Date published: 2025-9-12

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HoxA13 Activators

HoxA13, a critical transcription factor in embryonic development, is modulated by a diverse array of chemical compounds that intricately influence its activity. Retinoic Acid (302-79-4) and Estradiol (50-28-2) are paramount in this regulation, with Retinoic Acid binding to RARs to modulate HoxA13 transcription in developmental pathways, and Estradiol enhancing HoxA13 expression via estrogen receptors, especially in female reproductive tissues. Dihydrotestosterone (521-18-6) also plays a significant role, particularly in male genital development, by augmenting HoxA13 expression through androgen receptor interaction. Nutrient-related compounds such as Folic Acid (59-30-3) contribute by ensuring proper methylation and DNA synthesis, pivotal for HoxA13 function in embryogenesis, while Vitamin D3 (67-97-0) enhances HoxA13 expression in vitamin D responsive tissues through its receptor-mediated action.

The functionality of HoxA13 is further influenced by compounds that modify chromatin and DNA states. Sodium Butyrate (156-54-7) and Trichostatin A (58880-19-6), as histone deacetylase inhibitors, facilitate transcriptionally active chromatin states near the HOXA13 gene, promoting its expression. 5-Azacytidine (320-67-2), by inhibiting DNA methylation, can activate silenced genes, potentially enhancing HoxA13 expression. Additionally, Lithium Chloride (7447-41-8), through its influence on the Wnt signaling pathway, and Forskolin (66575-29-9), via elevating cAMP levels, contribute to the regulation of HoxA13 through signaling pathways that intersect with Hox gene regulation. Epigallocatechin Gallate (989-51-5) and Bisphenol A (80-05-7) also play roles in modulating HoxA13 activity, the former through its effects on oxidative stress-related pathways, and the latter by mimicking estrogenic activity, influencing Hox gene expression in estrogen-sensitive tissues. Collectively, these compounds enhance the functional activity of HoxA13, pivotal for its roles in development and organogenesis.

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