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Here the ‘p’ indicates we are discussing the amino acid series of the proteins that correspond to the cDNA or mRNA sequence. It says that Jackson’s PLP1 will have a serine (S) substituted in at position 65 in place of the normal isoleucine. Isoleucine is a hydrophobic amino serine and acid is a polar and uncharged amino acid.

These are pretty different animals completely and it is normally assumed that kind substitution should have some significant influence on protein structure or function. The relevant question is what impact? The canonical membrane structures of some of the various splice variants of the standard PLP1 protein have been determined more than about ten years ago.

It is a highly conserved protein that is practically identical in several species from mouse to man. Recently, a few 3-D proteins conformations, the real crystal structures, have been determined also, in mixture with other bound proteins sometimes. The presumptive membrane topology is four transmembrane helices, with the position 65 serine (or thereabouts depending on where the amino acid start count is performed) lying at the extracellular apex of the first membrane helix.

While serine can be phosphorylated in a variety of proteins this might not be likely in the observed position. To this point, it is known that while transgenic mice that overexpress the PLP gene show neuronal degeneration and axonal disintegration, perhaps paradoxically, the absence of PLP/DM20 in PLP null mice also causes axonal swellings. Because this protein is generally so abundant, around 50% of the total myelin protein, small changes can have large effects.

It is not known if the serine place should affect splicing (but notice close by splice site in the picture below), or impact any of the protein’s cross-linked cysteines, or have an effect on any critical cysteine palmitoylations on the other hand, but further research would be needed. As the proteins is known to form dimers, and perhaps even higher old multimers also, likely linking to each other to across layers of compacted myelin up, the result of serine on such oligomerization might be an important question. It is important I believe to circulate Jackson’s details to any doctors and researchers who might be poised to help, namely, experts in the many ‘orphan’ progressive degenerative neurologic disease.

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This course would include experts in a variety of leukodystrophies and lysosomal storage space diseases that affect myelin and those that ultimately impact mitochondria and their role in energy creation and other key metabolic processes. Two guys who come to mind immediately, and who I have spoken to before for various articles are Bruno Benitez Washington University in St. Louis, and Doug Wallace at CHOP.

4 nucleotides in addition to the last exon nucleotide. This version is predicted to be always a “splice donor” which means that can alter the length of the resulting proteins, a different transcript. PGAP1 has 22 exons and at least 11-splice variations. This variant has a mutation in the intron downstream of nucleotide position 2525. This creates a splice junction failure where the intern will not be spliced out and thus the variant will include protein sequence corresponding to the intron. There’s a lot of uncertainty about whether that could affect the enzyme activity of PGAP1 straight. It’ll generate a protein of unexpected length.