Infectious and Inflammatory Disease Center, Sanford-Burnham Medical Research Institute, La Jolla, California, United States of America.
PLoS One. 2010 Jun 24;5(6):e11305. doi: 10.1371/journal.pone.0011305.
Furin, a specialized endoproteinase, transforms proproteins into biologically active proteins. Furin function is important for normal cells and also in multiple pathologies including malignancy and anthrax. Furin is believed to cycle between the Golgi compartment and the cell surface. Processing of anthrax protective antigen-83 (PA83) by the cells is considered thus far as evidence for the presence of substantial levels of cell-surface furin. To monitor furin, we designed a cleavage-activated FRET biosensor in which the Enhanced Cyan and Yellow Fluorescent Proteins were linked by the peptide sequence SNSRKKR / STSAGP derived from anthrax PA83. Both because of the sensitivity and selectivity of the anthrax sequence to furin proteolysis and the FRET-based detection, the biosensor recorded the femtomolar levels of furin in the in vitro reactions and cell-based assays. Using the biosensor that was cell-impermeable because of its size and also by other relevant methods, we determined that exceedingly low levels, if any, of cell-surface furin are present in the intact cells and in the cells with the enforced furin overexpression. This observation was in a sharp contrast with the existing concepts about the furin presentation on cell surfaces and anthrax disease mechanism. We next demonstrated using cell-based tests that PA83, in fact, was processed by furin in the extracellular milieu and that only then the resulting PA63 bound the anthrax toxin cell-surface receptors. We also determined that the biosensor, but not the conventional peptide substrates, allowed continuous monitoring of furin activity in cancer cell extracts. Our results suggest that there are no physiologically-relevant levels of cell-surface furin and, accordingly, that the mechanisms of anthrax should be re-investigated. In addition, the availability of the biosensor is a foundation for non-invasive monitoring of furin activity in cancer cells. Conceptually, the biosensor we developed may serve as a prototype for other proteinase-activated biosensors.
弗林是一种专门的内切蛋白酶,可将前体蛋白转化为具有生物活性的蛋白质。弗林的功能对正常细胞很重要,在包括恶性肿瘤和炭疽在内的多种病理中也很重要。人们认为弗林在高尔基体区室和细胞表面之间循环。迄今为止,细胞对炭疽保护抗原 83(PA83)的加工被认为是细胞表面存在大量弗林的证据。为了监测弗林,我们设计了一种切割激活的 FRET 生物传感器,其中增强型青色和黄色荧光蛋白通过源自炭疽 PA83 的肽序列 SNSRKKR/STSAGP 连接。由于炭疽序列对弗林蛋白水解的敏感性和选择性以及基于 FRET 的检测,生物传感器在体外反应和基于细胞的测定中记录了皮摩尔级别的弗林。使用由于其大小而不透细胞的生物传感器以及其他相关方法,我们确定在完整细胞中和强制过表达弗林的细胞中,如果存在细胞表面弗林,则其水平极低。这一观察结果与细胞表面弗林呈现和炭疽病机制的现有概念形成鲜明对比。接下来,我们使用基于细胞的测试证明,PA83 实际上是在细胞外环境中被弗林加工的,只有这样,产生的 PA63 才能结合炭疽毒素细胞表面受体。我们还确定,生物传感器(而非常规肽底物)允许在癌细胞提取物中连续监测弗林的活性。我们的结果表明,不存在生理相关水平的细胞表面弗林,因此应重新研究炭疽的机制。此外,生物传感器的可用性为非侵入性监测癌细胞中弗林的活性奠定了基础。从概念上讲,我们开发的生物传感器可以作为其他蛋白酶激活生物传感器的原型。