Did evolution autophosphorylate your kinases? (3)

By: James V. Kohl | Published on: October 24, 2016

Did evolution autophosphorylate your kinases? (1)
Did evolution autophosphorylate your kinases? (2)
See also:

N6-Methyladenosine in Flaviviridae Viral RNA Genomes Regulates Infection

Reported as: Chemical tags affect ability of RNA viruses to infect cells

Dynamics of Human and Viral RNA Methylation during Zika Virus Infection

Reported as:  Zika virus infection alters human and viral RNA

My comment: Virus-driven hecatombic evolution of all pathology is linked from the failure of energy-dependent phosphorylation to biophysically constrain the RNA-mediated damage to DNA via fixation of amino acid substitutions in the cell types of all living genera.

It is now perfectly clear to all serious scientists that evolution did not autophosphorylate their kinases.

See how nutrient energy-dependent phosphorylation must occur to regulate transcription in the context of chromatin remodeling, linked to supercoiled DNA and to chromosomal rearrangements that link RNA-mediated amino acid substitutions to all biodiversity via differences in energy-dependent morphological and behavioral phenotypes.

For example: Chromatin Kinases Act on Transcription Factors and Histone Tails in Regulation of Inducible Transcription

Chemical inhibition of MSKs selectively targets inducible transcription

My comment: Even C. David Allis has been forced to admit to the facts about chemical ecology that I placed into the context of this model.
Nutrient-dependent/pheromone-controlled adaptive evolution: a model

THIS MODEL DETAILS HOW CHEMICAL ECOLOGY DRIVES ADAPTIVE EVOLUTION VIA: (1) ecological niche construction, (2) social niche construction, (3) neurogenic niche construction, and (4) socio-cognitive niche construction. This model exemplifies the epigenetic effects of olfactory/pheromonal conditioning, which alters genetically predisposed, nutrient-dependent, hormone-driven mammalian behavior and choices for pheromones that control reproduction via their effects on luteinizing hormone (LH) and systems biology.

Everything published by serious scientists since then attests to the facts that link polycombic ecological adaptations from our 1996 review with its section on molecular epigenetics.
See: From Fertilization to Adult Sexual Behavior
Unfortunately, pseudoscientists and supporters of the evolution industry have tried to prevent the dissemination of accurate information about nutrient-dependent RNA-mediated cell type differentiation in the context of the pheromone-controlled physiology of reproduction in species from microbes to humans.
Others went so far as to invent the term oncohistone in an attempt to link virus-driven hecatombic evolution to beneficial mutations rather than admit that virus-driven energy theft is the link to all pathology in all living genera.
See: Histone H3K36 mutations promote sarcomagenesis through altered histone methylation landscape
Reported as: Gene regulatory mutation linked to rare childhood cancer

Because the DIPG mutation always changed the same amino acid in the same location in the histone gene, Lewis knew something was special about it.

My comment: Unfortunately, Lewis did not seem to know that energy-dependent changes in RNA-mediated amino acid substitutions are linked to healthy longevity in all living genera or that virus-driven energy theft links amino acid substitutions in viruses to all pathology.

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