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Glossary Ectodysplasin A

regulates development of skin, hair, teeth, and sweat glands

Ectodysplasin A (Eda) is a protein crucial for the development of ectodermal tissues, which include skin, hair, teeth, and sweat glands. Mutations in the EDA gene can lead to ectodermal dysplasias, a group of disorders characterized by abnormalities in these tissues, often resulting in sparse hair, missing teeth, and reduced ability to sweat.

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research Stimulation of ectodermal organ development by Ectodysplasin-A1

249 citations , May 2003 in “Developmental Biology”

Ectodysplasin-A1 is crucial for developing hair, teeth, and glands.

research Identification of dkk4 as a target of Eda-A1/Edar pathway reveals an unexpected role of ectodysplasin as inhibitor of Wnt signalling in ectodermal placodes

117 citations , April 2008 in “Developmental biology”

This study identified that Eda-A1 unexpectedly induces placode inhibitors dkk4 and lrp4, indicating the importance of tightly regulated signaling for proper ectodermal organ development.

research Enhanced ectodysplasin-A receptor (EDAR) signaling alters multiple fiber characteristics to produce the East Asian hair form

98 citations , June 2008 in “Human mutation”

This study found that a genetic variant in the EDAR gene leads to typical East Asian hair characteristics by increasing signaling output, as shown in transgenic mice experiments.

research Identification of Ectodysplasin Target Genes Reveals the Involvement of Chemokines in Hair Development

48 citations , January 2012 in “The journal of investigative dermatology/Journal of investigative dermatology”

This study identified chemokine receptor ligands cxcl10 and cxcl11 as new hair-specific transcriptional targets of the Eda pathway, suggesting chemokine signaling plays a role in primary hair follicle patterning.

research Expression of Foxi3 is regulated by ectodysplasin in skin appendage placodes

43 citations , February 2013 in “Developmental dynamics”

This study found that Eda and activin A regulate Foxi3 expression, which may contribute to the development of hypohidrotic ectodermal dysplasia by affecting Foxi3 activity in ectodermal appendages like hair and teeth.

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