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比较优化的 Syk siRNA 与 Syk 抑制剂在 FcepsilonRI 激活的 RBL-2H3 嗜碱性细胞中的抗过敏性活性。

Comparison of the anti-allergic activity of Syk inhibitors with optimized Syk siRNAs in FcepsilonRI-activated RBL-2H3 basophilic cells.

机构信息

Department of Pulmonary Diseases Research, Boehringer-Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany.

出版信息

Cell Immunol. 2010;262(1):28-34. doi: 10.1016/j.cellimm.2009.12.004. Epub 2009 Dec 14.

Abstract

Spleen tyrosine kinase (Syk) binds ITAM-bearing receptors in a wide variety of cell types. One such example is the activation of mast cells, basophils and eosinophils via the stimulation of the FcepsilonRI receptor by IgE/allergen complexes. The possible role of Syk in inflammatory signaling cascades has led to the development of pharmacological agents designed to block the Syk catalytic domain as potential novel therapeutics. Whilst the enzymatic activity of Syk lends towards the design of small-molecule inhibitors, other attention has focused on the possibility of targeting Syk expression using anti-sense oligonucleotides as an alternate means of anti-inflammatory therapy. In this study, we compared the ability of multiple optimized Syk siRNA sequences and small-molecule Syk inhibitors to block FcepsilonRI-mediated signal transduction, degranulation and TNFalpha secretion in the basophilic cell line RBL-2H3. We also characterized the specificity of each siRNA sequence with regards to off-target induction of the interferon-inducible gene IFIT1. We identified a single siRNA sequence, which displayed a favorable profile of efficient Syk knockdown, blockage of FcepsilonRI-mediated signal transduction, degranulation and TNFalpha secretion and a lack of IFIT1 induction. The effect of this siRNA was comparable to that of the Syk kinase domain inhibitors BAY61-3606 and R406. The identification of an active and specific Syk siRNA could be a basis for the development of therapeutic Syk siRNAs against inflammatory diseases.

摘要

脾脏酪氨酸激酶(Syk)结合 ITAM 受体在多种细胞类型中。一个这样的例子是通过 IgE/变应原复合物刺激 FcepsilonRI 受体激活肥大细胞、嗜碱性粒细胞和嗜酸性粒细胞。Syk 在炎症信号级联中的可能作用导致了设计旨在阻断 Syk 催化结构域的药理学制剂的发展,作为潜在的新型治疗方法。虽然 Syk 的酶活性有助于设计小分子抑制剂,但其他注意力集中在使用反义寡核苷酸靶向 Syk 表达作为替代抗炎治疗方法的可能性上。在这项研究中,我们比较了多种优化的 Syk siRNA 序列和小分子 Syk 抑制剂阻断嗜碱性细胞系 RBL-2H3 中 FcepsilonRI 介导的信号转导、脱颗粒和 TNFalpha 分泌的能力。我们还研究了每个 siRNA 序列针对干扰素诱导基因 IFIT1 的非靶诱导的特异性。我们确定了一个单一的 siRNA 序列,它显示了有效的 Syk 敲低、阻断 FcepsilonRI 介导的信号转导、脱颗粒和 TNFalpha 分泌以及缺乏 IFIT1 诱导的有利特征。该 siRNA 的效果可与 Syk 激酶结构域抑制剂 BAY61-3606 和 R406 相媲美。活性和特异性 Syk siRNA 的鉴定可能为开发针对炎症性疾病的治疗性 Syk siRNA 奠定基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/85f6/7124319/1a283ef66c76/gr1.jpg

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