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与瘤亡因子相关的可溶性形式的诱导亡的配体与S100P蛋白相互作用

Victoria A Rastrygina¹, Alexey S Kazakov¹, Roman S Fadeev²

¹Institute for Biological Instrumentation, Institutskaya str., 7, Pushchino, Moscow Region 142290, Russia.

International journal of biological macromolecules

|May 3, 2025

概括

该S100P蛋白特别结合可溶性瘤坏死因子 (TNF) 相关的亡诱导连接体 (TRAIL),降低其杀死癌细胞的能力. 这种相互作用可能解释S100P的存在.

科学领域:

分子生物学分子生物学
免疫学免疫学免疫学
生物化学生物化学

背景情况:

与瘤亡因子 (TNF) 相关的诱导亡的连接体 (TRAIL) 是亡和免疫反应中的关键蛋白质.
S100蛋白质是多功能结合蛋白质,在各种细胞过程中发挥作用.
以前的研究表明,可溶性TNF与S100蛋白结合,影响其活性.

研究的目的:

研究可溶性 TRAIL (sTRAIL) 和人类 S100 蛋白之间的相互作用.
为了确定S100蛋白是否调节sTRAIL的细胞毒性功能.
探索sTRAIL-S100P相互作用在癌症中的潜在作用.

主要方法:

表面等离子体共振光谱学
内在的光是一种内在的光.
化学交叉连接化学交叉连接
分子建模分子建模
局部导向的突变发生.
细胞毒性测定试验
生物信息学分析

主要成果:

只有S100P蛋白与sTRAIL有特定的相互作用 (K_d = 0.16 ± 0.07μM).
结合S100P的sTRAIL单体需要Ca2+,而结合sTRAIL三元体则没有.
突变和建模确定了S100P的""和C端区域对于sTRAIL结合至关重要.
S100P显著降低了sTRAIL对HT-1080纤维瘤细胞的细胞毒性.
生物信息学揭示了各种癌症中的TRAIL和S100P失调.

结论:

S100P直接结合并抑制了sTRAIL的细胞毒性活性.
特别是在癌症的背景下,S100P和sTRAIL之间的相互作用需要进一步研究.
通过抑制TRAIL介导的亡,S100P可能有助于瘤发生.

关键词:

细胞活力细胞活力蛋白质蛋白质相互作用在S100蛋白质中.在S100P中,它是S100P.这就是TNF超级家族.轨道的轨道是一个轨道.

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