{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hu Y"],"funding":["Science and Technology Support Program of Jiangsu Province","Key Laboratory in Science and Technology Development Project of Suzhou","National Natural Science Foundation of China","Suzhou International Joint Laboratory for Diagnosis and Treatment of Brain Diseases, the Interdisciplinary Basic Frontier Innovation Program of Suzhou Medical College of Soochow University","MOE Key Laboratory of Geriatric Diseases and Immunology"],"pagination":["140"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11977062"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["82(1)"],"pubmed_abstract":["Parkinson's disease (PD) is a common neurodegenerative movement disorder characterized by dopaminergic neuron loss in the substantia nigra pars compacta and striatal dopamine depletion. The NUS1 gene, which encodes the neurite outgrowth inhibitor B receptor (NgBR), has been recently identified as a novel risk gene for PD. However, its roles and mechanism in neurodegeneration are still unclear. Here, we demonstrate that NgBR deficiency triggers neuronal damage through a novel KAT7/RFX1/FGF1 axis. RNA sequencing and experimental verification revealed that NgBR depletion downregulates expression and secretion of fibroblast growth factor 1 (FGF1), which led to inactivation of the PI3K/AKT signaling pathway. Mechanistically, NgBR deletion suppresses lysine acetyltransferase 7 (KAT7) expression,"],"journal":["Cellular and molecular life sciences : CMLS"],"pubmed_title":["Loss of NgBR causes neuronal damage through decreasing KAT7-mediated RFX1 acetylation and FGF1 expression."],"pmcid":["PMC11977062"],"funding_grant_id":["YXY2303023","CXZX202231","JYN202401","SZ2024001","32271039","32170987, 32471047"],"pubmed_authors":["Ren H","Hu Y","Liu L","Guo J","Hong Y","Cao Y","Yang P","Ma Y","Tang B","Wang G"],"additional_accession":[]},"is_claimable":false,"name":"Loss of NgBR causes neuronal damage through decreasing KAT7-mediated RFX1 acetylation and FGF1 expression.","description":"Parkinson's disease (PD) is a common neurodegenerative movement disorder characterized by dopaminergic neuron loss in the substantia nigra pars compacta and striatal dopamine depletion. The NUS1 gene, which encodes the neurite outgrowth inhibitor B receptor (NgBR), has been recently identified as a novel risk gene for PD. However, its roles and mechanism in neurodegeneration are still unclear. Here, we demonstrate that NgBR deficiency triggers neuronal damage through a novel KAT7/RFX1/FGF1 axis. RNA sequencing and experimental verification revealed that NgBR depletion downregulates expression and secretion of fibroblast growth factor 1 (FGF1), which led to inactivation of the PI3K/AKT signaling pathway. Mechanistically, NgBR deletion suppresses lysine acetyltransferase 7 (KAT7) expression,","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2025-07-05T03:04:51.259Z","creation":"2025-07-05T03:04:51.259Z"},"accession":"S-EPMC11977062","cross_references":{"pubmed":["40192836"],"doi":["10.1007/s00018-025-05660-6"]}}