Short cell-penetrating peptides: a model of interactions with gene promoter sites.

Mechanism / theoretical grounding — not clinical validation.

Khavinson VKh, Tarnovskaya SI, Linkova NS, Pronyaeva VE, Shataeva LK, Yakutseni PP. Bull Exp Biol Med. 2013.

Organ: general-aging · Type: theoretical · Peptides: Vilon, Epitalon

Molecular-mechanics modeling of Lys-Glu and Ala-Glu-Asp-Gly against promoter motifs GCAG and ATTTC in CD5, IL-2, MMP2, and Tram1 — a three-dimensional docking model, not a cell binding assay.

Editorial summary of a 2013 original article in Bulletin of Experimental Biology and Medicine. Computational peptide–DNA modeling. Public pages cite PubMed only. Read the paper: PMID 23484211.

Methods

The authors analyzed molecular-mechanics parameters — hydrogen bonds, hydrophobic and electrostatic interactions, and DNA–peptide complex minimization energy — to quantify previously proposed qualitative models of peptide–DNA contact. From those estimates they built a three-dimensional model of Lys-Glu (Vilon / KE) and Ala-Glu-Asp-Gly (Epitalon / AEDG) interacting with DNA sites GCAG and ATTTC placed in promoter zones of genes encoding CD5, IL-2, MMP2, and Tram1. No electrophoretic mobility-shift or cellular reporter assay is described in the abstract.

Findings

The modeled contacts are offered as a quantitative validation of earlier complementary-binding pictures. The work assigns KE and AEDG to those promoter motifs in a docking/minimization framework.

This is a structural hypothesis. It does not demonstrate physical binding in cells, does not measure those gene products in people, and is not a clinical trial. Follow the PMID.