A substitution mutation where an amino acid changes, would impact the protein formed like this:
It would alter the primary structure of the protein, which in turn could affect the tertiary structure as it may alter bonds that form the protein’s specific 3D shape. As a result, a different tertiary structure resulrs, which may not be specific to the function of the protein, inhbiiting it from being able to perform its function.
Would say "alter the formation of bonds" rather than "alter bonds"
Rather than "may not be specific to the function of the protein" say that it results in a differently shaped active site and can therefore no longer function correctly.
Hey,
Just wondering, if all our cells have the same suite of antigens, then why do autoimmune diseases only affect certain types of cells?
Also, on second exposure to a pathogen, do the memory Th cells have to still activate the memory B cells and memory Tc cells, or is there another path that occurs?
Thankyou
The antigens presented on mhc 1 are peptide fragements - not all cells produce the same proteins, so they don't all present the same fragments.
Fairly sure they don't have to. I think Th cells still releases cytokines that help with the prolliferation and differentiaion, but there isn't a need for contact dependent signalling (what the B and Th cell do in a primary reaction) - this is initially needed to be sure that they've bound the same antigen to help prevent them wrongly attacking self. Don't quote me on that though. It's not something you need to know for the exam.
Hey there,
From the Sample VCAA examination 2017 :
1b) Would you use raw student data or mean data for oxygen concentration?
Would there be a fair argument in arguing that its better to use raw student data than the mean as the mean was affected by the one [possible contamination] result showing increase in oxygen concentration rather than decreasing and thus the mean shows constant oxygen concentration affecting the accuracy of the experiment
We discussed this last year and decided that you could probably do either so long as you could justify it.
hey,
i was curious as to - for the death receptor pathway of apoptosis (extrinsic pathway), are the death receptors on the damaged cell always there? and do they just become damaged or different, initiating this response?
or do they just be presented when the cell becomes damaged
Death receptors are always present. Death receptors respond to extrinsic apoptosis, so cytokine binds to receptor forming a ligang-receptor complex. Certain mutations in genes of cancer cells can cause changes in death receptors and hence preventing apoptosis. But ye, death receptors are always present.
The thing that binds to the death receptor and triggers that pathway is called a death ligand, you might not need to know that but if you do call it that and not a cytokine.
heyo, i just finished correcting my last practice exam - (neap bio 3&4 2018) one question was "describe the function of citrate synthase" in regards to its role in the krebs cycle.
I had never heard this term before, i could conclude that it was an enzyme but thats it I went back and searched for it in the study design and couldnt find it. So my question is should I have known this..?? would i need to know anything beyond this definition (from the answers) "Citrate synthase is an enzyme that catalyses specific chemical reactions, It combines two substrates (C4 and C2) to form one product (C6)"
Thanks!!!!
Definitely don't need to know that. It was in the old study design, no idea why neap had it in a 2018 exam. (Having said that, if it's function could be interpreted from the stem of the question or a diagram or something then you may have needed to work it out).
BTW let me know if I've missed any questions or if you still don't really understand. There's been heaps and I wouldn't be too surprised if some manage to slip by.