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内皮细胞中的磷酸化蛋白质组学特征可预测 CML 中酪氨酸激酶抑制剂的血管毒性。

A phosphoproteomic signature in endothelial cells predicts vascular toxicity of tyrosine kinase inhibitors used in CML.

机构信息

Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA; and.

Broad Institute of MIT and Harvard, Cambridge, MA.

出版信息

Blood Adv. 2018 Jul 24;2(14):1680-1684. doi: 10.1182/bloodadvances.2018020396.

DOI:10.1182/bloodadvances.2018020396
PMID:30021779
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6058230/
Abstract

Newer CML kinase inhibitors increase ischemia risk and are toxic to endothelial cells where they produce a proteomic toxicity signature. This phosphoproteomic EC toxicity signature predicts bosutinib to be safe, providing a potential screening tool for safer drug development.

摘要

新型 CML 激酶抑制剂会增加缺血风险，并对内皮细胞有毒性，在这些细胞中会产生蛋白质组毒性特征。这种磷酸化蛋白质组学 EC 毒性特征表明博舒替尼是安全的，为更安全的药物开发提供了一种潜在的筛选工具。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e406/6058230/850952e10056/advances020396absf1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e406/6058230/850952e10056/advances020396absf1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e406/6058230/850952e10056/advances020396absf1.jpg

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Mol Cancer. 2018 Feb 19;17(1):49. doi: 10.1186/s12943-018-0780-6.
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Dasatinib Reversibly Disrupts Endothelial Vascular Integrity by Increasing Non-Muscle Myosin II Contractility in a ROCK-Dependent Manner.
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