biostudies-literatureOrtolano NANICHD NIH HHSNINDS NIH HHSNCI NIH HHSNational Institutes of HealthNIGMS NIH HHSe0248000https://www.ebi.ac.uk/biostudies/studies/S-EPMC7951927biostudies-literatureUnknown16(3)CUL9 is a non-canonical and poorly characterized member of the largest family of E3 ubiquitin ligases known as the Cullin RING ligases (CRLs). Most CRLs play a critical role in developmental processes, however, the role of CUL9 in neuronal development remains elusive. We determined that deletion or depletion of CUL9 protein causes aberrant formation of neural rosettes, an in vitro model of early neuralization. In this study, we applied mass spectrometric approaches in human pluripotent stem cells (hPSCs) and neural progenitor cells (hNPCs) to identify CUL9 related signaling pathways that may contribute to this phenotype. Through LC-MS/MS analysis of immunoprecipitated endogenous CUL9, we identified several subunits of the APC/C, a major cell cycle regulator, as potential CUL9 interacting pPloS oneA proteomics approach for the identification of cullin-9 (CUL9) related signaling pathways in induced pluripotent stem cell models.PMC7951927F31NS108581R21CA227483-01A1P50 HD1035375T32HD7502-20F32 NS010858T32 HD007502R21 CA227483R35 GM1289151R35GM128915-01Joshi PConnelly JPKline LAPruett-Miller SMGama VRomero-Morales AIRose KLOrtolano NARasmussen MLBodnya CfalseA proteomics approach for the identification of cullin-9 (CUL9) related signaling pathways in induced pluripotent stem cell models.CUL9 is a non-canonical and poorly characterized member of the largest family of E3 ubiquitin ligases known as the Cullin RING ligases (CRLs). Most CRLs play a critical role in developmental processes, however, the role of CUL9 in neuronal development remains elusive. We determined that deletion or depletion of CUL9 protein causes aberrant formation of neural rosettes, an in vitro model of early neuralization. In this study, we applied mass spectrometric approaches in human pluripotent stem cells (hPSCs) and neural progenitor cells (hNPCs) to identify CUL9 related signaling pathways that may contribute to this phenotype. Through LC-MS/MS analysis of immunoprecipitated endogenous CUL9, we identified several subunits of the APC/C, a major cell cycle regulator, as potential CUL9 interacting p2021-01-01T00:00:00Z20212026-04-29T06:29:22.323Z2024-12-04T07:20:12.032ZS-EPMC79519273370543810.1371/journal.pone.0248000