CELF2 regulation in multiple myeloma
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1279000 | ENA |
REPOSITORIES: ENA
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Project description:In this study, we analyzed transcriptome sequencing data to compare CELF2 RNA binding protein regulation in multiple myeloma cell line
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Project description:Neurodevelopment relies on precise post-transcriptional regulation to coordinate neuronal differentiation, migration, and circuit formation. The CUGBP Elav-like family member 2 (CELF2) is an RNA-binding protein with established roles in alternative splicing and mRNA regulation, yet its function in the developing brain remains poorly defined. Here, we investigated the role of CELF2 during early postnatal neurodevelopment using a constitutive Celf2 knockout mouse model. Celf2 knockout pups exhibited neonatal lethality accompanied by impaired neuronal maturation and disrupted cortical organization. Bulk RNA sequencing revealed widespread transcriptional dysregulation, while splicing analyses identified reduced exon inclusion in multiple neurodevelopmental transcripts following CELF2 loss. Notably, Camk2a transcript and protein levels were markedly reduced in knockout brains, consistent with CELF2 binding to the Camk2a 3′UTR. Functional studies in Caenorhabditis elegans demonstrated that expression of human CAMK2A partially rescued synaptic puncta deficits in unc-75 (CELF ortholog) mutants, supporting a conserved role for CELF-family proteins in synaptic maturation. Histological analyses revealed reductions in Nestin- and Doublecortin-positive immature neurons, thinning of upper cortical layers, and decreased CAMK2A expression. Single-nucleus RNA sequencing further revealed selective reductions in upper layer II/III excitatory neuron populations in the cortex. Together, these findings establish CELF2 as a critical post-transcriptional regulator required for neuronal maturation and architectural stability during early brain development and highlight how disruption of RNA regulatory programs may contribute to neurodevelopmental disorders.
2026-06-03 | GSE319281 | GEO
Project description:Neurodevelopment relies on precise post-transcriptional regulation to coordinate neuronal differentiation, migration, and circuit formation. The CUGBP Elav-like family member 2 (CELF2) is an RNA-binding protein with established roles in alternative splicing and mRNA regulation, yet its function in the developing brain remains poorly defined. Here, we investigated the role of CELF2 during early postnatal neurodevelopment using a constitutive Celf2 knockout mouse model. Celf2 knockout pups exhibited neonatal lethality accompanied by impaired neuronal maturation and disrupted cortical organization. Bulk RNA sequencing revealed widespread transcriptional dysregulation, while splicing analyses identified reduced exon inclusion in multiple neurodevelopmental transcripts following CELF2 loss. Notably, Camk2a transcript and protein levels were markedly reduced in knockout brains, consistent with CELF2 binding to the Camk2a 3′UTR. Functional studies in Caenorhabditis elegans demonstrated that expression of human CAMK2A partially rescued synaptic puncta deficits in unc-75 (CELF ortholog) mutants, supporting a conserved role for CELF-family proteins in synaptic maturation. Histological analyses revealed reductions in Nestin- and Doublecortin-positive immature neurons, thinning of upper cortical layers, and decreased CAMK2A expression. Single-nucleus RNA sequencing further revealed selective reductions in upper layer II/III excitatory neuron populations in the cortex. Together, these findings establish CELF2 as a critical post-transcriptional regulator required for neuronal maturation and architectural stability during early brain development and highlight how disruption of RNA regulatory programs may contribute to neurodevelopmental disorders.
2026-06-03 | GSE319432 | GEO
Project description:<h4><strong>BACKGROUND:</strong> Multiple myeloma is characterized by clonal proliferation of malignant plasma cells in the bone marrow that produce monoclonal immunoglobulins. N-glycosylation changes of these monoclonal immunoglobulins have been reported in multiple myeloma, but previous studies only detected limited serum N-glycan features.</h4><h4><strong>METHODS:</strong> Here, a more detailed study of the human serum N-glycome of 91 multiple myeloma patients and 51 controls was performed. We additionally analyzed sequential samples from patients (n = 7) which were obtained at different time points during disease development as well as 16 paired blood serum and bone marrow plasma samples. N-glycans were enzymatically released and measured by mass spectrometry after linkage specific derivatization of sialic acids.</h4><h4><strong>RESULTS:</strong> A decrease in both α2,3- and α2,6-sialylation, galactosylation and an increase in fucosylation within complex-type N-glycans were found in multiple myeloma patients compared to controls, as well as a decrease in difucosylation of diantennary glycans. The observed glycosylation changes were present in all ISS stages, including the 'low-risk' ISS I. In individual patients, difucosylation of diantennary glycans decreased with development of the disease. Protein N-glycosylation features from blood and bone marrow showed strong correlation. Moreover, associations of monoclonal immunoglobulin (M-protein) and albumin levels with glycan traits were discovered in multiple myeloma patients.</h4><h4><strong>CONCLUSIONS & GENERAL SIGNIFICANCE: </strong>In conclusion, serum protein N-glycosylation analysis could successfully distinguish multiple myeloma from healthy controls. Further studies are needed to assess the potential roles of glycan trait changes and the associations of glycans with clinical parameters in multiple myeloma early detection and prognosis.</h4>
2022-04-27 | MTBLS676 | MetaboLights
Project description:Multiple myeloma is a plasma cell malignancy of the bone marrow. Despite therapeutic advances, multiple myeloma remains incurable and better risk stratification as well as new therapies are therefore highly needed. The proteome of multiple myeloma has not been systematically assessed before and holds the potential to uncover additional insight into disease biology and improved prognostic models. Here, we provide a comprehensive multi-omics analysis including deep tandem mass tag (TMT)-based quantitative global (phospho)proteomics, RNA sequencing and nanopore DNA sequencing of 138 primary patient-derived plasma cell malignancies encompassing treatment-naive multiple myeloma patients treated in clinical trials, plasma cell leukemia, and the premalignancy monoclonal gammopathy of undetermined significance (MGUS), as well as healthy controls. We found that the (phospho)proteome of malignant plasma cells is highly deregulated as compared to healthy plasma cells and is both defined by chromosomal alterations and extensive post-transcriptional regulation. A protein signature was identified that is associated with aggressive disease and more predictive for outcome than cytogenetic-based risk assessment in newly diagnosed multiple myeloma. Integration with functional genetics and single-cell sequencing revealed generally and genetic subtype-specific deregulated proteins and pathways in plasma cell malignancies that include novel potential targets for (immuno)therapies. These findings provide new insights in the biology of multiple myeloma and will be a unique resource for investigating new therapeutic approaches.
2024-07-09 | PXD043580 | Pride