Negative signaling in B lymphocytes induces tyrosine phosphorylation of the 145-kDa inositol polyphosphate 5-phosphatase, SHIP.
Negative signaling in B lymphocytes induces tyrosine phosphorylation of the 145-kDa inositol polyphosphate 5-phosphatase, SHIP.
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DOI：
10.4049/jimmunol.157.6.2234
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发表时间：
1996-09
影响因子：
4.4
通讯作者：
George Chacko;S. Tridandapani;J. Damen;L. Liu;G. Krystal;K. Coggeshall
中科院分区：
文献类型：
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作者：
George Chacko;S. Tridandapani;J. Damen;L. Liu;G. Krystal;K. Coggeshall
刺激B细胞Ag受体（BCR）已被报道诱导145-kDa蛋白的酪氨酸磷酸化及其与衔接蛋白Shc的缔合。我们已经确定这种蛋白质的新肌醇多磷酸5-磷酸酶（SHIP）。进一步的分析显示，SHIP的最大磷酸化及其与Shc的结合都需要与IgG的Fc受体（Fc γ RII）共聚簇，而不是单独刺激BCR。由于BCR和Fc γ RII的共同聚集也下调了Ag受体刺激诱导的增殖，因此我们假设SHIP的酪氨酸磷酸化及其与Shc的相关性通过影响肌醇和磷脂酰肌醇代谢而促进了负信号传导。
Stimulation of the B cell Ag receptor (BCR) has been reported to induce tyrosine phosphorylation of a 145-kDa protein and its association with the adapter protein Shc. We have identified this protein as the novel inositol polyphosphate 5-phosphatase (SHIP). Further analysis revealed that both maximal phosphorylation of SHIP and its association with Shc require co-clustering with the Fc receptor for IgG (Fc gamma RII) rather than stimulation of the BCR alone. Since co-clustering of the BCR and Fc gamma RII also down-regulates proliferation induced by Ag receptor stimulation, we hypothesize that tyrosine phosphorylation of SHIP and its association with Shc contribute to negative signaling through effects on inositol and phosphatidylinositol metabolism.