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1
Targeted disruption of SHIP leads to Steel factor-induced degranulation of mast cells.SHIP的靶向破坏导致肥大细胞的Steel因子诱导的脱颗粒。
EMBO J. 1998 Dec 15;17(24):7311-9. doi: 10.1093/emboj/17.24.7311.
2
Thapsigargin-induced degranulation of mast cells is dependent on transient activation of phosphatidylinositol-3 kinase.毒胡萝卜素诱导的肥大细胞脱颗粒依赖于磷脂酰肌醇-3激酶的短暂激活。
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3
SHIP's C-terminus is essential for its hydrolysis of PIP3 and inhibition of mast cell degranulation.SHIP的C末端对于其水解磷脂酰肌醇-3,4,5-三磷酸（PIP3）和抑制肥大细胞脱颗粒至关重要。
Blood. 2001 Mar 1;97(5):1343-51. doi: 10.1182/blood.v97.5.1343.
4
The src homology 2-containing inositol phosphatase (SHIP) is the gatekeeper of mast cell degranulation.含Src同源2结构域的肌醇磷酸酶（SHIP）是肥大细胞脱颗粒的守门人。
Proc Natl Acad Sci U S A. 1998 Sep 15;95(19):11330-5. doi: 10.1073/pnas.95.19.11330.
5
Protein kinase C-delta is a negative regulator of antigen-induced mast cell degranulation.蛋白激酶C-δ是抗原诱导肥大细胞脱颗粒的负调节因子。
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6
The inositol 5'-phosphatase SHIP-2 negatively regulates IgE-induced mast cell degranulation and cytokine production.肌醇5'-磷酸酶SHIP-2负向调节IgE诱导的肥大细胞脱颗粒和细胞因子产生。
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7
Insulin and insulin-like growth factor-1 promote mast cell survival via activation of the phosphatidylinositol-3-kinase pathway.胰岛素及胰岛素样生长因子-1通过激活磷脂酰肌醇-3-激酶途径促进肥大细胞存活。
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8
Dysregulated FcepsilonRI signaling and altered Fyn and SHIP activities in Lyn-deficient mast cells.Lyn 缺陷型肥大细胞中 FcepsilonRI 信号失调以及 Fyn 和 SHIP 活性改变。
J Immunol. 2004 Jul 1;173(1):100-12. doi: 10.4049/jimmunol.173.1.100.
9
SHIP negatively regulates IgE + antigen-induced IL-6 production in mast cells by inhibiting NF-kappa B activity.SHIP通过抑制核因子κB活性负向调节肥大细胞中IgE加抗原诱导的白细胞介素-6的产生。
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10
Phosphatidylinositol (3,4,5)P3 is essential but not sufficient for protein kinase B (PKB) activation; phosphatidylinositol (3,4)P2 is required for PKB phosphorylation at Ser-473: studies using cells from SH2-containing inositol-5-phosphatase knockout mice.磷脂酰肌醇（3,4,5）三磷酸对于蛋白激酶B（PKB）的激活至关重要，但并不充分；磷脂酰肌醇（3,4）二磷酸是PKB在丝氨酸473位点磷酸化所必需的：使用含SH2结构域的肌醇-5-磷酸酶基因敲除小鼠的细胞进行的研究。
J Biol Chem. 2002 Mar 15;277(11):9027-35. doi: 10.1074/jbc.M106755200. Epub 2002 Jan 7.

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Stimulus strength determines the BTK-dependence of the SHIP1-deficient phenotype in IgE/antigen-triggered mast cells.刺激强度决定了 IgE/抗原触发的肥大细胞中 SHIP1 缺陷表型对 BTK 的依赖性。
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5
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Inhibitory effects of quail egg on mast cells degranulation by suppressing PAR2-mediated MAPK and NF-kB activation.鹌鹑蛋通过抑制PAR2介导的MAPK和NF-κB激活对肥大细胞脱颗粒的抑制作用。
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Differential Lyn-dependence of the SHIP1-deficient mast cell phenotype.SHIP1 缺陷型肥大细胞表型对 Lyn 的不同依赖性。
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9
Mast cells in airway diseases and interstitial lung disease.气道疾病和间质性肺疾病中的肥大细胞。
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本文引用的文献

