Light-activated PTEN-dependent viral latency (3)

Combination of KRAS gene silencing and PI3K inhibition for ovarian cancer treatment 12/16/19

…we propose using small interfering RNA (siRNA) therapeutics to directly target the undruggable KRAS (siKRAS) in combination with the pan-PI3K inhibitor GDC-0941 (GDC) to simultaneously block both PI3K and RAS signaling, thereby exerting synergistic anti-tumor effects on ovarian cancers with PTEN deficiency and KRAS(G12D) mutation.

The synergistic anti-tumor effects have been linked to food energy-dependent pheromone-controlled biophysically constrained viral latency via the light-activated assembly of the microRNA-RNA-peptide nanocomplex in more tan 100 blog posts since 2/24/19.

See for instance: RNA processing and disease (4)

See also: Human microRNA‐30 inhibits influenza virus infection by suppressing the expression of SOCS1, SOCS3, and NEDD4 12/26/19

Our findings suggest that IAV utilises a novel strategy to restrain host type I IFN‐mediated antiviral immune responses by decreasing the expression of miR‐30 family members, and add a new way to understand the mechanism of immune escape caused by influenza viruses.

The escape mechanism requires the energy-dependent proliferation of viruses and the virus-driven degradation of messenger RNA that all serious scientists have linked to all virus-driven pathology via the creation of toxic peptides. Light-activated microRNA biogenesis has been linked to regulation of food energy-dependent pheromone-controlled fixation of amino acid substitutions in all peptides.

See: MicroRNA miR-7 regulates secretion of insulin-like peptides 12/26/19

Taken together, these results support a role for miR-7 regulation of an actin capping protein in insulin regulation, and highlight a conserved mechanism of action for an evolutionarily ancient microRNA.

The only experimental evidence for evolutionarily ancient microRNA links the light-activated assembly of the microRNA-RNA-peptide nanocomplex to disease prevention during the last 5-10,000 years of ecological adaptations and sympatric speciation in all living genera via substitution of achiral glycine in position 6 of the gonadotropin releasing hormone (GnRH) decapeptide of all jawed vertebrates.

See: Evolution of gonadotropin-releasing hormone (GnRH) structure and its receptor  3/15/12

It is very surprising and fascinating that the coordinated evolutionary selection of amino acids participating in binding GnRH has resulted in such perfection, that no substitution with a natural amino acid in any position improves binding potency.

For comparison to claims about evolutionary selection of amino acids, see: Past 5,000 years prolific for changes to human genome  11/28/12

The findings confirm their earlier work suggesting that the majority of variants, including potentially harmful ones, were picked up during the past 5,000–10,000 years.

See also:

Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants 1/10/13

Our results better delimit the historical details of human protein-coding variation, show the profound effect of recent human history on the burden of deleterious SNVs segregating in contemporary populations, and provide important practical information that can be used to prioritize variants in disease-gene discovery.

Prioritizing variants in disease-disease gene discovery can be removed from consideration since all diseases are caused by the virus-driven degradation of messenger RNA, which is biophysically constrained by the food that organisms eat and the physiology of reproduction in all living genera.


Author: James Kohl

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