And here's a patent request involving an enzyme encoded by gene UGCG that is involved in keratinocyte differentiation. They want to use it as a treatment for acne and any other condition that involves hyperkeratinization:
More info on UGCG: http://en.wikipedia.org/wiki/UGCG
And here: http://www.genecards...sp.pl?gene=UGCG Where it includes a chart with its genomic location.
And under Epigenetics it says:
'QIAGEN PyroMark CpG Assay predesigned Pyrosequencing DNA Methylation assays for UGCG'
I, of course, have no idea what that means, but epigenitics are things that we change in our life time due to environment and the things we do to ourselves that become part of our genetic makeup and can get passed down to our kids. And it seems they've identified something.
Good Things for Hyperkeratinization:
Also, there's at least 3 genes/enzyme mutations identified as being involved in the linoleic acid deficiency found in mammalian skin prone to skin irritations of all sorts. http://www.acne.org/...pical-solution/
-Acne prone skin has found to be deficient in retinoids, possible due to mutations in CYP26AI gene that causes it to be metabolized too fast to be used.
Polymorphisms in the human cytochrome P-450 1A1 gene (CYP1A1) as a factor for developing acne.
Paraskevaidis A, Drakoulis N, Roots I, Orfanos CE, Zouboulis CC.
Department of Dermatology, University Medical Center Benjamin Franklin, Free University of Berlin, Germany.
Cytochromes P-450 are a supergene family of enzymes involved in the metabolism of a wide range of endogenous and foreign compounds. The existing genetic variations of the distinct isozymes lead to interindividually different metabolic capacity. Since vitamin A, endogenous retinoids and their natural metabolites are morphogenic for the sebaceous gland, we investigated the polymorphisms of cytochrome P-450 1A1, as being one of the most active isozymes involved in their interconversion. From the known mutations, two were investigated; an additional cleavage site for MspI in the 3'-flanking region identified as a thymine-to-cytosine transition 1,194 bp downstream of exon 7 (m1) and an adenine-to-guanine transition at position 4889 in exon 7 (m2). We studied 96 acne patients for m1 and m2 mutations by restriction fragment length polymorphism and allele-specific polymerase chain reaction, respectively, and compared the results with 408 reference individuals. No statistically significant difference was found in the distribution of m2 alleles; the frequency was 3.13 and 3.06% of the alleles, respectively (odds ratio = 1.02, confidence limits 0.41-2.52, p = 0.96). In contrast,a trend to an overrepresentation of m1 alleles in acne patients was observed; allele frequency was 8.33 in the patients and 6.99% in the control subjects, respectively (odds ratio 1.21, 95% confidence limits 0.68-2.16, p = 0.52). As the m1 mutation might define a marker for alterations on regulatory sites, the biological efficacy of natural retinoids could be greatly impaired by their rapid metabolism to inactive compounds. The resulting deficit of active natural retinoids may lead to abnormal sebocyte differentiation and hyperkeratinization of the follicular canal implicating the development of acne in some patients.
Also, according to this article, the genome of p acnes has been mapped. or at least that of P. acnes strain KPA171202 http://www.acne.org/...#entry3257204.. Somewhere I have read research that has found a mutated strain or species in acne prone skin. Perhaps it's that strain and the info is in that paper.
And that's just a few. See also this thread:
Edited by alternativista, 31 December 2012 - 02:59 PM.