1
Growth factors and insulin stimulate tyrosine phosphorylation of the 51C/SHIP2 protein.生长因子和胰岛素刺激51C/SHIP2蛋白的酪氨酸磷酸化。
J Biol Chem. 1998 Jul 17;273(29):18605-9. doi: 10.1074/jbc.273.29.18605.
2
Targeted disruption of SHIP leads to hemopoietic perturbations, lung pathology, and a shortened life span.SHIP的靶向破坏会导致造血紊乱、肺部病变以及寿命缩短。
Genes Dev. 1998 Jun 1;12(11):1610-20. doi: 10.1101/gad.12.11.1610.
3
SHIP modulates immune receptor responses by regulating membrane association of Btk.SHIP通过调节Btk的膜结合来调节免疫受体反应。
Immunity. 1998 Apr;8(4):509-16. doi: 10.1016/s1074-7613(00)80555-5.
4
Sphingosine kinase-mediated Ca2+ signalling by G-protein-coupled receptors.鞘氨醇激酶介导的G蛋白偶联受体Ca2+信号传导
EMBO J. 1998 May 15;17(10):2830-7. doi: 10.1093/emboj/17.10.2830.
5
Involvement of Bruton's tyrosine kinase in FcepsilonRI-dependent mast cell degranulation and cytokine production.布鲁顿酪氨酸激酶参与FcεRI依赖性肥大细胞脱颗粒和细胞因子产生。
J Exp Med. 1998 Apr 20;187(8):1235-47. doi: 10.1084/jem.187.8.1235.
6
The SH2-containing inositol polyphosphate 5-phosphatase, ship, is expressed during hematopoiesis and spermatogenesis.含SH2结构域的肌醇多磷酸5-磷酸酶SHIP在造血和精子发生过程中表达。
Blood. 1998 Apr 15;91(8):2753-9.
7
Btk/Tec kinases regulate sustained increases in intracellular Ca2+ following B-cell receptor activation.Btk/Tec激酶调节B细胞受体激活后细胞内钙离子（Ca2+）的持续增加。
EMBO J. 1998 Apr 1;17(7):1973-85. doi: 10.1093/emboj/17.7.1973.
8
Phosphatidylinositol-3,4,5-trisphosphate (PtdIns-3,4,5-P3)/Tec kinase-dependent calcium signaling pathway: a target for SHIP-mediated inhibitory signals.磷脂酰肌醇-3,4,5-三磷酸（PtdIns-3,4,5-P3）/Tec激酶依赖性钙信号通路：SHIP介导的抑制性信号的靶点。
EMBO J. 1998 Apr 1;17(7):1961-72. doi: 10.1093/emboj/17.7.1961.
9
Wortmannin-sensitive phosphorylation, translocation, and activation of PLCgamma1, but not PLCgamma2, in antigen-stimulated RBL-2H3 mast cells.在抗原刺激的RBL - 2H3肥大细胞中，wortmannin敏感的PLCγ1而非PLCγ2的磷酸化、易位及激活。
Mol Biol Cell. 1998 Feb;9(2):483-96. doi: 10.1091/mbc.9.2.483.
10
Activation of phospholipase C gamma by PI 3-kinase-induced PH domain-mediated membrane targeting.磷脂酰肌醇3激酶诱导的PH结构域介导的膜靶向作用激活磷脂酶Cγ 。
EMBO J. 1998 Jan 15;17(2):414-22. doi: 10.1093/emboj/17.2.414.

SHIP的靶向破坏导致肥大细胞的Steel因子诱导的脱颗粒。

Targeted disruption of SHIP leads to Steel factor-induced degranulation of mast cells.

作者信息

Huber M, Helgason C D, Scheid M P, Duronio V, Humphries R K, Krystal G

机构信息

Terry Fox Laboratory, BC Cancer Agency, 601 West 10th Avenue, Vancouver, BC, V5Z IL3, Canada.

出版信息

EMBO J. 1998 Dec 15;17(24):7311-9. doi: 10.1093/emboj/17.24.7311.

DOI:10.1093/emboj/17.24.7311
PMID:9857188
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1171077/
Abstract

To investigate the role of the src homology 2 (SH2)-containing inositol 5' phosphatase (SHIP) in growth factor-mediated signalling, we compared Steel factor (SF)-induced events in bone marrow-derived mast cells (BMMCs) from SHIP-/- and SHIP+/+ littermates. We found SF alone stimulated massive degranulation from SHIP-/- but none from SHIP+/+ BMMCs. This SF-induced degranulation, which was not due to higher c-kit levels in SHIP-/- cells, correlated with higher intracellular calcium than that in SHIP+/+ cells and was dependent on the influx of extracellular calcium. Both this influx and subsequent degranulation were completely inhibited by PI-3-kinase inhibitors, indicating that SF-induced activation of PI-3-kinase was upstream of extracellular calcium entry. A comparison of phosphatidylinositol-3,4,5-trisphosphate (PIP3) levels following SF stimulation of SHIP+/+ and SHIP-/- BMMCs suggested that SHIP restricted this entry by hydrolyzing PIP3. Although PI-3-kinase inhibitors blocked the release of intracellular calcium, implicating PIP3, and PLCgamma-2 was slightly more tyrosine phosphorylated in SHIP-/- cells, the increase in inositol-1,4,5-trisphosphate (IP3) and intracellular calcium levels were identical in SHIP-/- and SHIP+/+ BMMCs. These results suggest that SHIP prevents SF from triggering degranulation of normal BMMCs, and does so by hydrolyzing PIP3, which in turn limits extracellular calcium entry at a step after the release of intracellular calcium.

摘要

为了研究含src同源2（SH2）结构域的肌醇5'磷酸酶（SHIP）在生长因子介导的信号传导中的作用，我们比较了SHIP基因敲除小鼠（SHIP-/-）和野生型同窝小鼠（SHIP+/+）骨髓来源肥大细胞（BMMCs）中，干细胞因子（SF）诱导的相关事件。我们发现单独的SF可刺激SHIP-/- BMMCs大量脱颗粒，但对SHIP+/+ BMMCs无此作用。这种SF诱导的脱颗粒，并非由于SHIP-/-细胞中c-kit水平较高，其与SHIP+/+细胞相比，细胞内钙水平更高，且依赖于细胞外钙的内流。这种内流及随后的脱颗粒均被PI-3激酶抑制剂完全抑制，表明SF诱导的PI-3激酶激活位于细胞外钙内流的上游。比较SF刺激SHIP+/+和SHIP-/- BMMCs后磷脂酰肌醇-3,4,5-三磷酸（PIP3）的水平，提示SHIP通过水解PIP3来限制这种内流。尽管PI-3激酶抑制剂可阻断细胞内钙的释放，提示PIP3参与其中，且SHIP-/-细胞中PLCγ-2的酪氨酸磷酸化略增加，但SHIP-/-和SHIP+/+ BMMCs中肌醇-1,4,5-三磷酸（IP3）和细胞内钙水平的升高是相同的。这些结果表明，SHIP可阻止SF触发正常BMMCs的脱颗粒，其机制是通过水解PIP3，进而在细胞内钙释放后的一个步骤限制细胞外钙的内流。