PTD-DBM (5mg)

PTD-DBM Peptide

PTD-DBM stands for Protein Transduction Domain-fused Disheveled Binding Motif. It is a synthetic peptide which has been studied within a wide range of research areas, including tissue damage, hair follicle development. Researchers have focused on the peptide specifically within the context of follicle development, suggested it may exert stimulating action through interaction with the endogenous proteins linked to follicle damage, CXXC5.^[1] It was discovered by Professor Kang-Yell Choi and his team of researchers at the Yonsei University in South Korea. The researchers studied the mechanism of hair follicle loss, and suggested that the cellular pathway Wnt/β-catenin may be crucial for follicle development. The signaling modulated by this pathway appears to control hair morphogenesis, growth, and regeneration.

Specifications

Molecular Formula: C₁₂₄H₂₂N₆₁O₂₈S₂

Molecular Weight: 3082.65

Sequence: H-Arg-Arg-Arg-Arg-Arg-Arg-Arg-Arg-Gly-Gly-Gly-Gly-Arg-Lys-Thr-Gly-His-Gln-Ile-Cys-Lys-Phe-Arg-Lys-Cys-OH

PTD-DBM Research

PTD-DBM Peptide and Androgenetic Alopecia
Hair follicle growth is considered to occurs in three phases, anagen phase (growth phase), catagen phase (regression phase), and telogen phase (resting phase).The excessive secretion of androgens such as testosterone, may lead to a shorter duration of the anagen phase. In research models of androgenetic alopecia, Wnt/β-catenin signaling appears to be primary among several cellular pathways involved in hair follicle development. This signaling pathway starts with the secretion of Wnt proteins.^[2] These proteins appear to bind with the Low-Density Lipoprotein-Related Protein (LRP), which, in turn, may deactivate glycogen synthase kinase-3β (GSK-3β). GSK-3β is an enzyme that is considered to deactivate the β-catenin in the hair follicle. Once stabilized, β-catenin appears to bind with the T-cell factor (TCF)/lymphoid enhancer factor (LEF). The proteins generated by the activation of β-catenin-TCF/LEF are considered to lead to the regulation of hair follicle cellular proliferation.

While in the course of their research, Professor Kang-Yell Choi and team consistently reported that a specific protein called CXXC-type zinc finger protein 5 (CXXC5) appeared to be excessively expressed research models of alopecia. CXXC5 appears to trigger the signaling pathways leading to a downregulation of Wnt/β-catenin. This observation has been confirmed by ancillary studies where murine models not expressing CXXC5 did not exhibit baldness or patching.^[3] CXXC5 appears to act by binding with another type of protein called Dvl protein. The CXXC5 and Dvl Protein-Protein Interaction (PPI) may lead to the downregulation of the Wnt/β-catenin pathway. As the Wnt/β-catenin pathway becomes downregulated, it may interfere with the generation of new hair follicles and the growth of existing ones. Based on the findings in various scientific studies, PTD-DBM is assumed to interfere with CXXC5 and Dvl Protein to Protein Interaction (PPI). It may lead to increased growth of hair follicles and due to this interaction, the hair follicles spend more time in the anagen phase of the hair cycle. The action of PTD-DBM appears to be further enhanced when symbiotically combined as with the case of valproic acid.

PTD-DBM Peptide and Tissue Repair
The Wnt/β-catenin pathway is considered to play a crucial role in tissue repair and the fibrosis of skin breaks. One of the regulators of this pathway is CXXC-type zinc finger protein 5 (CXXC5). It appears to function by negative feedback regulation. CXXC5 interacts with the Disheveled (Dvl) protein and downregulates the action of the Wnt/β-catenin signaling pathway.^[4] The researchers conclude that “these data suggest that CXXC5 would represent a potential target for future therapies aimed at improving wound healing.” The CXXC5−/−knockout mice examined in the quoted research study exhibited reportedly accelerated healing of skin lesions. They also exhibit increased keratin and collagen synthesis. PTD-DBM may exhibit the potential to function in a preventative action of the CXXC5-Dvl domain. It has been noted by researchers to enact this potential by preventing the Protein-Protein Interaction (PPI) between CXXC5 and Dvl proteins. This may result in an upregulation of the Wnt/β-catenin pathway. This upregulation may lead to hastened tissue repair processes through increasing keratin and collagen synthesis and by accelerating dermal fibrosis.

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References