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pubmed-article:21683687pubmed:abstractTextThe high affinity IgE Fc receptor (Fc?RI) ? chain is well implicated as a signal amplifier through the immunoreceptor tyrosine-based activation motif (ITAM) in its C-terminal intracellular region. Our previous study, however, demonstrated that mutation in all of the three tyrosine residues within the Fc?RI? ITAM did not impair Fc?RI-induced cytokine production, suggesting a possible functional region other than the ITAM. To investigate the ITAM-independent mechanism by which Fc?RI? regulates Fc?RI-induced cytokine production, mouse mast cells expressing various Fc?RI? mutants were generated. We observed that truncation of the Fc?RI? C-terminus downstream of the ITAM resulted in a considerable decrease in Fc?RI-induced IL-6 production but not degranulation. Furthermore, mutagenesis of a single C-terminal aspartic acid (D234) to alanine (?-D234A) also significantly impaired IL-6 production. In addition, the similarity between the circular dichroism (CD) spectra of the wild type and ?-D234A suggests that the secondary structure of the Fc?RI? C-terminus was not affected by the D234A mutation. Consistently, we did not observe any effect of this mutation on Fc?RI-induced tyrosine phosphorylation of Fc?RI?. These observations strongly suggest a novel signaling pathway mediated by the cytoplasmic tail downstream of the Fc?RI? ITAM.lld:pubmed
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pubmed-article:21683687pubmed:authorpubmed-author:TeradaTomoyos...lld:pubmed
pubmed-article:21683687pubmed:copyrightInfoCopyright © 2011 Elsevier Inc. All rights reserved.lld:pubmed
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pubmed-article:21683687pubmed:articleTitleFc?RI-induced mast cell cytokine production critically involves an aspartic acid residue (D234) in the C-terminal intracellular domain of the Fc?RI? chain.lld:pubmed
pubmed-article:21683687pubmed:affiliationDivision of Molecular Cell Immunology and Allergology, Nihon University Graduate School of Medical Science, Tokyo, Japan.lld:pubmed
pubmed-article:21683687pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:21683687pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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