作者: Karin U. Schallreuter , Stefanie Behrens-Williams , Tahira P. Khaliq , Steven M. Picksley , Eva M. J. Peters
DOI: 10.1034/J.1600-0625.2003.00084.X
关键词: Pigmentation disorder 、 Oxidative stress 、 Wild type 、 Biology 、 Nuclear protein 、 Vitiligo 、 Cancer research 、 Epidermis (botany) 、 Melanin 、 Skin cancer
摘要: Despite the lack of protective melanin and increased oxidative stress due to mM concentrations epidermal H2O2 in vitiligo, there is no significantly risk for chronic actinic damage non-melanoma skin cancer. Therefore question arises, which mechanisms could be involved these patients preventing initiation cancers. Recently an overexpression p53 has been shown vitiligo. Unfortunately was further characterization this elevated p53. Employing a functional colour yeast assay, study presented herein demonstrates first time functioning wild-type protein both depigmented 'normal' pigmented epidermis with vitiligo compared healthy controls. Surprisingly long-term narrowband UVB (311 nm) treatment does not alter expression. Moreover, MDM-2, PCNA p21 expression remain unchanged This coincides decreased thioredoxin reductase (TR) levels whereas mRNA unaffected. Because TR one transcriptional target p53, results support functionality, supported by specific FASAY test. To our knowledge example persistent humans. Based on we hypothesize that low incidence damage, basal cell squamous carcinoma as documented well reside function up-regulated