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The proposed mechanism involves: DNA binding: Short peptides bind in the major or minor groove of DNA at specific nucleotide sequences complementary to their amino acid structure Chromatin remodeling: Peptide binding alters local chromatin accessibility, either activating or repressing gene transcription Tissue specificity: Different peptide sequences preferentially bind different DNA sequences, explaining organ-specific effects Age-related depletion: Endogenous short peptide pools decline with aging, contributing to gene silencing and functional decline Restoration: Exogenous administration of the correct peptide sequence restores youthful gene expression patterns This theory has been supported by molecular modeling studies from the Khavinson group showing theoretical peptide-DNA interactions, and by gene expression studies showing that bioregulator peptides alter transcription of specific gene sets

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