Recombinant Human EDA protein

Supplementary information

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

EDA also known as Ectodysplasin A is a protein encoded by the EDA gene. It is a member of the tumor necrosis factor (TNF) family and is expressed in epithelial cells. The molecular mass of EDA is approximately 47 kDa. EDA plays a mechanical role in signaling processes that are important for developmental pathways. Its expression is observed in tissues like skin hair follicles and some glandular cells where it contributes to cellular communication.

Biological function summary

Ectodysplasin A influences the development and differentiation of epithelial tissues. It plays a role in the formation of hair shafts sweat glands and other ectodermal structures. EDA operates as part of a signaling complex influencing cell fate decisions through binding to its receptor EDA receptor (EDAR). This interaction initiates processes for the development and maintenance of these structures impacting cell proliferation and differentiation.

Pathways

Not only does EDA interact in the TNF signaling pathway it also engages in the NF-kB pathway. The NF-kB pathway initiates transcription of genes responsible for cell survival and inflammatory responses. EDA interaction with EDAR also involves signaling pathways intersecting with NF-kB leading to activation of downstream proteins like TRAF6 and NEMO. These proteins orchestrate cell proliferation and apoptotic regulation confirming EDA's role in strategic developmental and signaling pathways.

Abnormal function or mutations in EDA link to conditions such as X-linked hypohidrotic ectodermal dysplasia (XLHED) and immune system irregularities. XLHED occurs due to EDA gene mutations leading to missing or improperly developed ectodermal structures like hair and teeth. EDA's association with XLHED connects it to EDAR and down to other proteins such as NF-kB indicating the broader genetic mutations' impact on downstream signaling which results in specific phenotype alterations seen in the disorder.