Healing a natural knockout of epithelial organogenesis

Trends in Molecular Medicine

Volumn 8, Issue 5, 2002, Pages 197-200

  Kere, Juha ^a,b   Elomaa, Outi ^b  

^a KAROLINSKA INSTITUTE   (Sweden)

^b UNIVERSITY OF HELSINKI   (Finland)

Author keywords

[No Author keywords available]

Indexed keywords

ANHIDROTIC ECTODERMAL DYSPLASIA; ARTICLE; CHROMOSOMAL LOCALIZATION; CHROMOSOME 13Q; CHROMOSOME 1Q; CHROMOSOME 2Q; CHROMOSOME XQ; ECTODERMAL DYSPLASIA; GENE FUNCTION; HUMAN; KNOCKOUT MOUSE; MOLECULAR CLONING; NONHUMAN; PATHOPHYSIOLOGY; SIGNAL TRANSDUCTION;

EID: 0036256086     PISSN: 14714914     EISSN: None     Source Type: Journal    
DOI: 10.1016/S1471-4914(02)02342-0     Document Type: Short Survey

References (26)

1. Ectodysplasin-A1 is sufficient to rescue both hair growth and sweat glands in Tabby mice
2. X-linked anhidrotic (hypohidrotic) ectodermal dysplasia is caused by mutation in a novel transmembrane protein
3. Cloning of Tabby, the murine homolog of the human EDA gene: Evidence for a membrane-associated protein with a short collagenous domain
4. The Tabby phenotype is caused by mutation in a mouse homologue of the EDA gene that reveals novel mouse and human exons and encodes a protein (ectodysplasin-A) with collagenous domains
5. The TNF and TNF receptor superfamilies; integrating mammalian biology
6. Ectodysplasin is a collagenous trimeric type II membrane protein with a tumor necrosis factor-like domain and co-localizes with cytoskeletal structures at lateral and apical surfaces of cells
7. Ectodysplasin, a protein required for epithelial morphogenesis, is a novel TNF homologue and promotes cell-matrix adhesion
8. Involvement of a novel Tnf receptor homologue in hair follicle induction
9. Mutations in the human homologue of mouse dl cause autosomal recessive and dominant hypohidrotic ectodermal dysplasia
10. The anhidrotic ectodermal dysplasia gene (EDA) undergoes alternative splicing and encodes ectodysplasin-A with deletion mutations in collagenous repeats
11. Two-amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors
12. Ectodysplasin is released by proteolytic shedding and binds to the EDAR protein
13. Mutations within a furin consensus sequence block proteolytic release of ectodysplasin-A and cause X-linked hypohidrotic ectodermal dysplasia
14. Mutations leading to X-linked hypohidrotic ectodermal dysplasia affect three major functional domains in the tumor necrosis factor family member ectodysplasin-A
15. The ectodermal dysplasia receptor activates the nuclear factor-κB, JNK, and cell death pathways and binds to ectodysplasin A
16. Signaling and subcellular localization of the TNF receptor Edar
17. Gene defect in ectodermal dysplasia implicates a death domain adapter in development
18. Genomic rearrangement in NEMO impairs NF-κB activation and is a cause of incontinentia pigmenti
19. The IKK complex: An integrator of all signals that activate NF-κB?
20. X-linked anhidrotic ectodermal dysplasia with immunodeficiency is caused by impaired NF-κB signaling
21. A novel X-linked disorder of immune deficiency and hypohidrotic ectodermal dysplasia is allelic to incontinentia pigmenti and due to mutations in IKK-γ (NEMO)
22. Requirement of NF-κB/Rel for the development of hair follicles and other epidermal appendices
23. 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
24. Development of several organs that require inductive epithelial-mesenchymal interactions is impaired in LEF-1-deficient mice
25. β-catenin controls hair follicle morphogenesis and stem cell differentiation in the skin
26. Mutations in GJB6 cause hidrotic ectodermal dysplasia