BIOL 355 Study Guide - Midterm Guide: Glycosaminoglycan, Mmp2, Proteoglycan

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ochreporcupine180

21 Apr 2017

School

Department

Biology

Course

BIOL 355

Professor

Linda Martin- Morris

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Document Summary

If tumor cells want to divide in order for the tumor to grow, it needs space to enlarge into; the ecm gets in the way. They are made inside the cell, secreted and used to modify the extracellular matrix. Mmp2 is not found in general purpose cells. It would be beneficial for a tumor cell to be able to modify its ecm to make room for growth and migration. If mmp2 is eliminated from cells tumor paint still binds. Mmps can have their production turned up based on growth factors, the need for cells to migrate and grow. Helps activate mmps (perhaps annexin is turned up in cells that want to manufacture more. Mmps- when they need to grow tumors or move cells: dapi: stains nucleus (blue) Isolectin: a protein that is found on blood vessel walls on epithelial cells: blood vessels will not be as present (upregulated) in annexin a2 loss of function genotypes.

Related Questions

1.In 1971, Dr. Judah Folkman published the âangiogenic hypothesisâ suggesting that a tumor cannot grow beyond 1â2 millimeters without the development of new blood vessels (angiogenesis) that provide access to oxygen and nutrients. During the 1990s, it was discovered that vascular endothelial growth factor (VEGF) stimulates migration and proliferation of the cells that form blood vessels, leading to the formation of new blood vessels. VEGF binds to receptor tyrosine kinases (RTKs) on the cell surface and causes the RTKs to dimerize and become active, thereby initiating an intracellular signaling cascade that stimulates cell division and inhibits apoptosis. Many cancer cells secrete high levels of VEGF and increased VEGF expression in a tumor is correlated with a poor medical outcome for the patient. You work for a biotechnology company that seeks to create anti-cancer drugs that prevent growth of tumors and/or cause tumors to shrink, while leaving normal cells relatively untouched. Your company has purchased the rights to therapeutic uses of VEGF derived proteins as anti-tumor drugs. You have found that the VEGF protein has 2 domains, one involved in receptor binding, the other is required for dimerization of VEGF. You propose to make mutant versions of the protein that will act as antagonists of the receptor to be given to patients as an IV treatment as a way to inhibit the endogenous VEGF secreted by the tumor.

a.Which of the 2 domains should you mutate (receptor binding or dimerization)?

b. How do you expect the introduction of the mutant protein into the bloodstream of patients to block tumor progression (in other words, why did you change the domain in part a)?

peachmoose600

1. Inflammation is generally a protective response, which would normally be beneficial. Is it an exclusively beneficial response? Explain 2 pts

2. You are a physician and your patient has had a heart attack resulting in decreased blood flow to the heart tissue. Once blood flow is reestablished, what might be a major concern? 2pts

3. One of the first steps in inflammation is the development of increased adhesiveness of neutrophils to the endothelium cells of venules. How does this occur? Give details 3 pts

4. What approach might stop the P- and E-selectin-mediated step in inflammation, thus blocking the process? 2pts

5. What sequence of events is triggered by the initial adhesion of neutrophils? 2pts

6. For no known reason, a person is found to make autoimmune antibodies against the ?2 subunit of leukocyte integrins. What symptoms, if any, is s/he likely to exhibit? (2pts each)

How might leukocyte adhesion deficiency be treated?

How might antibodies against the ?2 subunit of integrins prove useful medically?

7. Cancer cells from a person suffering from malignant melanoma are analyzed and found to have an elevated ability to bind to laminin; they also secrete much higher than normal levels of a certain proteolytic enzyme activity. How would these differences from normal, control cells promote metastasis of these cancer cells? Explain 4 pts

8. Why would cells that express less E-cadherin be more likely to become malignant and give rise to epithelial cell tumors? Explain 3 pts

9. What would happen if you were able to inject the gene for ?5?1 integrin (a fibronectin receptor) into some tumor cells in such a way that it was expressed extremely efficiently? Explain 3pts

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BIOL 355 Study Guide - Midterm Guide: Glycosaminoglycan, Mmp2, Proteoglycan

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