The tipping point (revisited): 82,000 publications (4)

MicroRNA Items: 1 to 20 of 81970

See for example: Oligonucleotide Therapeutics as a New Class of Drugs for Malignant Brain Tumors: Targeting mRNAs, Regulatory RNAs, Mutations, Combinations, and Beyond 1/14/19

 …synthetic gRNAs guiding CRISPR-Cas9 editing technologies have a tremendous potential to further expand the applications of oligonucleotide therapeutics and take them beyond RNA targeting.

See also: Reduced Expression of Brain-Enriched microRNAs in Glioblastomas Permits Targeted Regulation of a Cell Death Gene 9/2/11

In conclusion, the data presented here provide a comprehensive analysis of the miRNA signature in glioblastoma and demonstrate the potential application of miRNA-regulated genes in the therapeutic treatment of brain cancers— an approach that could be readily extended to cancers of other organs.

According to one reputable source (a Harvard and MIT-trained physicist), the so-called cell “death gene” was discovered by researchers at Abcam in the 1990s. The discovery has now been “monetized” for delivery as a “billion dollar baby” in therapy.

See Abcam’s “Interactive Pathways,” which link epigenetics and autophagy to cancer or to cancer prevention.

See also their resources for RNA interference, which includes this one on epigenetics. Epigenetics in cancer

Until it was monetized, oligonucleotide therapeutics was known as naturally occurring RNA interference.

See the original patent application: RNA-Guided Human Genome Engineering

5. Repetitive elements or endogenous viral elements can be targeted with engineered Cas+gRNA systems in microbes, plants, animals, or human cells to reduce deleterious transposition or to aid in sequencing or other analytic genomic/transcriptomic/proteomic/diagnostic tools (in which nearly identical copies can be problematic).

Get Well in the RNAi Way-RNAi, A Billion Dollar Baby in Therapy 3/3/16

RNAi has targeted exogenous genes in models of viral infection

See also: Special Issue “Non-Coding RNAs in Viral Infections” 9/21/18

See also: Microglial memory of early life stress, epigenetic mechanisms and susceptibility to neurodegeneration in adulthood (a preprint)

Epigenetic mechanisms, including DNA methylation, post-transcriptional histone modification and microRNA signaling networks directly modulate gene expression and are dynamically regulated in post-mitotic neurons, with crucial functions in memory formation and synaptic plasticity, modified by chronic stress exposure for example (Day & Sweatt, 2010; Herrera et al., 2015; Shaltiel et al., 2013).

Ultimately, the fact that viral microRNAs link stress-induced changes in the microRNA/messenger RNA balance to all pathology was placed into the context of this question:

Can Viruses in the Genome Cause Disease? 1/1/19

Clinical trials that target human endogenous retroviruses to treat multiple sclerosis, ALS, and other ailments are underway, but many questions remain about how these sequences may disrupt our biology.

Instead of asking the question and making claims about what was unknown, this was published and linked to effective treatment as “Viral Resurrection” in The Scientist 33 (1) 2019 pp 23-29.

Ancient retroviruses embedded in our DNA could hold the key to treating complex disease.

For a historical perspective on what is know to all serious scientists about viral resurrection via the works of science fiction author Greg Bear, see:

Evolution rising from the grave (2000)

Reactivation of a dormant message signals the dawn of a new humanity.

Biophysical constraints on reactivation of virus-driven pathology were placed into the context of this review: Living with the Neanderthals (2003)

He also seeks to teach readers about science, to highlight our utilitarian politics and our inability to get along with each other, and to provide a quasi-rational basis for theology and morality.

He failed to convince most people that the nutrient-dependent pheromone-controlled physiology of reproduction in bacteria could “provide a quasi-rational basis for theology and morality.”

Instead, most people got stuck with ridiculous theories about evolution.

See: Infographic: Human Endogenous Retroviruses and Disease

1/1/19

Human endogenous retroviruses that colonized vertebrate DNA millions of years ago have long been dismissed as junk DNA, but researchers now know that they may play important roles in cancer, neurodegeneration, and other ailments.

Over the course of evolution, several groups of ancient viruses colonized our ancestors’ genomes, leaving thousands of fragments of viral code in modern-day human DNA.

No experimental evidence of biophysically constrained top-down causation and epigenetic effects on cell type differentiation have been linked to more than ~10,000 years of our history of life on this planet.

For contrast see, Gorillas have been infected with the HERV-K (HML-2) endogenous retrovirus much more recently than humans and chimpanzees 1/4/19 and Analysis of 6,515 exomes reveals the recent origin of most human protein-coding variants (11/28/12)

See for comparison:  Epstein-Barr virus microRNAs regulate B cell receptor signal transduction and lytic reactivation 1/7/19

Stress-linked lytic reactivation has been linked from the virus-driven degradation of messenger RNA in bacteria to all pathology.

The late Eshel Ben-Jacob led the way towards Greg Bear’s understanding of the facts during the same time I detailed the facts about human pheromones in my published works and in presentatons from 1995 until 2002, and again from 2006 to 2018.

See:

These are some of the last of the late Eshel Ben-Jacobs published works:

MicroRNA-based regulation of epithelial–hybrid–mesenchymal fate determination (2013)

Modeling putative therapeutic implications of exosome exchange between tumor and immune cells (2014)

Stability of the hybrid epithelial/mesenchymal phenotype (2016)

See also: Seeking the foundations of cognition in bacteria: From Schrödinger’s negative entropy to latent information (2006)