Molecular mechanism of kallikrein‐related peptidase 8/neuropsin‐induced hyperkeratosis in inflamed skin
Molecular mechanism of kallikrein‐related peptidase 8/neuropsin‐induced hyperkeratosis in inflamed skin
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DOI：
10.1111/j.1365-2133.2010.09864.x
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发表时间：
2010-09
影响因子：
10.3
通讯作者：
K. Shingaki;S. Matsuzaki;M. Taniguchi;T. Kubo;T. Fujiwara;S. Kanazawa;A. Yamamoto;H. Tamura;T. Maeda;K. Ooi;K. Matsumoto;Sadao Shiosaka;M. Tohyama
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文献类型：
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作者：
K. Shingaki;S. Matsuzaki;M. Taniguchi;T. Kubo;T. Fujiwara;S. Kanazawa;A. Yamamoto;H. Tamura;T. Maeda;K. Ooi;K. Matsumoto;Sadao Shiosaka;M. Tohyama
背景角化过度和棘皮症发生在发炎的皮肤。角质形成细胞的增殖和分化是炎症后表皮修复的重要过程。已报道Neuropsin及其人类同源物激肽释放酶相关肽酶8（KLK 8）参与表皮增殖和分化，但所涉及的分子机制尚不清楚。
Background Hyperkeratosis and acanthosis occur in inflamed skin. Proliferation and differentiation of keratinocytes are important processes during epidermal repair after inflammation. Neuropsin and its human homologue kallikrein‐related peptidase 8 (KLK8) have been reported to be involved in epidermal proliferation and differentiation, but the involved molecular mechanisms are obscure.