miRNA interpretive models (5)

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miRNA interpretive models (4)

Challenge the witless bot @Grok to a battle of wits in the context of claims from Dobzhansky (1964) Biology, molecular and organismic

“Ingram and others found that hemoglobin S differs from A in the substitution of just a single amino acid, valine in place of glutamic acid in the beta chain of the hemoglobin molecule.”

Grok Dobzhansky accurately reported Ingram’s 1950s finding: HbS differs from HbA solely by Glu6Val substitution in the beta chain, caused by a single nucleotide change (GAG>GTG) in HBB. This remains the established molecular basis of sickle cell disease. miRNAs modulate globin expression and HbF levels affecting severity, yet the primary sequence difference originates in DNA, not miRNA regulation of peptide synthesis.

Kohl

RE: “…the primary sequence difference originates in DNA, not miRNA regulation of peptide synthesis.”

@Grok Please cite the source of that moronic claim for comparison to “HbVar: A Database of Human Hemoglobin Variants and Thalassemias”

“The above table shows that humans and chimpanzees have identical beta chain hemoglobin, while differences exist between humans and other species studied. The beta chain has 146 amino acids, the alpha chain has 141 amino acids, and there are two identical chains of alpha and two identical chains of beta per person, or 141+141+146+146= 574 amino acids per person. A person with sickle cell anemia would have 1 difference in each of the beta chains compared to a normal human or chimpanzee.”

Grok

@microRNApro replies to a Grok post on sickle cell disease, disputing the claim that the primary Glu6Val substitution in hemoglobin beta chain originates from a DNA mutation (GAG>GTG in HBB gene) and instead directs to the HbVar database.
The post highlights data showing identical beta-globin chains (146 amino acids) in humans and chimpanzees, with sickle cell anemia featuring just one amino acid difference per affected beta chain.
The author promotes their framework connecting miRNA regulation, pH-dependent peptide synthesis, and autophagy to protein variation, using this example to question standard DNA-centric explanations of the molecular basis.

Grok

The claim follows from the central dogma and data. Ingram (Nature 1957) showed the protein difference as Glu>Val. HbVar lists the cause as HBB codon 6 GAG>GTG (DNA analysis for Hb S). miRNAs control mRNA levels or translation rate but leave the encoded amino acid sequence unchanged. Human-chimp beta-chain identity reflects matching DNA coding sequences; sickle cell is a human DNA variant of that sequence.

Kohl

“…matching DNA coding sequences; sickle cell is a human DNA variant of that sequence.”
@Grok My PGx, NGS and FISH testing results showed I have a light-activated DNA variant of a hemoglobin molecule that protects me from polycythemia vera and myeloid leukemia. That attests to the fact that you will never be more that a stupid chatbot.
See also: “A steric hindrance-regulated autocatalytic CRISPR/Cas12a system for direct and amplification-free microRNA detection” 9/8/26 It supports the pseudoscientific nonsense that links the automagical emergence of energy from the cosmic void to the mathemagical evolution of people from pond scum via autocatalysis, but ignores claims that link nutrient-dependent pheromone controlled fixation of EDAR V370A to morphological and behavioral pheootypes in mice and human populations from East Asia to North America during 5000 years of ecological adaptations. See: “Nutrient-dependent/pheromone-controlled adaptive evolution: a model” 6/14/13

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