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Sunday, October 6, 2013

FMO3 gene : E158K and E308G

There are a few ways that people can have 'faults' in their DNA that cause them an inability to develop a fully functioning protein of some sort (eg FMO3 protein). Most errors will only affect function by a certain %, say meaning 90% function etc. It's 'null mutants' and deletions that are probably the worst type of errors, that can cause almost total inability to create the protein (usually people have maybe 20% function even if severe). Currently with TMAU, the severe genetic type is associated with having 2 copies of null mutants.

However the most common type of 'errors' are 'Single Nucleotide Polymoprhisms', 'variants' that are missense changes which mean the wrong amino acid is inserted in the 532 amino acids track that go to make a full FMO3 protein. Usually there are many of these missense changes in a gene pool and often do not have any 'clinical' effect on protein formation. However sometimes a missense copy here and there in your FMO3 DNA can compound to possibly affect function to some degree.

2 common polymorphisms for the FMO3 protein are what are known as E158K and E308G. This means that on the 532 amino acid 'DNA railtrack', at codons ('track') 158 and 308 there are missense amino acids. At both 158 and 308 they should be E (Glutamic acid) but instead it is :
158 : should be glutamic acid : instead is lysine
308 : should be glutamic acid : instead is glycine

Apparently, it is estimated that around 50% of the white population carry a copy of the E158K error, and about 20% carry a copy of the E308G error

What researchers do is in the lab use FMO3 DNA and check to see how the 'faults' may affect total formation of the (FMO3) protein. Currently it is thought that carrying a copy of E158K and E308G on the same allelle (i.e. from the same parent) may affect FMO3 function to some degree (say meaning 70%-90% function)

Whether later it will be thought carrying them on either allelle is enough to cause some deficiency is unknown. However it does seem that these little 'SNPs' (not just at 158 and 308) compounded may in the future be predicted to cause problems in the FMO3 DNA 532-track railtrack. To have a copy of one 'null-mutant' as well as these little SNP faults may be enough to put people in the 'risk zone' at times. We will need to wait and see the full picture

Link: amino acid symbols
Link: letter to editor about compound heterozygosity and FMO3 function



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1 comments:

Anonymous said...

mój problem nieświeży oddech już 7 lat , jedyne po czym jest gorzej to amfetamina, gdy zażyje amfetaminę pogarsza się bardzo

przeczytałem ten artykuł

http://jpet.aspetjournals.org/content/288/3/1251?ijkey=d34d01b2247dfb8cd3a932a5beb09e2ea1b7be3c&keytype2=tf_ipsecsha

i pytam- czy jeśli pogarsza się po amfetaminie to mogę mieć tmau1?

Dec 27, 2016, 11:00:00 AM
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