I will also plug my thread on APOB structure and function:
Behe’s book as resulted in a lot of attention being focused onto one gene: ApoB. I thought it might be useful for the scholars here at PS to do some background work on what ApoB does, what effects mutations may have, and possibly what effects the specific changes in the polar bear ApoB gene may have.
I found a useful review article:
It would appear that ApoB has two main functions: getting cholesterol into the blood stream and getting it out of the blood stream. Therefore, high or low levels of lipids in the blood stream can be affected by lipid production and lipid clearance. I have only briefly skimmed the abstract of the paper and thought it would be a great topic for the scholar forum.
Interestingly, ApoB is found in two isoforms through post-transcriptional modification: apoB-48 and apoB-100. It would appear that the smaller isoform is responsible for transferring dietary lipids into the blood stream. This may hold a key for understanding possible active sites for lipid…
Of interest is the relative cholesterol levels in both polar bears and brown bears. From what I can see, both brown bears and polar bears have comparable cholesterol numbers. From the other thread:
So what are the cholesterol levels in polar bears, and in brown bears for that matter?
Brown bears: 7.89 ± 1.96 mmol/L (11.08 ± 1.04 mmol/L while hibernating)ref
Polar bears: females (median): 8.58 ± 1.31 mmol/L, males: 6.61 ± 2.06 mmol/Lref
For reference, it is suggested that humans have less than 200 mg/dL cholesterol which is 5.5 mmol/L. Hibernating brown bears have twice that level, while active brown and polar bears are about 50% above that (i.e. 300 mg/dL).
If damaged APOB results in hyper or hypocholesterolemia per Behe’s claims, then why isn’t that seen in those figures? Behe or the DI needs to explain this.
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