Predicting who wins the 2017 Nobel Prizes (3)
Summary: The unique mechanism detailed in the context of “Roles of APOBEC3A and APOBEC3B in Human Papillomavirus Infection and Disease Progression” is obviously not a unique mechanism. The mechanism exemplifies the fact that RNA-directed DNA methylation is energy-dependent and the fact that virus-driven energy theft causes the degradation of messenger RNA, which serious scientists have linked to all pathology.
My failure to accurately predict who would win the 2017 Nobel Prize in Physiology or Medicine can now be placed into the context of more experimental evidence of biophysically constrained energy-dependent pheromone-controlled biologically-based cause and effect.
I mentioned the evidence published on 21 August 2017 as Roles of APOBEC3A and APOBEC3B in Human Papillomavirus Infection and Disease Progression in the context of my blog post about Viral infection linked to cancer via a “unique mechanism,” which was reported as: “Unique mechanism links viral infection by HPV with cancer through function of a single enzyme”
The so-called unique mechanism is obviously the virus-driven degradation of messenger RNA, which has repeatedly been linked to all pathology, including the suicides of veterans who have served overseas.
See also experimental evidence of virus-driven degradation portrayed in the 2 October 2017 publication: Histone H3K4 monomethylation catalyzed by Trr and mammalian COMPASS-like proteins at enhancers is dispensable for development and viability
Drosophila embryos with trr alleles encoding catalytic mutants manifest subtle developmental abnormalities when subjected to temperature stress or altered cohesin levels. Collectively, our findings suggest that animal development can occur in the context of Trr or mammalian COMPASS-like proteins deficient in H3K4 monomethylation activity and point to a possible role for H3K4me1 on cis-regulatory elements in specific settings to fine-tune transcriptional regulation in response to environmental stress.
The ability to fine-tune transcriptional regulation via energy-dependent changes in RNA-directed DNA methylation was reported as: Unexpected findings uncover new understanding of gene expression
“What is it about the whole body of the enzyme itself that functions in development and its mutations that can result in cancer? That’s what we need to figure out.”
Thanks for asking. The unique mechanism detailed in the context of Roles of APOBEC3A and APOBEC3B in Human Papillomavirus Infection and Disease Progression is obviously not a unique mechanism. The mechanism exemplifies the fact that RNA-directed DNA methylation is energy-dependent and the fact that virus-driven energy theft causes the degradation of messenger RNA, which serious scientists have linked to all pathology.
Clearly, the serious scientists are not asking questions about energy-dependent RNA-mediated cell type differentiation or attempting to place what is known back into the context of theories about the role of “enhancers.”
There are now more than 65,000 indexed published works that link pre-mRNAs, which are also called microRNAs, to biophysically constrained protein folding chemistry via the physiology of pheromone-controlled reproduction in species from microbes to humans. See for examples: microRNA or pre mrna.
Theorists and/or other biologically uninformed science idiots who use terms like enhancers, promoters, QTLs, et al., in their attempts to obfuscate what is known to serious scientists about the biophysically constrained energy of supercoiled DNA will be faced with the possibility of even more ridicule than was delivered in the context of this parody.