Kljuic, A and Bazzi, H and Sundberg, J. P. and Martinez-Mir, A. and O'Shaughnessy, R. and Mahoney, M. G. and Levy, M. and Montagutelli, X. and Ahmad, W. and Aita, V. M. and Gordon, D. and Uitto, J. and Whiting, D. and Ott, J. and Fischer, S. and Gilliam, T. C. and Jahoda, C. A. B. and Morris, R. J. and Panteleyev, A. A. and Nguyen, V. T. and Christiano, A. M. (2003) 'Desmoglein 4 in hair follicle differentiation and epidermal adhesion : evidence from inherited hypotrichosis and acquired pemphigus vulgaris.', Cell., 113 (2). pp. 249-260.
Cell adhesion and communication are interdependent aspects of cell behavior that are critical for morphogenesis and tissue architecture. In the skin, epidermal adhesion is mediated in part by specialized cell-cell junctions known as desmosomes, which are characterized by the presence of desmosomal cadherins, known as desmogleins and desmocollins. We identified a cadherin family member, desmoglein 4, which is expressed in the suprabasal epidermis and hair follicle. The essential role of desmoglein 4 in skin was established by identifying mutations in families with inherited hypotrichosis, as well as in the lanceolate hair mouse. We also show that DSG4 is an autoantigen in pemphigus vulgaris. Characterization of the phenotype of naturally occurring mutant mice revealed disruption of desmosomal adhesion and perturbations in keratinocyte behavior. We provide evidence that desmoglein 4 is a key mediator of keratinocyte cell adhesion in the hair follicle, where it coordinates the transition from proliferation to differentiation.
|Full text:||Full text not available from this repository.|
|Publisher Web site:||http://dx.doi.org/10.1016/S0092-8674(03)00273-3|
|Date accepted:||No date available|
|Date deposited:||No date available|
|Date of first online publication:||April 2003|
|Date first made open access:||No date available|
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