MicroRNAs as therapeutic agents

By: James V. Kohl | Published on: November 21, 2018

Excerpt: See for comparison: Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems (2018) Twitter is blocking my tweets when I include links to this open access article about the fact that microRNAs buffer genetic variation.
MicroRNAs as therapeutic agents: The future of the battle against cancer

MicroRNAs bind to their target mRNAs to act as either oncogenes or tumour suppressors. With the near-complete elucidation of the biogenesis pathway…

It has become perfectly clear to all serious scientists that light-activated microRNA biogenesis biophysically constrains viral latency in all living genera in the context of the physiology of reproduction and healthy longevity.
See Daev (1994) Pheromonal regulation of genetic processes: research on the house mouse (Mus musculus L.)
See also: Feedback loops link odor and pheromone signaling with reproduction (2005)
See for comparison:  Alice and Bob Meet the Wall of Fire: The Biggest Ideas in Science from Quanta
Contributors: Philip Ball, K. C. Cole, Robbert Dijkgraaf, Dan Falk, Courtney Humphries, Ferris Jabr, Katia Moskvitch, George Musser, Michael Nielsen, Jennifer Ouellette, John Pavlus, Emily Singer, Andreas von Bubnoff, Frank Wilczek, Natalie Wolchover, Carl Zimmer
See for instance: A Fight for the Soul of Science

“Maybe someday things will change,” Achinstein added, “and the speculations will become testable; and maybe not, maybe never.” We may never know for sure the way the universe works at all distances and all times, “but perhaps you can narrow the live possibilities to just a few,” he said. “I think that would be some progress.”

The contributors have individually and collectively failed to make any scientific progress. See for comparison: Nutrient-dependent Pheromone-Controlled Ecological Adaptations: From Angstroms to Ecosystems (2018) Twitter is blocking my tweets when I include links to this open access article.
I invalidated the pseudoscientific nonsense touted by biologically uninformed journalists at Quanta, and my review of nutritional epigenetics also invalidated the patent for naturally occurring RNA interference, a billion dollar baby in therapy.
See: Church et al., RNA-Guided Human Genome Engineering.
I provided details and citations to works that link what all serious scientists know about how RNA interference biophysically constrains viral latency, which links naturally occurring light-activated microRNA biogenesis from RNA-guided genome organizations to healthy longevity via the physiology of reproduction in all living genera.
See also: Artificial MicroRNA-Mediated Inhibition of Japanese Encephalitis Virus Replication in Neuronal Cells (2018)

…RNA interference based on amiRNAs targeting viral conserved regions at 3’UTR was a useful approach for improvements of nucleic acid inhibitors against JEV.

Dynamic changes in global microRNAome and transcriptome reveal complex miRNA-mRNA regulated host response to Japanese Encephalitis Virus in microglial cells (2016)

…our data provide a uniquely comprehensive view of the changes in the host miRNAs induced by JEV during cellular infection and identify Notch pathway in modulating microglia mediated inflammation.

Toward the human cellular microRNAome (2017)

These microRNA expression patterns from 42 cell types are the first step toward a complete understanding of microRNA expression across all cells and establishing a human cell atlas. Our data also demonstrate general consistencies, but not without some concerning differences, between primary cells and immortalized/cancer cell lines. This work brings a new realization to the importance of cellular microRNA localization and enhances our understanding of this powerful regulatory RNA species.

MicroRNA expression patterns do not exist outside the context of light-activated microRNA biogenesis. Cold Springs Harbor Press, Harvard, and MIT will continue to obfuscate the facts that link light-activated microRNA biogenesis to biophysically constrained viral latency because the facts prevent them from profiting by linking expensive therapies and unnecessary treatments to naturally occurring RNA interference.
See: The Bull Sperm MicroRNAome and the Effect of Fescue Toxicosis on Sperm MicroRNA Expression
See also: A novel regulatory axis, CHD1L-miR-486 -MMP2, controls spermatogonial stem cell properties

…MMP2 regulates SSC stemness gene expression and growth properties through activating beta-catenin signaling by cleaving N-cadherin and increasing beta-catenin nuclear translocation. Our data demonstrates that Chd1l-miR-486-MMP2 is a novel regulatory axis governing SSC stemness gene expression and growth properties, offering a novel therapeutic opportunity for treating male infertility.

See also: The biochemical basis of microRNA targeting efficacy

This model substantially improved prediction of cellular repression, thereby providing a biochemical basis for quantitatively integrating miRNAs into gene-regulatory networks.

One feature that was not captured in our model is the evolutionary conservation of sites…

The epic failure to capture anything that attests to the evolutionary conservation of sites can be place into the context of allele-specific RNA decay.
But see the twist:  Pervasive allele-specific regulation on RNA decay in hybrid mice

…changes in RNA decay could serve as important means to stabilize RNA abundances during mammalian evolution.

RNA decay is linked to evolution  54 years after McEwen et al., (1964) linked the creation of ATP and the creation of RNA to all biodiversity.
Dependence of RNA synthesis in isolated thymus nuclei on glycolysis, oxidative carbohydrate catabolism and a type of “oxidative phosphorylation”

The synthesis of RNA in isolated thymus nuclei is ATP dependent.

Each time you see a claim that suggests mammals evolve outside the context of the energy-dependent creation of RNA, try to remember three things:
1) Changes in the rate of RNA decay are food energy-dependent and biophysically constrained by the pheromone-controlled physiology of reproduction in species from bacteria to primates.
2) The growth of plants clearly links light-activated microRNA biogenesis to healthy longevity.
3) The virus-driven degradation of messenger RNA link mutations to all pathology.
For a historical perspective, see: On the Influence of the Human Instinct in the Prevention and Cure of Disease, Chiefly in Reference to Diet (1855).
Compare the claims about food to Darwin’s “conditions of life” in Origin of Species (1859)
Chapter 4
Chapter 5
Chapter 6
See also, my review of Kevin J. Mitchell’s “Innate.” Ignoring light-activated microRNA biogenesis

He frames his claims in the context of random mutations and evolved biodiversity despite the facts that serious scientists have detailed. For example, ages 10+ can learn how the creation of subatomic particles must be linked from cytosis to biophysically constrained viral latency and sympatric speciation.

The physiology of reproduction is linked to heredity in species from soil bacteria to humans via EDAR V370A (an amino acid substitution) in mice; in populations found in North and East Asia; and in populations in the New World.

I could go on about the facts about cell type differentiation for hours or refer you to MicroRNA.pro or one of my other domains. Alternatively, you could see the work that was published today: “MicroRNAs buffer genetic variation at specific temperatures during embryonic development” for comparison to our 1996 review of molecular epigenetics: “From Fertilization to Adult Sexual Behavior”

See also: Extracts of Polypore Mushroom Mycelia Reduce Viruses in Honey Bees 

Bees have been observed foraging on mushroom mycelium, suggesting that they may be deriving medicinal or nutritional value from fungi.

Stamets et al., (2018) failed to link the physiology of microRNA-mediated food energy-dependent pheromone-controlled behavior in the model organism I used to refute the pseudoscientific nonsense about neo-Darwian evolution.
See: Nutrient-dependent/pheromone-controlled adaptive evolution: a model (2013)
In my model, no bioinformatics expertise is required. Organisms that do not eat die too quickly to compete with those that find food and reproduce in the context of Darwin’s “conditions of life” and common sense.

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