FREE* SAMPLE: Histone modification

By: James V. Kohl | Published on: October 29, 2015

Histone Modification Antibodies


See also — as used in ad copy excerpt for their products:

Histone modification antibodies are notorious for binding non-specifically to similar, but off-target histone modifications and/or having their specific binding inhibited by steric hindrance from modifications on neighboring residues.
CST addresses these issues by using including a peptide array assay similar to the one described by Fuchs, S.M., et al. (1) to our validation testing. In a single experiment, the peptide arrays assess reactivity against known modifications across all histone proteins as well as the effects of neighboring modifications on the ability of the antibody to detect a single modification site.
We recognize that breakthrough discoveries require both hard work and reliable reagents, so as our epigenetics portfolio expands….

In context:
Residue (as used above): Amino Acid Residues Contributing to Function of the Heteromeric Insect Olfactory Receptor Complex
Peptide (as used above): Peptide synthesis triggered by comet impacts: A possible method for peptide delivery to the early Earth and icy satellites
Protein (as used below): A universal trend of amino acid gain and loss in protein evolution
My comment: In my model, the nutrient-dependent RNA-mediated fixation of the “residues” links what others refer to as “amino acids” to the peptides and proteins that link supercoiled DNA to the protection of organized genomes from virus-driven genomic entropy via nutrient-dependent DNA repair in the context of the innate immune system. This limits claims about where peptides came from and claims about protein evolution to what is known to serious scientists about the experience-dependent de novo creation of olfactory receptor genes in all vertebrates and invertebrates.
Arguably, you might not understand the facts about histones and cell type differentiation if you could not first translate the language they used in the ad copy and use the same language to explain how their products help to link epigenetic cause and effect from metabolic networks to genetic networks. The epigenetic links from metabolic networks to genetic networks require details of how the epigenetic landscape is linked to the physical landscape of DNA via the conserved molecular mechanism of biophysically constrained RNA-mediated protein folding chemistry that links amino acid substitutions from histones to supercoiled DNA.
Unfortunately, by the time anyone begins to use their products for discoveries or validation of links from atoms to ecosystems via what is currently know about physics, chemistry, and molecular epigenetics, they have typically already been taught to place their results into the context of neo-Darwinian theory. Results are virtually guaranteed to be presented by academics in that context along with all the pseudoscientific nonsense researchers were taught to believe linked mutations to the creation of new genes.
Many academics seem to think that mutated new genes link natural selection to the evolution of biodiversity via de Vries definition of mutation and the assumptions of population geneticists who calculated how long it might take for accumulated mutations to lead to the evolution of a new species.
No experimental evidence of biologically-based cause and effect suggests that any species has evolved from another species. That fact can be addressed by asking an evolutionary theorist where amino acids come from, or  where histones came from, and why the amino acid substitutions in the histones were needed to protect organized genomes from virus-driven genomic entropy.
Eugene Koonin would probably tell you the viruses evolved first, and that everything known to serious scientists about virus-driven pathology should be taken with a grain of salt before including it in links from nutritional epigenetics to pharmacogenomics in the context of personalized/precision medicine. See: Riding the Evolution Paradigm Shift With Eugene Koonin

[T]he entire ideology of personalized medicine should be taken with many grains of salt.

See also: A virocentric perspective on the evolution of life

Virus–host arms races and cooperation were among the decisive factors in the evolution of all life forms.

My comment: Did you or anyone else you know cooperate with an influenza virus or any other virus to ensure the survival of similar life forms? Are viruses our domesticated friends?
See also: Breakthrough DNA Editor Borne of Bacteria


In a new paper in Nature Reviews Genetics, Koonin and Mart Krupovic of the Pasteur Institute in Paris argue that the CRISPR-Cas system got its start when mutations transformed casposons from enemies into friends. Their DNA-cutting enzymes became domesticated, taking on a new function: to store captured virus DNA as part of an immune defense.

My comment: When did the DNA-cutting enzymes evolve? How? When did the need to store captured virus DNA evolve?
See also: Beyond species recognition: somatic state affects long-distance sex pheromone communication
Abstract excerpt:

We show that the emission of the long-distance sex pheromone of the burying beetle, Nicrophorus vespilloides is highly condition-dependent and reliably reflects nutritional state, age, body size and parasite load—key components of an individual’s somatic state.

My comment: No experimental evidence of biologically based cause and effect suggests that sex differences “evolved” or that pheromonal communication “evolved.” However, experimental evidence of biologically-based cause and effect linked the “re-evolution” of bacterial flagellum to its innate immune system via its nutrient-dependent pheromone-controlled physiology of reproduction. The “re-evolution” of this functional structure occurred in four days.
Let’s try to place that into the context of 700 million years of evolution, shall we? You first!

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