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pubmed-article:18289606pubmed:abstractTextMast cells play a central role in allergic disease and host defense against several pathogens through the release of various bioactive compounds via degranulation. In this study, we found that a myristoylated pseudosubstrate of PKC-zeta (zeta-PS; myristoyl-SIYRRGARRWRKL, a PKC-zeta inhibitor) regulates mast cell degranulation. zeta-PS increased [Ca+2]i level at nanomolar concentrations in a PKC-zeta activity-independent manner in HMC-1 cells. Moreover, zeta-PS-induced [Ca+2]i generation was completely abrogated by phospholipase C (PLC), IP3 receptor or Galpha i/o inhibitor and zeta-PS potently induced degranulation in HMC-1 cells which was significantly inhibited by pretreating PLC inhibitors or a calcium chelator. Therefore, our results suggest that zeta-PS can induce degranulation in HMC-1 cells by triggering the calcium signal via a PKC-zeta-independent but Galpha i/o, PLC and IP3-dependent pathways.lld:pubmed
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pubmed-article:18289606pubmed:articleTitleA myristoylated pseudosubstrate peptide of PKC-zeta induces degranulation in HMC-1 cells independently of PKC-zeta activity.lld:pubmed
pubmed-article:18289606pubmed:affiliationDepartment of Life Science, Division of Molecular and Life Science, Biotech Center, Pohang University of Science and Technology, San 31 Hyoja-Dong, Nam-Gu, Pohang, Kyungbuk 790-784, Republic of Korea.lld:pubmed
pubmed-article:18289606pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:18289606pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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