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Peptide mapping of SRSF7_RS-GFP isoforms in murine P19 cells

ABSTRACT: Here we mapped peptides of mouse SRSF7_RS-GFP purified from P19 cells.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture

SUBMITTER: Ilka Wittig

LAB HEAD: Michaela Müller-McNicoll

PROVIDER: PXD016871 | Pride | 2020-05-27

REPOSITORIES: pride

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			Action	DRS
	P17_143_SRSF7_Michaela_GFP_Chymo.mgf	Mgf
	P17_143_SRSF7_Michaela_GFP_Chymo.pride.mgf.gz	Mgf
	P17_143_SRSF7_Michaela_GFP_Chymo.raw	Raw
	P17_143_SRSF7_Michaela_GFP_Chymo_171215025403.mgf	Mgf
	P17_143_SRSF7_Michaela_GFP_Chymo_171215025403.pride.mgf.gz	Mgf

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Publications

SRSF7 maintains its homeostasis through the expression of Split-ORFs and nuclear body assembly.

Königs Vanessa V de Oliveira Freitas Machado Camila C Arnold Benjamin B Blümel Nicole N Solovyeva Anfisa A Löbbert Sinah S Schafranek Michal M Ruiz De Los Mozos Igor I Wittig Ilka I McNicoll Francois F Schulz Marcel H MH Müller-McNicoll Michaela M

Nature structural & molecular biology 20200302 3

SRSF7 is an essential RNA-binding protein whose misexpression promotes cancer. Here, we describe how SRSF7 maintains its protein homeostasis in murine P19 cells using an intricate negative feedback mechanism. SRSF7 binding to its premessenger RNA promotes inclusion of a poison cassette exon and transcript degradation via nonsense-mediated decay (NMD). However, elevated SRSF7 levels inhibit NMD and promote translation of two protein halves, termed Split-ORFs, from the bicistronic SRSF7-PCE transc ...[more]

PMID: 32123389

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Peptide mapping of SRSF7_RRM isoforms in murine P19 cells

Project description:Here we mapped peptides of mouse SRSF7_RRM purified from P19 cells.

2020-05-27 | PXD016884 | Pride

High-resolution analysis of SRSF3 and SRSF4 binding sites by iCLIP

Project description:Endogenous SRSF3 and SRSF4 RNA binding sites were identified genome-wide by iCLIP in P19 BAC trangenic cell lines using GFP-epitope tag.

2012-03-21 | E-MTAB-747 | biostudies-arrayexpress

Differential expression of mature miRNAs in P19 cells during neuronal differentiation and by Rbfox3 depletion.

Project description:To investigate whether Rbfox3 could alter the expression level of miRNAs during neuronal differentiation of P19 cells, we performed miRNA microarray analysis using the RNAs extracted from untreated (undifferentiated) P19-GFP, RA-treated (neuronally differentiated) P19-GFP, or RA-treated P19-T2 cells. Total 9 samples were analyzed. We compared expression levels of P19-GFP (-) vs P19-GFP (+) vs P19-T2 (+) to identify miRNAs which had changes in expression levels with p < 0.01. From this miRNA list, we compared among P19-GFP (-) vs P19-GFP (+) vs P19-T2 (+) to identify the miRNAs which appeared to correlate with Rbfox3 expression.

2014-09-21 | E-GEOD-52377 | biostudies-arrayexpress

The intracellular domain of amyloid precursor protein induces the dynamic change of the gene expression profile in P19 cells.

Project description:As previously reported (Neuroscience letters 444(2008)127-131), we established embryonic carcinoma P19 cell line expressing the intracellular domain of APP (AICD). Although neurons could be differentiated from these cell lines with RA treatment, expression of AICD gave rise to neuron-specific apoptosis. To identify the genes that are involved in this cell death, we evaluated changes of gene expressions that was induced by AICD through this process of cell death. The expression profiles of almost forty thousands transcripts were monitored by DNA microarrays. AICD-expressing P19 cell lines (AICD/P19) and control P19 cell lines (pCDNA/P19) that carry vector alone were used and cultured. To induce neural differentiation of these P19 cell lines, cells were allowed to aggregate in culture medium with 5×10-7 M all-trans-retinoic acid (RA) for 4 days (aggregated state). After aggregation, cells were replated onto cell culture grade dishes or poly-L-Lysine coated cell-disks for two days (differentiated state). RNAs were isolated at each states.

