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Global analysis of excitotoxicity-induced alterations in RNA structure and RNA-protein binding in neurons identifies subsets of transcripts and RNA-binding proteins involved in synaptic plasticity and neurodegenerative disorders [PIP-seq]

ABSTRACT: Global analysis of excitotoxicity-induced alterations in RNA structure and RNA-protein binding in neurons identifies subsets of transcripts and RNA-binding proteins involved in synaptic plasticity and neurodegenerative disorders [PIP-seq]

PROVIDER: PRJNA1119026 | ENA |

REPOSITORIES: ENA

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Global analysis of excitotoxicity-induced alterations in RNA structure and RNA-protein binding in neurons identifies subsets of transcripts and RNA-binding proteins involved in synaptic plasticity and neurodegenerative disorders [PIP-seq]

Project description:Excitotoxicity and altered RNA regulation by RNA-binding proteins (RBPs) are two prevalent hallmarks in multiple neurodegenerative disorders. However, global analysis of RNA-protein interactions in primary neurons in the context of excitotoxicity has not been assessed. To address this, in this work we have applied the protein interaction profile sequencing (PIP-seq) method to primary neurons treated with NMDA to induce excitotoxicity. Our results reveal that NMDA dramatically changes RNA secondary structure at the UTR regions, and that specific RNA structure reduction at the 3’UTR correlates with increased mRNA abundance as assessed by mRNA-Seq. Protein binding sites increase in response to excitotoxicity and, interestingly, different RNA-protein binding in this context defines subsets of transcripts functionally associated with synaptic functions and neurodegenerative disorders. We also identify two RNA motifs enriched in protein binding in the context of excitotoxicity and a list of proteins binding to them in vitro. Accordingly, we observe that two of these RBPs, CELF6 and YBX3 alter their protein levels in response to NMDA treatment, suggesting their involvement in RNA regulation in the context of excitotoxicity. Overall, we describe for the first time the global RNA-protein interactions of primary cortical neurons in baseline conditions and in an in vitro model of excitotoxicity, providing extensive datasets that can be leveraged to bridge the mechanistic gap between two major hallmarks common in multiple neurodegenerative disorders: excitotoxicity and RNA regulation by RBPs

2025-04-28 | GSE268840 | GEO

2025-04-28 | GSE268844 | GEO

Project description:Global analysis of excitotoxicity-induced alterations in RNA structure and RNA-protein binding in neurons identifies subsets of transcripts and RNA-binding proteins involved in synaptic plasticity and neurodegenerative disorders [RNA-seq]

| PRJNA1119030 | ENA

N-terminomics Analysis of Mouse cultured cortical neuron during excitotoxicity

Project description:Excitotoxicity is a primary pathological process directing neuronal cell death in both acute neurological disorders and neurodegenerative diseases such as ischemic stroke and Alzheimer’s disease. We use mouse cultured cortical neuron treated with 100uM of Glutamate for a model of excitotoxicity and applied N-terminomics (TAILS) method to identify the neuronal proteins aberrantly modified in excitotoxicity

2023-04-07 | PXD040648 | Pride

Dynamic changes in proteome and phosphoproteome following glutamate excitotoxicity in cultured primary cortical neurons

Project description:Excitotoxicity caused by over-stimulation of the ionotropic glutamate receptors is a key neuronal cell death process underpinning brain damage in acute and chronic neurological disorders such as ischaemic stroke, traumatic brain injury, and neurodegenerative diseases. Exactly how neurons die in excitotoxicity still remains unclear and is an important area of research in the field of neuroscience. In this current project we wanted to explore the global changes in proteome and phosphoproteome following glutamate excitotoxicity in cultured primary cortical neurons.

2019-03-07 | PXD008353 | Pride

CROP-seq + PIP-seq

Project description:We used PIP-seq with a CROP-seq library to evaluate the feability of PIP-seq for large pooled CRISPR screens

2023-01-12 | GSE202915 | GEO

Compound PIP-RBPJ-1 treated human neural stem cells

Project description:The study of the compond PIP-RBPJ-1‘ function on neural stem cell. Synthetic DNA-binding inhibitors capable of gaining precise control over neurogenesis factors could obviate the current clinical barriers associated with small molecule use in regenerative medicine. Here, we show the design and bio-efficacy of a synthetic ligand PIP-RBPJ-1 to cause promoter-specific suppression of neurogenesis-associated HES1, and its downstream genes. Furthermore, PIP-RBPJ-1 alone could alter the neural system-associated notch signaling factors and remarkably induce neurogenesis with an efficiency that is comparable to a conventional approach. Here is one day treatment of the PIP-RBPJ-1 on neural stem cells.

2018-07-19 | GSE109916 | GEO

CROP-seq + PIP-seq

Project description:CROP-seq + PIP-seq

| PRJNA923463 | ENA

PIP protein binding in CD4+ T cells

Project description:Proteins were pulled down using PIP beads to determine what proteins may be interacting with different PIPs

2024-12-16 | PXD046124 | Pride

A functional and regulatory network associated with PIP expression in human breast cancer

Project description:Background The PIP (prolactin-inducible protein) gene has been shown to be expressed in breast cancers, with contradictory results concerning its implication. As both the physiological role and the molecular pathways in which PIP is involved are poorly understood, we conducted a combined gene expression profiling and network analysis studies on selected breast cancer cell lines presenting distinct PIP expression levels and hormonal receptor status, to explore the functional and regulatory network of PIP co-modulated genes. Results Microarray analysis allowed identification of genes co-modulated with PIP independently of modulations resulting from hormonal treatment or cell line heterogeneity. Relevant clusters of genes that can discriminate between [PIP+] and [PIP-] cells were identified. Functional and regulatory network analyses based on knowledge database revealed a master network of PIP co-modulated genes, including many interconnecting oncogenes and tumor suppressor genes, half of which were detected as differentially expressed through high-precision measurements. The networks identified appear associated with an inhibition of proliferation coupled with an increase of apoptosis and an enhancement of cell adhesion in breast cancer cell lines. Finally, the STAT5 motif was identified in promoters of an important part of genes belonging to the PIP networks. Conclusion Our global exploratory approach was found to be an effective strategy to identify the biological pathways modulated along with the PIP expression, thus supporting good prognostic value of disease-free survival time in breast cancer based on previous reports focusing on PIP’s favorable signature. Moreover, our data allowed us to provide the first insight in its regulatory subnetwork in which STAT5 appears as a potential key regulator.

2009-03-06 | GSE11627 | GEO

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