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Post by lazerlee on Feb 17, 2022 3:58:23 GMT -5
Here is a link to the genetic study of HFI patients... It indicates that the patients share specific mutation in the non-coding promoter section of the Gene. This area of the gene does not appear to be used to define the variation/mutation. www.ncbi.nlm.nih.gov/pmc/articles/PMC2993836/ |
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Post by lazerlee on Feb 17, 2022 4:40:00 GMT -5
I am curious if anyone is studying HFI diagnosed patients and the same promoter region defects of "normal" genes for AldoB functionality?
(From the nature of the HFI genetic Identification studies, a normal protein Identification has not been made. Curiosity is about if the promoter region is somehow negated by something in the protein coding section.)
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Post by lazerlee on Feb 17, 2022 5:09:18 GMT -5
An older article that seems to indicate when Aldalose B is created by HNF-3 the promoter region is ignored, while HNF-1 uses it. pubmed.ncbi.nlm.nih.gov/8383844/ |
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Post by lazerlee on Feb 17, 2022 5:40:39 GMT -5
HNF-1 is the Transcription Factor used in the kidneys...
The theory about HNF-3 ignoring the Promoter region of the AldoB gene (placement location/adjustment) seems to be in dispute. Both Transcription Factors are present in the liver.
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Post by lazerlee on Feb 17, 2022 14:35:21 GMT -5
I am curious about how (or if) the protein encoding of a normal Gene limits the use of Carboxypeptidase A. Molecular derivatives, and how this interaction with the promoter region affects the ability to bind the protein to the cell wall? And function of the protein/enzyme
(Does the combination [alternative coding, varient promoter region and a normally benign molecule to humans] make "normal"/healthy bacteria in the intestines become toxic?)
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