Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Roth_Isoforms_BioID_Chtop_Sap30bp_VS30_VS32_2023_DDA

ABSTRACT: BioID data (DDA files) associated with the manuscript by Roth et al. 2023 describing the identification and characterization of neural alternative splicing events and associated PPI changes for 17 gene regulatory factors. BioID experiments were performed for two isoforms of Chtop and Sap30bp with/without inclusion of a neural-regulated exon. For Chtop, cells were also treated with MS023, an arginine methyltransferase inhibitor, at 3 concentrations (DMSO, 1uM and 4uM).

INSTRUMENT(S): TripleTOF 6600

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Anne-Claude Gingras

PROVIDER: MSV000091298 | MassIVE | Thu Feb 16 09:32:00 GMT 2023

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Similar Datasets

Roth_Isoforms_BioID_Chtop_Sap30bp_VS31_VS33_2023_DIA

Project description:BioID data (DIA files) associated with the manuscript by Roth et al. 2023 describing the identification and characterization of neural alternative splicing events and associated PPI changes for 17 gene regulatory factors. BioID experiments were performed for two isoforms of Chtop and Sap30bp with/without a neural-regulated exon. For Chtop, cells were also treated with MS023, an arginine methyltransferase inhibitor, at 3 concentrations (DMSO, 1uM and 4uM).

2023-02-12 | MSV000091274 | MassIVE

Roth_Isoforms_FLAG_Chtop_Isoforms_MS023_VS34_2023_DIA

Project description:FLAG AP-MS data (DIA) associated with the manuscript by Roth et al. 2023 describing the identification and characterization of neural alternative splicing events and associated PPI changes for 17 gene regulatory factors. This dataset includes Chtop AP-MS data from N2a cells treated with and without the arginine methyltransferase inhibitor MS023.

2023-08-06 | MSV000092608 | MassIVE

Roth_Isoforms_FLAG_Chtop_Isoforms_MS023_VS35_2023_DDA

Project description:FLAG AP-MS data (DDA) associated with the manuscript by Roth et al. 2023 describing the identification and characterization of neural alternative splicing events and associated PPI changes for 17 gene regulatory factors. This dataset includes Chtop AP-MS data from N2a cells treated with and without the arginine methyltransferase inhibitor MS023.

2023-08-06 | MSV000092607 | MassIVE

Roth_Isoforms_FLAG_P105_VS28_2023_DDA

2023-02-16 | MSV000091297 | MassIVE

Roth_Isoforms_FLAG_P105_VS29_2023_DIA

2023-02-12 | MSV000091275 | MassIVE

A global regulatory mechanism for activating an exon network required for neurogenesis

Project description:The vertebrate and neural-specific SR-related protein nSR100/SRRM4 regulates an extensive program of alternative splicing with critical roles in nervous system development. However, the mechanism by which nSR100 controls its target exons is poorly understood. We demonstrate that nSR100-dependent neural exons are associated with a unique configuration of intronic cis-elements that promote rapid switch-like regulation during neurogenesis. A key feature of this configuration is the insertion of specialized intronic enhancers between polypyrimidine tracts and acceptor sites that bind nSR100 to potently activate exon inclusion in neural cells, while weakening 3' splice site recognition and contributing to exon skipping in non-neural cells. nSR100 further operates by forming multiple interactions with early spliceosome components bound proximal to 3' splice sites. These multifaceted interactions achieve dominance over neural exon silencing mediated by the splicing regulator PTBP1. The results thus illuminate a widespread mechanism by which a critical neural exon network is activated during neurogenesis.

2014-09-11 | GSE57278 | GEO

A global regulatory mechanism for activating an exon network required for neurogenesis

2014-09-11 | E-GEOD-57278 | biostudies-arrayexpress

Homo sapiens isolate:HeLa cervical carcinoma cells

Project description:Massively parallel exon inclusion assay

| PRJNA420342 | ENA

Neuron-specific protein network mapping of autism risk genes identifies shared biological mechanisms and disease relevant pathologies

Project description:There are hundreds of risk genes for autism spectrum disorder (ASD), but signaling networks at the protein level remain unexplored. We used neuron-specific proximity-labeling proteomics (BioID) to identify protein-protein interaction (PPI) networks for 41 ASD-risk genes. Neuron-specific PPI networks included synaptic transmission proteins, which are disrupted by de novo missense variants. The PPI network map revealed convergent pathways including mitochondrial/metabolic processes, Wnt signaling, ion channel activity and MAPK signaling. CRISPR knockout validations revealed an association between mitochondrial activity and ASD-risk genes. The PPI network showed an enrichment of 112 additional ASD-risk genes and differentially expressed genes from post-mortem ASD patients. Clustering of risk genes based on PPI networks identified gene groups corresponding to clinical behavior score severity. Our data reveal that cell type-specific PPI networks can identify previously unknown individual and convergent ASD signaling networks, provide a method to assess patient variants, and reveal biological insight into disease mechanisms and sub-cohorts of ASD.

2022-09-24 | GSE213899 | GEO

Targeting PRMT1-mediated SRSF1 Methylation to Suppress Exon Inclusion within Oncogenic Transcripts and Breast Tumorigenesis

Project description:PRMT1 is highly expressed in breast tumors, and has been suggested to play a vital role in breast tumorigenesis, but the underlying molecular mechanisms remain to be fully characterized. Here, we reveal that PRMT1 exhibits a wide-spreading role in RNA alternative splicing based on transcriptome analysis, with a preference for exon inclusion in a large cohort of oncogenic genes. Profiling PRMT1 methylome reveals that the arginine/serine-rich splicing factor SRSF1 is heavily arginine-methylated by PRMT1, which is critical for SRSF1 phosphorylation, SRSF1 binding with RNA, and PRMT1-induced exon inclusion. In breast tumors, the overexpression of PRMT1 is associated with high levels of SRSF1 arginine methylation and aberrant exon inclusion in those oncogenic genes. Accordingly, PRMT1-mediated SRSF1 methylation and exon inclusion events are found to be critical for the malignant behaviors of breast cancer cells. Furthermore, we identified and characterized a selective PRMT1 inhibitor iPRMT1, which is potent in inhibiting PRMT1-mediated SRSF1 methylation and exon inclusion events, and breast cancer cell growth both in vitro and in vivo. Combination treatment with iPRMT1 and inhibitor targeting SRSF1 phosphorylation, SPHINX31 or SRPIN340, exhibits synergistic effects on suppressing breast cancer cell growth, strengthening the cross-talk between arginine methylation and phosphorylation in SRSF1. In conclusion, our data uncover a key mechanism underlying PRMT1-mediated gene alternative splicing, demonstrating targeting PRMT1 has great potential to treat breast cancer in clinic.

2023-10-02 | GSE212049 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data