Journal Article

Anhidrotic Ectodermal Dysplasia (EDA) Protein Expressed in MCF-7 Cells Associates with Cell Membrane and Induces Rounding

Sini Ezer, David Schlessinger, Anand Srivastava and Juha Kere

in Human Molecular Genetics

Volume 6, issue 9, pages 1581-1587
Published in print September 1997 | ISSN: 0964-6906
Published online September 1997 | e-ISSN: 1460-2083 | DOI: http://dx.doi.org/10.1093/hmg/6.9.1581
Anhidrotic Ectodermal Dysplasia (EDA) Protein Expressed in MCF-7 Cells Associates with Cell Membrane and Induces Rounding

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Anhidrotic ectodermal dysplasia (EDA) is a rare X-linked recessive disorder characterized by the absence or hypoplasia of hair, teeth and sweat glands. The gene responsible for the disorder has recently been cloned. The predicted gene product is a 135 amino acid protein with no significant homology to previously known proteins. As a first step to analyze function, we have studied the subcellular localization of the EDA gene product expressed in two epithelial cell lines, COS-1 and MCF-7. Biochemical fractionation and confocal imaging analysis show that, in agreement with a single putative transmembrane domain inferred from its sequence, the EDA protein is transported to the plasma membrane. Moreover, in MCF-7 cells expression of EDA is associated with rounding and detachment of the cells. These results suggest that the EDA protein may be involved in cellular dynamics or signaling.

Journal Article.  4745 words.  Illustrated.

Subjects: Genetics and Genomics

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