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Comments ...

 +0  (nbme22#35)

Why is this not increased binding of DNA polymerase?

This mutation should cause cellular division ie DNA replication and cause increased binding to origin replication sequences ie TATA by DNA polymerase.

brise  It's talking about mutations on the transcription of genes that inhibit the cell division. Also RNA polymerase binds to the promoter region.
nwinkelmann  Also, the question specifically (though in a very wordy, convoluted way) asked what the effect of the mutation on transcription was. DNA pol is not used in transcription, it is used in replication. RNA pol is used in transcription. In terms of increased or decreased binding, argining is polar/positively charged and proline is neutral/nonpolar, so there are fewer H-bonding sites, and thus decreased binding of the RNA pol.
medn00b  Could this convoluted question also mean.......... that since the gene to make p53 is messed up due to the hydrogen bonds, RNA polymerase will not be able to bind to make the mRNA ... So there will be cancer? Because P53 is a tumor suppressor... lemme know thanks guys

 +0  (nbme22#44)

Babies don't have mature activity of this enzyme when first born...Tx with phototherapy...not same mechanism as enzyme but makes bilirubin more soluble

Subcomments ...

submitted by lodododo(1),

There’s a UWorld question on this. Once the healthy axon retracts and the distal (injured) axon degenerates, there’s a bunch of myelin debris in the way that remains there for a long time. This blocks regeneration of the axon.

alacran763  Reinnervation *is* assisted by schwann cells, but the process is very delicate. After Wallerian degeneration, the schwann cells basically have to line up perfectly along where the nerve is supposed to grow, but it does not happen perfectly and the schwann cell disorganization often prevents proper reinnervation. +2  
dantescuttlefish  I thought the Uworld question said that in the CNS myelin debris is there for months even years....the PNS it gets cleared much quicker. +1