Khakpour Niloofar, Zahmatkesh Amin, Hosseini Seyed Younes, Ghamar Hassan, Nezafat Navid
Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
Shiraz Transplant Center, Shiraz University of Medical Sciences, Shiraz, Iran.
Mol Biotechnol. 2024 Sep 13. doi: 10.1007/s12033-024-01278-4.
The human adenovirus (HADV) early region 4 open reading frame 4 (E4orf4) protein plays a regulatory role in promoting viral infection by interacting with various cellular proteins. E4orf4 can induce death in cancer cells. One of the death pathways that is induced by this protein is related to the formation of membrane blebbing following the phosphorylation of tyrosine amino acids. The activation of this pathway requires the interaction of E4orf4 with Src family kinases (SFKs). The modulation mechanism of Src-dependent signaling via E4orf4 is not yet fully understood. However, evidence suggests that a physical association between the Src kinase domain and the arginine-rich motif of E4orf4 is crucial. Physically connecting E4orf4 to Src kinase leads to the deregulation of the Src-related signaling pathway, thereby inducing cytoplasmic death. In this study, we mapped the E4orf4 interaction site in Src to investigate the interaction between E4orf4 and Src in detail. We also compared the binding strength of E4orf4 proteins from different HADV groups. To this end, we performed bioinformatics structural analysis of the Src kinase domain and E4orf4 to identify E4orf4 interaction sites. The group with the lowest binding energy was predicted to be the most likely candidate for the highest cytoplasmic death in tumor cells based on the energy of the E4orf4-Src complex in various HADV groups. These results show that HADV-A and HADV-C have minimal binding energies to the E4orf4-Src complex, while the dissociation constant (Kd) of HADV-A was less than that of HADV-C. According to the obtained results, E4orf4 of the HADV-A group is more effective at triggering cytoplasmic death based on its most robust interaction with the Src kinase domain.
人类腺病毒(HADV)早期区域4开放阅读框4(E4orf4)蛋白通过与多种细胞蛋白相互作用,在促进病毒感染方面发挥调节作用。E4orf4可诱导癌细胞死亡。该蛋白诱导的死亡途径之一与酪氨酸氨基酸磷酸化后膜泡形成有关。该途径的激活需要E4orf4与Src家族激酶(SFK)相互作用。E4orf4对Src依赖性信号传导的调节机制尚未完全明确。然而,有证据表明,Src激酶结构域与E4orf4富含精氨酸的基序之间的物理关联至关重要。将E4orf4与Src激酶物理连接会导致Src相关信号通路失调,从而诱导细胞质死亡。在本研究中,我们绘制了E4orf4在Src中的相互作用位点,以详细研究E4orf4与Src之间的相互作用。我们还比较了不同HADV组E4orf4蛋白的结合强度。为此,我们对Src激酶结构域和E4orf4进行了生物信息学结构分析,以确定E4orf4相互作用位点。根据不同HADV组中E4orf4-Src复合物的能量,结合能最低的组被预测为最有可能在肿瘤细胞中导致最高细胞质死亡的候选组。这些结果表明,HADV-A和HADV-C与E4orf4-Src复合物的结合能最小,而HADV-A的解离常数(Kd)小于HADV-C。根据所得结果,基于其与Src激酶结构域最强烈的相互作用,HADV-A组的E4orf4在触发细胞质死亡方面更有效。