes via protein destruction instead of some other method that does not require the re-synthesis of a cyclin protein the next time the cell divides?arrow_forward
- After a cell "clears" the G₁ restriction checkpoint, it can proceed into S phase. This S phase entry is achieved by a cyclin dependent kinase (Cdk2) and its cyclin (Cyclin E), but additionally requires the action of a protein kinase (CDC2) as well as a phosphatase (CDC25) enzyme. Explain how these 4 proteins work together to orchestrate S phase entry.arrow_forwardI just read an abstract of the paper “Disulfide bond-disrupting agents activate the tumor necrosis family-related apoptosis-inducing ligand/death receptor 5 pathway” and noted that “DDAs and TRAIL synergize to kill cancer cells and are cytotoxic to HER2+ cancer cells with acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib.” For the last sentence, I am not sure the meaning of the “acquired resistance to the EGFR/HER2 tyrosine kinase inhibitor Lapatinib”. Is the “acquired resistance ... to inhibitor” a good thing or bad thing, as far as the synergize effect of DDAs and TRAIL”? Hope that expert can help.arrow_forwardRTKs are receptors made of an extracellular ligand binding domain and an intracellular kinase domain (see image). Insulin binds to its RTK Insulin receptor, causing an increase in glucose absorption and storage in liver cells. EGF binds to its own RTK, EGFR and promotes cell growth through the Ras pathway. a) Explain why the same type of tyrosine kinase in two RTKs can lead to very different cellular responses. Give an example of potential cellular outputs for each of these two RTKs.arrow_forward
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