Polycomb repressive complex 2 (PRC2) maintains repression of cell-type-specific genes but also associates with genes ectopically in cancer.
These data support a model in which pre-mRNA evicts PRC2 during gene activation and provides the means to selectively remove PRC2 from specific genes.
Reported as: Method discovered to reactivate tumour fighting genes ‘silenced’ by cancer 9/23/19
Healthy cells use PRC2 to silence genes whose instructions should only be read by other cell types. Cancer cells ‘hijack’ this silencing function of PRC2 to switch off ‘tumour suppressor’ genes. When active, these genes stop cells from dividing, so if PRC2 could be removed from these genes it could halt tumour growth.
Using healthy cells grown in the lab, the researchers found that PRC2 also binds to RNA, the information molecule that is produced by active genes. When PRC2 binds RNA, it can no longer bind and silence the gene.
The information molecule, RNA links the light-activated assembly of the microRNA-RNA-peptide nanocomplex to biophysically constrained viral latency and all pathology via what also is called the polycomb repressive complex 2.
We referred to it as “polycomb” in the molecular epigenetics section of our 1996 review of RNA-mediated cell type differentiation. From Fertilization to Adult Sexual Behavior
Yet another kind of epigenetic imprinting occurs in species as diverse as yeast, Drosophila, mice, and humans and is based upon small DNA-binding proteins called “chromo domain” proteins, e.g., polycomb. These proteins affect chromatin structure, often in telomeric regions, and thereby affect transcription and silencing of various genes…
Others have ignored the evidence that links pre-mRNAs to what is known about how microRNAs (also known as pre-mRNAs) link the Creation of RNA to biophysically constrained viral latency and healthy longevity.
But see: Ultrastructural localization of DREADDs in monkeys 5/18/19
Sympatric speciation was placed into the context of DREADD/tag combinations that link a food energy-dependent surface glycoprotein to the infectivity of the human virus from mice to monkeys via fixation of amino acid substitutions or the virus-driven degradation of messenger RNA that prevents fixation. The human influenza hemagglutinin (HA) tag is derived from the HA-molecule corresponding to amino acids 98-106.
See: A two-amino acid change in the hemagglutinin of the 1918 influenza virus abolishes transmission (2007) via the energy-dependent Creation of the information molecule, RNA.
The facts about influenza virus replication have since been placed into the context of all viral replication via the conserved molecular mechanisms that biophysically constrain host methyltransferase SETD3.
Our results reveal a crucial role of a host protein in viral pathogenesis, and suggest targeting SETD3 as a potential mechanism for controlling viral infections.
This was reported (with my emphasis) as: Disabling a single protein could “cure” the common cold
Viruses, like those that cause colds and flu, are some of the fastest-evolving forms of life on Earth. That’s why there are no permanent cures for these common illnesses. Any time scientists come up with a vaccine, it doesn’t affect all strains of the virus and even those that are inhibited by it can evolve resistance to the drug pretty quickly.
Serious scientists do not consider viruses to be evolving life forms. Replication requires them to steal the energy from living cells that is required for biophysically constrained cell type differentiation via the information molecule, RNA and fixation of amino acid substitutions.
In a search of Tweets that mention chemogenetic kinetics, I found a conversation that was initiated by Jessica Raper. She inadvertently linked microRNAs in the milk exosomes of all mammals from the information molecule, RNA to biophysically constrained viral latency via EDAR V370A in mice and non-human primates.
I wrote: Hi Jessica. Standing on the shoulders of giants may not be a good idea if the giants stepped on the toes of biologically uninformed science idiots who failed to link EDAR V370A from mice to humans in the context of the requirement for biophysically constrained viral latency.
See the refutation of neo-Darwinian pseudoscientific nonsense in: Environmental selection…through breast milk.
The frequency of the human-specific EDAR V370A allele appears to be uniquely elevated in North and East Asian and New World populations….”
Simply put, the human-specific EDAR V370A allele links the information molecule, RNA to virus-driven vector-induced species differences in exogenous proteins that link the degradation of the information molecule, also known as messenger RNA to food energy-dependent pheromone-controlled ecological adaptations in species from yeasts to mammals. The adaptations are “All about that base”
An energy-dependent catalytic hairpin assembly-based in vitro diagnostic (CIVD) system detected subnanomolar levels of target miRNAs and distinguished the link to single-base mismatches and the information molecule, RNA.
…this CIVD kit has shown excellent detection performance in real intracellular RNA samples and confirmed results similar to those of conventional methods (microarray and quantitative real-time polymerase chain reaction).
Pheromones are species-specific chemicals that biophysically constrain food energy-dependent viral latency. That is how insect pheromones have been linked to disease prevention in humans.
To prevent further obfuscation of facts about the energy-dependent expression of GPCRs (G protein coupled receptors), I added that virus-driven vector-induced species differences in exogenous proteins were linked from the energy-dependent Creation of RNA and GPCRs to biophysically constrained viral latency in Feedback loops link odor and pheromone signaling with reproduction