Posted: December 17th, 2016
surfaces of the epithelium. What cytoskeletal elements are associated with each junction? What is the function of each junction? 3) A stem cell divides into two daughter cells. One of the daughter cells goes on to become a terminally differentiated cell. What is the typical fate of the other daughter cell? 4) Your friend is a pioneer in ES cell research. In her research, she uses an ES cell line that originated from an inbred strain of laboratory mice called FG426. She has just figured out methods that allow her to grow an entire liver from an ES cell and has successfully grown 10 livers. She demonstrates that the newly grown livers are functional by successfully transplanting one of the new livers into a FG426 laboratory mouse. You are particularly excited about this, because you have a sick pet mouse, Squeaky. You are very attached to Squeaky, as you found him when you were out camping in New Hampshire. Unfortunately, Squeaky has developed liver disease and will not live much longer without a liver transplant. After you see your friend on TV talking about her new method for growing mouse livers, you immediately grab your cell phone to ask her whether Squeaky could have one of the newly grown livers. Just as you are about to dial your friend, you remember something you learned in cell biology and realize that instead, you should ask your friend about possibly using therapeutic cloning for Squeaky’s benefit. A. Why do you think that one of the newly grown livers may not work in Squeaky? B. Explain why therapeutic cloning would solve this problem. 5) Cancer is a disease of enhanced proliferation and cell survival. DNA repair mechanisms are normally important for cell survival. When a cell senses DNA damage, the cell cycle is inhibited until the damage is fixed. Given the importance of DNA repair mechanisms, how can their failure can lead to the production of cancer cells with a competitive advantage over normal cells? 6) Ras is a GTP-binding protein that is often defective in cancer cells. A signal from a growth factor through a receptor tyrosine kinase often stimulates normal cells to divide. When the receptor tyrosine kinase binds the growth factor, Ras is stimulated to bind GTP. Ras in turn activates proteins that promote cell proliferation. A common mutation in cancerous cells causes Ras to behave as though it were bound to GTP all the time. A. B. Why is this mutation advantageous to cancerous cells? Your friend decides that the signaling pathway involving the Ras protein is a good target for drug design, because the Ras protein is often defective in cancer cells. Your friend designs a drug that will turn off the receptor tyrosine kinase by preventing it from dimerizing. Do you think that this drug will affect cells that have a defective Ras protein that acts as if it were always bound to GTP? Why or why not? 7) What do integrin receptors bind to extracellularly? intracellularly? 8) What are the features of stem cells? 9) What is therapeutic cloning? What is reproductive cloning? What is the difference between them? 10) What are iPS cells and how are they made? 11) Why are malignant tumors more dangerous than benign tumors? 12) What kind of mutations can convert a proto-oncogene into an oncogene? 13) What is a tumor suppressor? What are the differences between a tumor suppressor and an oncogene? Essential Cell Biology, 4th Edition textbook Alberts et al., Garland Science, publisher.
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