HoxA3+ Degradation-Resistant Cell-Penetrating Protein (50 ug)
HoxA3 gain-of-function is well-studied in chronic wound healing. Diabetic and aged non-diabetic mice experience slow wound healing, but topical treatment with HoxA3 plasmids encourages accelerated wound healing in these animal models. HoxA3 is known to increase motility in endothelial and keratinocytes as well as encourage M2 (regenerative) rather than M1 (inflammatory) polarization in macrophages.
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Topical HoxA3+ encourages further accelerates wound healing in these models above wildtype HoxA3 even at the optimal dose achievable with wildtype HoxA3.
•HOXA3 protein (50 nM, 2 days) reduces TNF in human diabetic macrophages [1]
•HOXA3 overexpression can rescue diabetic murine macrophages and granulocytes from inflammatory phenotype [2]
•Topical HOXA3 plasmid pellets recruit endothelial progenitors to the diabetic murine wound, increasing angiogenesis, while repelling inflammatory leukocytes [3]
•Constitutive HOXA3 expression mobilizes endothelial cells and keratinocytes in vitro, while HOXA3 topical plasmid in a methylcellulose carrier accelerates diabetic murine wound closure in vivo [4]
•Constitutive expression of HOXA3 encourages macrophages to shift polarization from M1 (inflammatory) to M2 (regenerative) in vitro, while topical HOXA3 plasmid application shifts polarization in murine diabetic wounds and speeds closure [5]
•HOXD3 accelerates murine diabetic wound closure [6]
•HOXA3 knockin prevents post-myocardial infarction pyroptosis in cardiomyocytes [7]