{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu X"],"funding":["MOST | National Natural Science Foundation of China (NSFC)","| Jilin Provincial Scientific and Technological Development Program (Jilin Scientific and Technological Development Program)","吉林省科学技术厅 | Jilin Provincial Scientific and Technological Development Program","MOST | National Natural Science Foundation of China"],"pagination":["e0060624"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11264595"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["98(7)"],"pubmed_abstract":["Rabies virus (RABV) is highly lethal and triggers severe neurological symptoms. The neuropathogenic mechanism remains poorly understood. Ras-related C3 botulinum toxin substrate 1 (Rac1) is a Rho-GTPase that is involved in actin remodeling and has been reported to be closely associated with neuronal dysfunction. In this study, by means of a combination of pharmacological inhibitors, small interfering RNA, and specific dominant-negatives, we characterize the crucial roles of dynamic actin and the regulatory function of Rac1 in RABV infection, dominantly in the viral entry phase. The data show that the RABV phosphoprotein interacts with Rac1. RABV phosphoprotein suppress Rac1 activity and impedes downstream Pak1-Limk1-Cofilin1 signaling, leading to the disruption of F-actin-based structure f"],"journal":["Journal of virology"],"pubmed_title":["RABV induces biphasic actin cytoskeletal rearrangement through Rac1 activity modulation."],"pmcid":["PMC11264595"],"funding_grant_id":["32272984","20220101303JC","31702238"],"pubmed_authors":["Liu X","Zhao M","Duan M","Guan Z","Guo Y","Guo X","Zhang M","Wang H","Xu J"],"additional_accession":[]},"is_claimable":false,"name":"RABV induces biphasic actin cytoskeletal rearrangement through Rac1 activity modulation.","description":"Rabies virus (RABV) is highly lethal and triggers severe neurological symptoms. The neuropathogenic mechanism remains poorly understood. Ras-related C3 botulinum toxin substrate 1 (Rac1) is a Rho-GTPase that is involved in actin remodeling and has been reported to be closely associated with neuronal dysfunction. In this study, by means of a combination of pharmacological inhibitors, small interfering RNA, and specific dominant-negatives, we characterize the crucial roles of dynamic actin and the regulatory function of Rac1 in RABV infection, dominantly in the viral entry phase. The data show that the RABV phosphoprotein interacts with Rac1. RABV phosphoprotein suppress Rac1 activity and impedes downstream Pak1-Limk1-Cofilin1 signaling, leading to the disruption of F-actin-based structure f","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2025-05-18T13:26:16.312Z","creation":"2025-05-18T13:26:16.312Z"},"accession":"S-EPMC11264595","cross_references":{"pubmed":["38809020"],"doi":["10.1128/jvi.00606-24"]}}