Questions on apoptosis and autoimmunity article

To answer some of these questions, you may want to review your notes from earlier in the semester on apoptosis. You may also want to look at the poster of apoptosis that I put on the web site and look at the panel on proteins in the Bcl-2 family.

1.       How does Bcl-2, Bcl-X_L, Bax, Bak, affect apoptosis?

2.       What other factors are involved in the mitochondrial pathway of apoptosis?

3.      Would you expect apoptosis to be increased or decreased in autoimmune diseases?

4.       How does ABT-737 affect apoptosis and autoimmunity?

5.      Name a few autoimmune diseases (which may or may not be discussed in this paper).

6.       If you were going to design an anti-cancer treatment, would you want to increase or decrease Bcl-2?

7.       If you gave ABT-737 to animals with tumors, would this cause their tumors to grow or to shrink?

8.      What is the difference or similarity in the way that ABT-737 affects T and B cell proliferation in human cells as compared to mouse cells (look at figures 1A -C)?  How does ABT-737 affect apoptosis in these cells (figure 1 D)?

9.      What factors does ABT-737 affect in disease progression for RA (rheumatoid arthritis)?  Look at figure 4.

10.  How does ABT-737 affect Lupus (SLE)?  Look at figure 5.

11.  What happens in the Fas-ligand apoptotic pathway (as mentioned in the discussion)?

12.  The discussion mentions that Bcl-2 transgenic mice would cause SLE-like symptoms?   Why do you think this would occur?  Why?

13.  The discussion mentions that Bim knockout mice would cause SLE-like symptoms?   What role does Bim play in apoptosis and why would Bim knockout mice cause SLE-like symptoms?