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首页> 外文期刊>Signal transduction: Receptors, mediators and genes: Official journal of the Signal Transduction Society >Study of SHIP-binding cell surface proteins suggests c-kit as a SHIP-interacting receptor in mast cells
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Study of SHIP-binding cell surface proteins suggests c-kit as a SHIP-interacting receptor in mast cells

机译：SHIP结合细胞表面蛋白的研究表明c-kit是肥大细胞中与SHIP相互作用的受体

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Mast cells play a central role in a wide range of immunological and pathological processes, but are most noted for their role in IgE-dependent allergic responses. Aggregation of the high-affinity receptor for IgE, FcεRI, stimulates mast cell degranulation, production of lipid mediators, and the synthesis and secretion of cytokines and chemokines. FcεRI-induced mast cell activation is subject to regulation by inhibitory receptors that transduce intracellular signals via associating phosphatases. The inositol 5-phosphatase SHIP has been implicated in FcγRIIB-mediated inhibition of FcεRI-induced mast cell activation. However, SHIP also negatively regulates FcεRI signaling independent of FcγRIIB, suggesting the existence of additional receptors that mediate SHIP recruitment into sites where it mediates its inhibitory function. Here we show that SHIP associates with numerous phosphoproteins from pervanadate-stimulated mast cells. Based on their sensitivity to PNGase F treatment and cell surface biotinylation, some of these molecules may represent cell surface receptors. A prominent 120-130 kDa SHIP-binding phosphoprotein was identified in untreated RBL-2H3 cells and BMMC stimulated with stem cell factor. Based on its molecular weight, sensitivity to PNGase F, and reactivity with an anti-c-kit antibody, we conclude that this phosphoprotein is c-kit. Furthermore, tyrosine phosphorylation of SHIP is enhanced following SCF stimulation. Taken together, these data suggest that SHIP may function as a negative regulator of SCF signaling via direct association with phosphorylated c-kit.
机译：肥大细胞在广泛的免疫学和病理学过程中起着核心作用，但最著名的是它们在依赖IgE的过敏反应中的作用。 IgE的高亲和力受体FcεRI的聚集会刺激肥大细胞脱粒，脂质介体的产生以及细胞因子和趋化因子的合成和分泌。 FcεRI诱导的肥大细胞活化受到抑制性受体的调节，该抑制性受体通过磷酸酶转导细胞内信号。肌醇5-磷酸酶SHIP与FcγRIIB介导的对FcεRI诱导的肥大细胞活化的抑制有关。但是，SHIP还独立于FcγRIIB负调节FcεRI信号传导，表明存在其他受体，这些受体介导SHIP募集进入介导其抑制功能的位点。在这里，我们显示SHIP与过氧钒酸盐刺激的肥大细胞中的许多磷蛋白相关。基于它们对PNGase F处理和细胞表面生物素化的敏感性，其中一些分子可能代表细胞表面受体。在未处理的RBL-2H3细胞和干细胞因子刺激的BMMC中鉴定出一个突出的120-130 kDa SHIP结合磷蛋白。基于其分子量，对PNGase F的敏感性以及与抗c-kit抗体的反应性，我们得出结论，该磷蛋白是c-kit。此外，在SCF刺激后，SHIP的酪氨酸磷酸化增强。综上所述，这些数据表明SHIP可能通过与磷酸化的c-kit直接缔合而充当SCF信号传导的负调节剂。

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