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Gene Review

Edar  -  ectodysplasin-A receptor

Mus musculus

Synonyms: Anhidrotic ectodysplasin receptor 1, Dl, Downless, ED1R, ED3, ...
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Disease relevance of Edar


Psychiatry related information on Edar


High impact information on Edar

  • Mice with mutations in the downless (dl) gene have defects in hair follicle induction, lack sweat glands and have malformed teeth [3].
  • The mutated locus has been physically mapped in this family, and a 200-kb mouse YAC clone, YAC D9, has been identified and shown to rescue the dl phenotype in the spontaneous dl(Jackson) (dl(J), recessive) and Dl(sleek) (Dl(slk), dominant negative) mutants [3].
  • One branch of the family, dl(OVE1B), carries an approximately 600-kb deletion at the dl locus caused by transgene integration [3].
  • Edar is a death domain protein of the TNFR family that is required for the development of hair, teeth and other ectodermal derivatives [4].
  • The crux of this patterning mechanism is rapid Edar-positive feedback in the epidermis coupled with induction of dermal BMP4/7 [5].

Biological context of Edar

  • Edar/Eda interactions regulate enamel knot formation in tooth morphogenesis [6].
  • We could not, however, reproduce the downless phenotype, suggesting the existence of yet another ligand or receptor, or of ligand-independent activation mechanisms for Edar [6].
  • Catagen development accompanied by increased apoptosis in the outer root sheath was significantly accelerated in downless mice or after treatment of wild-type mice by a fusion protein that inhibits Edar signaling, compared with the corresponding controls [7].
  • Ectodysplasin, Edar and TNFRSF19 are expressed in complementary and overlapping patterns during mouse embryogenesis [8].
  • Genetic and experimental studies suggest that Edar signaling is involved in the control of cell fate decision in embryonic epidermis, as well as in the regulation of cell differentiation programs in the HF [9].

Anatomical context of Edar

  • Regulation of hair follicle development by the TNF signal ectodysplasin and its receptor Edar [10].
  • We show that Eda and Edar expression is confined to the ectoderm and occurs in a pattern that suggests a role of ectodysplasin/Edar signaling in the interactions between the ectodermal compartments and the formation and function of hair placodes [10].
  • By adding a soluble form of Edar to tooth germs, we were able to mimic the tabby enamel knot phenotype, demonstrating the involvement of endogenous Eda in tooth development [6].
  • tabby and downless mutant mice have apparently identical defects in teeth, hair and sweat glands [6].
  • Thus, our data demonstrate that in addition to its well-established role in HF morphogenesis, Edar signaling is also involved in hair cycle control and regulates apoptosis in HF keratinocytes during catagen [7].

Associations of Edar with chemical compounds

  • Ectodysplasin (Eda), a member of the tumor necrosis factor (TNF) superfamily, and its receptor Edar are necessary components of ectodermal organ development [8].
  • THC most closely resembled DPH in the tests with chemical convulsant agents, but a sedative action of THC, resembling that of PB and CDP, was indicated by low ED5 0 for increased latency and for prevention of mortality in the MES test [11].

Regulatory relationships of Edar


Other interactions of Edar


Analytical, diagnostic and therapeutic context of Edar


  1. Ectodysplasin signaling in development. Mikkola, M.L., Thesleff, I. Cytokine Growth Factor Rev. (2003) [Pubmed]
  2. Reversal of adenine-induced depression of mouse locomotor activity by amphetamine. Akintonwa, A., Auditore, J.V. Archives internationales de pharmacodynamie et de thérapie. (1978) [Pubmed]
  3. Involvement of a novel Tnf receptor homologue in hair follicle induction. Headon, D.J., Overbeek, P.A. Nat. Genet. (1999) [Pubmed]
  4. Gene defect in ectodermal dysplasia implicates a death domain adapter in development. Headon, D.J., Emmal, S.A., Ferguson, B.M., Tucker, A.S., Justice, M.J., Sharpe, P.T., Zonana, J., Overbeek, P.A. Nature (2001) [Pubmed]
  5. Generation of the primary hair follicle pattern. Mou, C., Jackson, B., Schneider, P., Overbeek, P.A., Headon, D.J. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  6. Edar/Eda interactions regulate enamel knot formation in tooth morphogenesis. Tucker, A.S., Headon, D.J., Schneider, P., Ferguson, B.M., Overbeek, P., Tschopp, J., Sharpe, P.T. Development (2000) [Pubmed]
  7. Involvement of the edar signaling in the control of hair follicle involution (catagen). Fessing, M.Y., Sharova, T.Y., Sharov, A.A., Atoyan, R., Botchkarev, V.A. Am. J. Pathol. (2006) [Pubmed]
  8. Ectodysplasin, Edar and TNFRSF19 are expressed in complementary and overlapping patterns during mouse embryogenesis. Pispa, J., Mikkola, M.L., Mustonen, T., Thesleff, I. Gene Expr. Patterns (2003) [Pubmed]
  9. Edar signaling in the control of hair follicle development. Botchkarev, V.A., Fessing, M.Y. J. Investig. Dermatol. Symp. Proc. (2005) [Pubmed]
  10. Regulation of hair follicle development by the TNF signal ectodysplasin and its receptor Edar. Laurikkala, J., Pispa, J., Jung, H.S., Nieminen, P., Mikkola, M., Wang, X., Saarialho-Kere, U., Galceran, J., Grosschedl, R., Thesleff, I. Development (2002) [Pubmed]
  11. Anticonvulsant activity of delta9-tetrahydrocannabinol compared with three other drugs. Sofia, R.D., Solomon, T.A., Barry, H. Eur. J. Pharmacol. (1976) [Pubmed]
  12. Mucosal addressin cell adhesion molecule 1 plays an unexpected role in the development of mouse guard hair. Nishioka, E., Tanaka, T., Yoshida, H., Matsumura, K., Nishikawa, S., Naito, A., Inoue, J., Funasaka, Y., Ichihashi, M., Miyasaka, M., Nishikawa, S. J. Invest. Dermatol. (2002) [Pubmed]
  13. NF-kappaB transmits Eda A1/EdaR signalling to activate Shh and cyclin D1 expression, and controls post-initiation hair placode down growth. Schmidt-Ullrich, R., Tobin, D.J., Lenhard, D., Schneider, P., Paus, R., Scheidereit, C. Development (2006) [Pubmed]
  14. Mapping of six dominant cataract genes in the mouse. Everett, C.A., Glenister, P.H., Taylor, D.M., Lyon, M.F., Kratochvilova-Loester, J., Favor, J. Genomics (1994) [Pubmed]
  15. Embryonic dermal condensation and adult dermal papilla induce hair follicles in adult glabrous epidermis through different mechanisms. Inamatsu, M., Tochio, T., Makabe, A., Endo, T., Oomizu, S., Kobayashi, E., Yoshizato, K. Dev. Growth Differ. (2006) [Pubmed]
  16. TNF signaling via the ligand-receptor pair ectodysplasin and edar controls the function of epithelial signaling centers and is regulated by Wnt and activin during tooth organogenesis. Laurikkala, J., Mikkola, M., Mustonen, T., Aberg, T., Koppinen, P., Pispa, J., Nieminen, P., Galceran, J., Grosschedl, R., Thesleff, I. Dev. Biol. (2001) [Pubmed]
  17. YAC rescue of downless locus mutations in mice. Majumder, K., Shawlot, W., Schuster, G., Harrison, W., Elder, F.F., Overbeek, P.A. Mamm. Genome (1998) [Pubmed]
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