Peter Pedersen

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p63-specific activation of the BPAG-1e promoter.

Motonobu Osada; Yuichi Nagakawa; Hannah Lui Park; Keishi Yamashita; Guojun Wu; Myoung Sook Kim; Alexey Fomenkov; Barry Trink; David Sidransky (Profiled Authors: David Sidransky; Myoung Kim; Barry Trink)

Department of Otolaryngology, Division of Head and Neck Cancer Research, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. osadamotonobu@yahoo.com
The Journal of investigative dermatology 2005;125(1):52-60.

p63, a member of the p53 superfamily, is an essential cell fate determinant for stratified epithelium. Deficiency of p63 leads to lack of differentiated epithelium from the skin and the presence of trace undifferentiated cells left in the dermis. We found that transcriptionally active isoforms of p63, TAp63beta and TAp63gamma, activated the skin-specific promoter of bullous pemphigoid antigen 1 (BPAG-1). The p63-response element was localized between bases -177 and -153 upstream of exon 1 in the BPAG-1e promoter, whereas regions surrounding the response element suppressed transcriptional responses to p53 and TAp73beta, resulting in p63-specific activation of the promoter. This represents a novel molecular mechanism by which target gene induction by p63 is distinguished from induction by other p53 family members.

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