Edexcel A2 Biology Unit 5 (6BIO5) - 22/06/2011- OFFICIAL THREAD !

Im confused again. It says on the first page of article on the 5th paragraph line 5 that 'epo receptor should shut down epo production.' istnt it the kidneys that produce epo and arent epo receptors on the bone marrow?? soo confusedd

Can someone help me answer these questions?

1)Why might AAVs be less vulnerable to attack from the immune system?
2) Why is the fact that IGF-1 doesn't alter blood sugar an important consideration for tennis players?
3)How might muscle wastage be controlled by a complex genetic pathway?
4) How may proteasome be compared to lysosomes?
5) Why might myostatin keep the satellite cells in check and stop the developing into new muscle cells?

Thank youuuuuu to whoever helps me out with this

epo receptors aren't in the bone marrow. Bone marrow produces red blood cells.

I know 1.) Because they are smaller (AAV's are smaller than adenoviruses)

Also, do you know what topic viruses being used as vectors was it, and what do we need to know for it (details)

Can someone help me answer these questions?

1)Why might AAVs be less vulnerable to attack from the immune system?
2) Why is the fact that IGF-1 doesn't alter blood sugar an important consideration for tennis players?
3)How might muscle wastage be controlled by a complex genetic pathway?
4) How may proteasome be compared to lysosomes?
5) Why might myostatin keep the satellite cells in check and stop the developing into new muscle cells?

Thank youuuuuu to whoever helps me out with this

ok, thanks rof reply.so how does epo stimulate production of rbc?

Hi, I just double checked in the mark scheme for june 2010, and you are both wrong! Actually, it is the idea that the potassium ions re-enter the axon through the membrane which is still permeable to them. this removes the + from the outside- restores the equilibrium between the diffusion gradient and the potential difference.

I'll answer them as best as I can, as I'm not sure we'll be expected to know some of them:

1) It says in the text that AAVs are smaller than adenoviruses, being small decreases the likelihood that a macrophage or other non-specific immune cells will recognise the antigen as being non-self. (just because of size)

I'll answer them as best as I can, as I'm not sure we'll be expected to know some of them:

1) It says in the text that AAVs are smaller than adenoviruses, being small decreases the likelihood that a macrophage or other non-specific immune cells will recognise the antigen as being non-self. (just because of size)

2) I guess it would be important in the sense that the fact it doesn't alter blood sugar levels is that you can continue to play with enhanced performance without the fear of suffering symptoms of a diabetic etc.

3) The pathway is the ubiquitin-ligase pathway,
ubiquitin tags are placed onto muscle cells, labelling them for destruction the complex formed binds to the proteosome and the protein starts to be hydrolyzed into its component amino acids, ubiquitin is released.

4) They can be compared similarly as they both involved with programmed destruction, the differences however is that a lysosome releases digestive enzyme that is involved with apoptosis of a cell, whereas a proteosome is only involved with the destruction of proteins, so it's on a smaller scale

5) Perhaps myostatin is a repressor molecule, in its presence the gene that codes for new satellite cells cannot be expressed, therefore when it is blocked this allows the synthesis of the satellite cells and results in more muscles.

But then all viruses must have a less chance of being detected than bacteria by that reasoning. Surely how detectable they are varies from virus to virus and bacteria to bacteria?

You are actually amazing! Thank you so much

**************************************
How are viruses used to insert genes into cells ?
**************************************

Are there any specific things (like enzymes) we need to know about