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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Protein tyrosine phosphatase PTPN21 acts as a negative regulator of ICAM-1 by dephosphorylating IKKモ in TNF-メ-stimulated human keratinocytes
Young-Chang Cho1, Ba Reum Kim1, Sayeon Cho1,*
1College of pharmacy, Chung-Ang University
Intercellular adhesion molecule-1 (ICAM-1), which is induced by tumor necrosis factor (TNF)-メ, contributes to the entry of immune cells into the site of inflammation in the skin. Here, we show that protein tyrosine phosphatase non-receptor type 21 (PTPN21) negatively regulates ICAM-1 expression in human keratinocytes. PTPN21 expression was transiently induced after stimulation with TNF-メ. When overexpressed, PTPN21 inhibited the expression of ICAM-1 in HaCaT cells but PTPN21 C1108S, a phosphatase activity-inactive mutant, failed to inhibit ICAM-1 expression. Nuclear factor-リB (NF-リB), a key transcription factor of ICAM-1 gene expression, was inhibited by PTPN21, but not by PTPN21 C1108S. PTPN21 directly dephosphorylated phospho-inhibitor of リB (IリB)-kinase モ (IKKモ) at Ser177/181. This dephosphorylation led to the stabilization of IリBメ and inhibition of NF-リB activity. Taken together, our results suggest that PTPN21 could be a valuable molecular target for regulation of inflammation in the skin by dephosphorylating p-IKKモ and inhibiting NF-リB signaling.
Abstract, Accepted Manuscript(in press) [Submitted on August 26, 2017, Accepted on September 28, 2017]
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