Anti-EDAR antibody [EPR8020]

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

The ectodysplasin A receptor also known as EDAR is a transmembrane protein involved in various developmental processes. It has a molecular mass of approximately 63 kDa. You can find EDAR expression in tissues such as the skin hair follicles and teeth. As a member of the tumor necrosis factor receptor (TNFR) family EDAR plays an important mechanical role by binding ectodysplasin A ligand (EDA) which initiates downstream signals important for developmental pathways.

Biological function summary

The interaction between EDAR and its ligand EDA influences morphogenesis of ectodermal-derived structures. This receptor-ligand binding is integral to the EDAR/NF-kappaB signaling complex. It affects processes such as the formation of hair follicles sweat glands and teeth. The receptor facilitates cell communication necessary for the proper development of these structures ensuring the correct activation of related signaling pathways.

Pathways

EDAR functions within the NF-kappaB and Wnt signaling pathways. These pathways regulate cellular differentiation and proliferation. The receptor collaborates with adapter proteins such as EDARADD to effectively transmit signals downstream. Furthermore it shares significant relationships with other TNF receptor family members highlighting the importance of signaling specificity and coordination within these biological pathways.

Associated diseases and disorders

Mutations in the EDAR gene associate with ectodermal dysplasia a genetic disorder affecting hair teeth and sweat glands. Additionally EDAR influences the development of hypohidrotic ectodermal dysplasia (HED). The receptor's link with EDA and other TNFR family members highlights the complex genetic interactions contributing to these conditions. Understanding these relationships provides insights into targeted therapeutic strategies addressing developmental abnormalities.