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首页> 外文期刊>Journal of Cellular Physiology >Cholesterol and Its Derivatives Reversibly Inhibit Proteinase K
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Cholesterol and Its Derivatives Reversibly Inhibit Proteinase K

机译：胆固醇及其衍生物可逆地抑制蛋白酶K

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摘要

Microorganisms express a variety of proteases that degrade many proteins of the host body and subvert host immune response. While elucidating the mechanism/s of an immune stimulatory drug that contains bile lipid, regulation of proteolytic activity was investigated. The drug and bile lipids both stabilize Proteinase K, an aggressive protease of fungal origin against auto-digestion. Among the components of bile lipids, only cholesterol and its derivatives stabilize the enzyme. Biophysical evidences such as scattering of light, intrinsic and extrinsic fluorescence emission spectra, circular dichroism spectra, atomic force microscopy, and transmission electron microscopy images indicated that cholesterol and its derivatives interact with Proteinase K. Inhibition kinetics using esterolysis of ATEE revealed non-competitive inhibition by cholesterol. Surface Plasmon Resonance and mass spectrometric analysis indicated 1:1 stoichiometry of binding and with dissociation constant in the M range. Further, the presence of four cholesterol recognition amino acid consensus motifs (CRAC motifs I-IV) was identified in Proteinase K. Bioinformatics analysis revealed that the whole stretch of cholesterol interacts very well with the hydrophobic groove of motif II only among the four CRAC motifs. Variation of cholesterol content of HepG2 human liver carcinoma cells showed positive correlation with binding of fluorescence tagged Proteinase K. Under these conditions, binding of Proteinase K to the cells did not affect their morphology, viability and growth kinetics. Cell bound Proteinase K could be released by an excess of its substrate, thereby restoring reversibly its proteolytic activity. J. Cell. Physiol. 232: 596-609, 2017. (c) 2016 Wiley Periodicals, Inc.
机译：微生物表达的各种蛋白酶降解宿主的身体和许多蛋白质破坏宿主的免疫反应。免疫刺激药物的机制/ s含有胆汁脂质,调节蛋白水解活性研究。和胆汁脂质稳定蛋白酶K,一个积极的真菌来源的蛋白酶auto-digestion。脂质,只有胆固醇及其衍生物稳定的酶。作为光散射,内在和外在荧光发射光谱、圆二色性光谱、原子力显微镜和透射电子显微镜图像显示胆固醇及其衍生品进行交互与蛋白酶k .抑制动力学esterolysis ATEE显示非竞争性抑制胆固醇。共振和质谱分析1:1的绑定和化学计量学离解常数在米的范围内。四个胆固醇识别的存在氨基酸共识图案(CRAC主题I-IV)蛋白酶k .生物信息学被确认分析显示,整个的胆固醇与互动很好疏水只第二主题的槽中四个CRAC图案。人类肝癌细胞HepG2的内容显示绑定的正相关荧光标记的蛋白酶k下这些条件,结合蛋白酶K的细胞不影响他们的形态、生存能力和生长动力学。发布的过量的底物,从而恢复可逆的蛋白水解活性。细胞。期刊、公司。

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