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A more recent version of this article appeared on November 26, 2004
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M406322200v1
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Papers In Press, published online ahead of print September 12, 2004
J. Biol. Chem, 10.1074/jbc.M406322200
Submitted on June 7, 2004
Revised on August 30, 2004
Accepted on September 12, 2004

p51/p63 controls subunit alpha3 of the major epidermis integrin anchoring the stem cells to the niche

Shun-ichi Kurata, Takeshi Okuyama, Motonobu Osada, Tatsuya Watanabe, Yoshiya Tomimori, Shingo Sato, Aki Iwai, Tsutomu Tsuji, Yoji Ikawa, and Iyoko Katoh

Ikawa Laboratory, RIKEN, Institute of Physical and Chemical Research, Wako, Saitama 351-0198

Corresponding Author: peace{at}postman.riken.jp

p51/p63, a member of the tumor suppressor p53 gene family, is crucial for skin development. We describe here identification of itga3 encoding integrin alpha3 as a target of its trans-activating function, proposing that p51/p63 allows epidermal stem cells to express laminin receptor alpha3beta1 for anchorage to the basement membrane. When activated by genotoxic stress or overexpressed ectopically in non-adherent cells, p51/p63 transduced a phenotype to attach to extracellular matrices, which was accompanied by alpha3 expression. Motifs matching the p53-binding consensus sequence were located in a scattered form in intron 1 of human itga3, and served as p51/p63-responsive elements in reporter assays. In addition to the trans-activating ability of the TA isoform, we detected a positive effect of the deltaN isoform on itga3. The high level alpha3 production in human keratinocyte stem cells diminished upon elimination of p51/p63 by siRNA or by Ca(2+)-induced differentiation. Furthermore, a chromatin immunoprecipitation experiment indicated a physical interaction of p51/p63 with intron 1 of itga3. This study provides a molecular basis for the standing hypothesis that p51/p63 is essential for epidermal-mesenchymal interactions.


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