Summary: The virus-driven degradation of messenger RNA was reported in the context of a “unique mechnanism.”
DNA cytidine deaminases remove RNA-mediated amino acid substitutions from a cytosine and convert the cytosine uracil. The deamination causes the degradation of DNA and mutations if not repaired.
The family members of apolipoprotein B messenger RNA-editing, enzyme-catalytic, polypeptide-like 3 (APOBEC3; A3) are DNA cytidine deaminases that remove the amino group from a cytosine, converting it to uracil. Cytosine deamination by A3 results in DNA degradation or mutations if not repaired (Figure 1A) [1,2,3]
The family members and friends of the DNA cytidine deaminases that remove the amino group from a cytosine can be compared to some of my former friends and family members. They let social scientists and other pseudoscientists convince them that the virus-driven degradation of messenger RNA did not cause all mutations. The pseudoscientists said nothing about how food energy-dependent endogenous RNA interference links ATP as energy to RNA-mediated DNA repair.
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.
Those who have seen others come to my personal Facebook page and claim that the facts about suicide and cancer are “bullspit” and that “nobody cares,” please watch what happens when everyone starts to care about the “bullspit” that’s still being taught to children as neo-Darwinian theory.
The children grow up to be pseudoscientists who cannot compete in an international market of scientific expertise, since all serious scientists have abandoned claims about mutation-driven evolution and the claims of “Big Bang” cosmologists who claim that energy “emerged” from nothing.
Stephen Hawking and Neil deGrasse Tyson are the big butt of jokes and the parodies of serious scientists. The future of science in the United States of America is a future that does not tolerate the ignorance of evolutionary theorists.
Although the G protein-biased D2R-agonist hordenine shares structural similarities to the balanced agonist dopamine, receptor–ligand interactions obtained after docking and energy minimisation in presence of a D2R homology model appear to be different. Hordenine lacks a meta-hydroxyl group compared to dopamine, rendering it unable to form hydrogen bonds to both residues Ser1935.42 and Ser1975.46 as dopamine does42 (Fig. 6).
…hordenine activates the receptor solely through G proteins, potentially leading to a more prolonged effect on the reward centre of the brain. The team is now investigating whether hordenine levels in beer are sufficient to have a significant effect on the reward centre.