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HeLa cell response to overexpression of wild type and mutated forms of the P19 splice variant of c-H-ras

Project description:The c-H-ras proto-oncogene undergoes alternative splicing of the exon termed IDX giving rise to a novel protein of the Ras family, p19 (H-RasIDX). The experiment tests the effect on the transcriptome of overexpressing the wild type and W164A mutated forms of p19. Keywords: genetic modification Three-condition experiment, where wild type p19 H-ras transfection or transfection with a mutated form (p19W164A) were compared to transfection with the negative control (empty pRK5 expression vector) which was used as the common reference. Biological replicates: 3 of each set of treatments, independently grown and harvested. Two technical replicates with dye swapping per comparison.

2009-12-29 | E-GEOD-12059 | biostudies-arrayexpress

Knockdown of SR protein family in P19 cells and RNA-seq of cytoplasmic and whole cell polyA+ RNA

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Project description:P19 differentiating cells were spread a two densities and mRNA from the two densities were compared

2007-06-30 | E-MEXP-1061 | biostudies-arrayexpress

Conversion of MyoD to a neurogenic factor: binding site specificity determines lineage [RNA-seq]

Project description:MyoD and NeuroD2 are master regulators of myogenesis and neurogenesis and bind to a "shared" E-box sequence (CAGCTG) and a "private" sequence (CAGGTG or CAGATG, respectively). To determine whether private-site recognition is sufficient to confer lineage-specification, we generated a MyoD-mutant with the DNA binding specificity of NeuroD2. Our results demonstrate that redirecting MyoD binding from MyoD-private sites to NeuroD2-private sites, despite preserved binding to the MyoD/NeuroD2-shared sites, is sufficient to change MyoD from a master regulator of myogenesis to a master regulator of neurogenesis. RNA-seq profiling of mouse P19 cells transfected with MyoD, NeuroD2 and chimera mutants. The chimeric mutants are MyoD with the bHLH domain replaced with the NeuroD2 bHLH domain.

2015-07-31 | E-GEOD-64622 | biostudies-arrayexpress

Global regulation of neuronal transcriptome by miR-9/tristetraprolin circuitry

Project description:Nervous system (NS) development relies on coherent up-regulation of extensive sets of genes in a precise spatiotemporal manner. How such transcriptome-wide effects are orchestrated at the molecular level remains an open question. Here we show that 3’-untranslated regions (3’UTRs) of multiple neuronal transcripts contain A/U-rich cis-elements (AREs) recognized by tristetraprolin (TTP/Zfp36), an RNA-binding protein previously reported to destabilize mRNAs encoding predominantly cytokines, growth factors and proto-oncogenes. We further demonstrate that the efficiency of ARE-dependent mRNA degradation declines during neural differentiation due to a decrease in the TTP protein expression mediated by the NS-enriched microRNA miR-9. Our experiments with transgenenic cell lines suggest that TTP down-regulation is essential for proper neuronal differentiation. Moreover, inactivation of TTP in neuroblastoma cells or mouse embryonic fibroblasts induces major changes in their transcriptomes accompanied by significantly elevated expression of NS-specific genes. We conclude that the newly identified miR-9/TTP circuitry limits unscheduled accumulation of neuronal mRNAs in non-neuronal cells and ensures coordinated up-regulation of these transcripts in neurons. 3'READS of undifferentiated and 3.5-day differentiated P19 cells

2015-04-01 | E-GEOD-61098 | biostudies-arrayexpress

Genetic and epigenetic determinants of neurogenesis and myogenesis [expression profiling]

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2012-03-26 | E-GEOD-34907 | biostudies-arrayexpress

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