This actin-sequestering peptide (molecular weight ~802.9 g/mol) plays a key role in cell migration, proliferation, and extracellular matrix remodeling
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The results were striking: Genes upregulated by GHK-Cu include: Collagen I, III, and VII synthesis genes (structural repair) Decorin and proteoglycan genes (extracellular matrix integrity) Antioxidant defense genes (SOD2, catalase, glutathione peroxidase) BDNF and nerve growth factor genes (neural repair and neuroprotection) Anti-inflammatory cytokine genes (IL-10, TGF-1) Angiogenesis genes (VEGF, angiopoietin new blood vessel formation) Stem cell self-renewal pathways Genes downregulated by GHK-Cu include: Pro-inflammatory cytokines (TNF-, IL-6, IL-1) Matrix metalloproteinases MMP-1, MMP-3 (enzymes that degrade collagen and connective tissue) Oxidative stress genes Pathways associated with cancer progression and metastasis The pro-inflammatory gene suppression is particularly notable
TB-500 vs GHK-Cu: Cell Migration vs Gene Modulation in Regenerative Peptide Research TB-500 and GHK-Cu are both studied for tissue repair, but they represent two different biological strategies
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4, and batoclimab and nipocalimab are specifically discussed in separate sections below