蛋白质组
计算生物学
化学
人类蛋白质组计划
热休克蛋白90
对接(动物)
GTP酶
蛋白质-蛋白质相互作用
血浆蛋白结合
二聚体
鉴定(生物学)
组合化学
生物化学
复印件
药物发现
生物
仿形(计算机编程)
生物信息学
串联质谱法
系统生物学
作者
Xuehan Zheng,Yanan Li,Hua Qin,Chengfei Ruan,Linlin Yao,Xian Liu,Mingliang Ye,Guangbo Qu,Guibin Jiang
标识
DOI:10.1021/acs.est.5c15707
摘要
Conventional target screening repertoires provide limited coverage of proteome-level interactions, leaving critical gaps in the mechanistic toxicology of per- and polyfluoroalkyl substances (PFAS). In this study, thermal proteome profiling (TPP) was applied for unbiased, proteome-wide characterization of PFAS-protein interactions across five representative PFAS, identifying 173 proteins with significant ligand-induced stabilization. Specifically, legacy PFAS converged on small COPII coat GTPase SAR1A/SAR1B, consistent with potential mechanistic Target of Rapamycin (mTOR)-linked metabolic reprogramming, whereas the replacement ether PFAS hexafluoropropylene oxide dimer acid (HFPO-DA, commercially known as GenX) showed a distinct targetome highlighted by WD repeat-containing protein 89 (WDR89), suggesting non-nuclear-receptor mechanisms plausibly related to chromatin/complex assembly. Cellular thermal shift assay and molecular docking independently verified target engagement and provided a structural rationale for the observed stabilization patterns. Further ontology-based annotation linked the stabilized targets to 279 standardized disease entities, with a predominance of neoplastic outcomes. These findings demonstrate TPP as a new approach methodology for PFAS target discovery, reveal divergent early events for legacy versus replacement chemistries, and provide a proteome-scale framework to prioritize mechanism-based validation and to support evidence-weighted risk assessment of emerging fluorinated alternatives.
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