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ectodysplasin A

La EDA gene provides instructions for making a protein called ectodysplasin A. This protein is part of a signaling pathway that plays an important role in development before birth. Specifically, it is critical for interactions between two embryonic cell layers called the ectoderm and the mesoderm. In the early embryo, these cell layers form the basis for many of the body's organs and tissues. Ectoderm-mesoderm interactions are essential for the formation of several structures that arise from the ectoderm, including the skin, hair, nails, teeth, and sweat glands.

Normal function

La EDA gene provides instructions for making a protein called ectodysplasin A. This protein is part of a signaling pathway that plays an important role in development before birth. Specifically, it is critical for interactions between two embryonic cell layers called the ectoderm and the mesoderm. In the early embryo, these cell layers form the basis for many of the body's organs and tissues. Ectoderm-mesoderm interactions are essential for the formation of several structures that arise from the ectoderm, including the skin, hair, nails, teeth, and sweat glands.

One version of the ectodysplasin A protein, known as ectodysplasin A1, interacts with a protein called the ectodysplasin A receptor (produced from the EDAR gene). On the cell surface, ectodysplasin A1 attaches to this receptor like a key in a lock. When these two proteins are connected, they trigger a series of chemical signals that affect cell activities such as division, growth, and maturation. Starting before birth, this signaling pathway controls the formation of ectodermal structures such as hair follicles, sweat glands, and teeth.

Conditions referring to this gene or chromosome

Other names

Ectodermal dysplasia protein

ectodysplasin

ectodysplasin-A

ED1

ED1-A1

EDA-A1

EDA-A2

EDA1

EDA_HUMAN

HED

XHED

XLHED

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Lectures complémentaires et références

Historique de l'article

Les informations sur cette page sont rédigées et examinées par des cliniciens qualifiés.
  • 18 Aug 2020 | Dernière version
  • 1 Nov 2018 | Publié à l'origine

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