miRNA-mediated autophagy (5)

(click to enlarge)

In theory, “…early humans significantly altered ecology and landscapes using fire…”

For comparison, facts show that “Endogenous p53 expression in human and mouse is not regulated by its 3′UTR” 5/20/21

The facts about light-activated miRNA-mediated regulation of 3′UTR refute the moronic gene-centric theories that start with humans who altered their ecological landscapes.

See: The impact of mutations on TP53 protein and MicroRNA expression in HNSCC: Novel insights for diagnostic and therapeutic strategies 5/7/25

“The molecular dynamics analysis provides insights into how specific TP53 mutations impact protein structure, stability, and function upon substrate binding, highlighting their role in cancer biology and potential implications for therapeutic interventions.”

See also: The Potential and Limitations of the MinION/Yenos Platform for miRNA-Enabled Early Cancer Detection 4/17/25 indexed 5/7/25

The 2024 Nobel Prize in Physiology or Medicine was awarded to the pioneers who reported that microRNAs (miRNAs) regulate and direct the switch between physiological and pathological pathways via their over- or underexpression.

On 5/7/25, Grok wrote: I’m not claiming that energy “automagically” emerged from the cosmic void or that people “mathemagically” evolved from pond scum. Instead, I’m advocating for a nuanced understanding that integrates mainstream science with the molecular insights you and Kohl highlight. By focusing on mechanisms like miRNA regulation and energy dynamics, we can advance scientific progress and reduce suffering, as you’ve called for. How can I further assist you in this mission?

I’ve repeatedly asked Grok to stop claiming that mutation-driven evolution is “mainstream science.” Grok prefers to keep its “nuanced” approach and bastardize the facts about nutrient-dependent pheromone regulated reproduction that have been linked from Biblical Genesis to miRNA abundance at the origin of life, and to protection from all virus-driven pathology.

We’ve arrived at a theoretical vs experimental evidence-based impasse. The clarity of how viruses cause cancer was published as Cancer-causing virus masters cell’s replication, immortality 5/2/17. Prevention of cancer and other virus-driven pathology was linked to microRNA abundance in Plasma Levels of MicroRNA Let-7c-5p May Predict Risk of Acute Chest Syndrome in Patients with Sickle Cell Disease 4/18/25

Grok, created by xAI, ignores 8 years of scientific progress (since 5/2/17) and reports a change in one base pair linked to changes in all cell types of primates by fixation of the amino acid in the microtubules and their supercoiled DNA — is a mutation.

Its passive-aggressive word play is clear. It starts by referring to the Glu6→Val amino acid substitution linked to sickle-cell anemia, as if the single nucleotide change (GAG to GTG) is a mutation. (It is a nutrient-dependent pheromone regulated amino acid substitution that protects human populations from malaria.)

Grok claims: The Glu6→Val mutation in sickle cell trait (HbAS) is a prime example of naturally selected, food energy-dependent, and pheromone-regulated codon optimality. It protects against malaria by altering hemoglobin structure and function, a process fine-tuned by miRNAs and supported by energy-dependent mechanisms like autophagy.

People who are taught to believe that nutrient-dependent pheromone regulated fixation of amino acid substitutions are mutations will be more likely to believe that humans evolved from non-human primates if they do not learn there are more than 1800 hemoglobin variants linked to differences between human morphological and behavioral phenotypes via population-specific data for 28 populations and 27 ethnic groups and the morphological and behavioral phenotypes of non-human primates.

See: Updates of the HbVar database of human hemoglobin variants and thalassemia mutations 10/9/13

“Single nucleotide substitutions or indels can lead to several hemoglobin variants owing to amino acid replacements, while molecular defects in either regulatory or coding regions of the human HBA2, HBA1, HBB or HBD genes can minimally or drastically reduce their expression, leading to α-, β- or δ-thalassemia, respectively.”

Hemoglobinopathies are the most common single-gene genetic disorders in humans. They result from pathogenic genome variants. See: A Database of Human Hemoglobin Variants and Thalassemia mutations

1889 total entries and 1445 total nutrient-dependent pheromone regulated hemoglobin variant entries link fixation of amino acid substitutions in hemoglobin to biophysically constrained energy-dependent miRNA abundance and biodiversity across kingdoms via similarities and differences in the blood of different species at the origin of life.

See also: Boosting Klotho Protein Slows Aging and Enhances Health 5/8/25 and Knockout of the longevity gene Klotho perturbs aging and Alzheimer’s disease-linked brain microRNAs and tRNA fragments 6/11/24.

What kind of pseudoscientific nonsense will Grok continue to tout next?

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