Browse
Submit Data
Databases
API
Help

Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

12 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ShRNA mediated knockdown of TRA2B and SRSF3 in HEK293 cell line

ABSTRACT: We have independently knocked down TRA2B and SRSF3 in HEK293 cells to identify the sum of alternative splicing changes that results from depletion of each factor. Each was compared to a control transfection of the hairpin vector alone. In this set, 9 total samples were analyzed. There were three biological replicates for each of three conditions: knockdown control, TRA2B knockdown and SRSF3 knockdown. Arrays were analyzed for gene expression using GeneBase and for alternative splicing using MADS+ and OmniViewer software.

ORGANISM(S): Homo sapiens

SUBMITTER: Erik Anderson

PROVIDER: E-GEOD-36069 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

Digitoxin treatment versus control in HEK293 cells

Project description:We treated HEK293 cells with the cardiotonic steroid digitoxin to identify alternative splicing changes as compared to DMSO treatment alone. In this set, 6 total samples were analyzed. There were three biological replicates for each of two conditions: DMSO treatment and Digitoxin treatment. Arrays were analyzed for gene expression using GeneBase and for alternative splicing using MADS+ and OmniViewer software.

2012-04-30 | E-GEOD-36058 | biostudies-arrayexpress

Regulation of exon definition and apoptosis by the Ewing's Sarcoma Protein

Project description:The Ewing's Sarcoma Protein EWS belongs to the TET family (FUS/TLS, EWS, TAF15) of RNA and DNA binding proteins, implicated in DNA transcription, pre-mRNA splicing and maintenance of genome integrity. To identify in vivo RNA targets of EWS we performed a combinatorial approach of CLIP-Seq In this dataset, we include the expression data obtained from three biological replicates of HeLa cells transfected with either scrambled or siEWS oligonucleotides. These data allowed us to identify 805 genes affected at the expression level by EWS knockdown, of which 395 upregulated and 410 downregulated. Moreover, HJAY identified 206 differentially regulated alternative splicing events in 114 genes. Three biological replicates were labeled and hybridized onto Affymetrix HJAY

2014-01-01 | E-GEOD-47790 | biostudies-arrayexpress

EGFRvIII vs. Control - xenograft glioblastomas

Project description:Glioblastoma cell lines were xenografted onto mice and resulting tumors were profiled by microarray. Xenograft recipient mice were NOD/SCID/gamma (NSG) male mice 3 months old. In this set, 6 total samples were analyzed. There were three biological replicates for each of two conditions: EGFRvIII containing tumors and control. Arrays were analyzed for gene expression using GeneBase and for alternative splicing using MADS+ software.

2013-07-01 | E-GEOD-46028 | biostudies-arrayexpress

TDP-43 can directly affect splicing profiles and isoform production of genes involved in the apoptotic and mitotic cellular pathways

Project description:In recent times, high throughput screening analyses have broadly defined the RNA cellular targets of TDP-43, a nuclear factor involved in neurodegeneration. A common outcome of all these studies is that changing the expression levels of this protein can alter the expression of several hundred RNAs within cells. What still remains to be clarified is which changes represent direct cellular targets of TDP-43 or just secondary variations due to the general role played by this protein in RNA metabolism. Using a HTS-based splicing junction analysis we have now identified 162 splicing events that are consistent with being directly controlled by TDP-43. Validation of the data, both in neuronal and non-neuronal cell lines demonstrated that TDP-43 substantially alters the levels of isoform expression in four genes potentially important for neuropathology: MADD/IG20, STAG2, FNIP1, and BRD8. Most importantly, for MADD/IG20 and STAG2 these changes could also be confirmed at the protein level. These alterations were also observed in a cellular model that successfully mimics TDP-43 loss of function effects following its aggregation. These novel splicing events may represent potential biomarkers to predict disease onset, progression, and to test the efficacy of novel therapeutic agents to recover TDP-43 functional properties. We have performed an HTS-based splicing junction analysis of a series of stable cell lines that lack TDP-43, overexpress this factor, or express an RNA-binding mutant, in order to find splicing events, potentially associated with neurodegenerativce diseases, regulated by this splicing factor. Samples were analyzed in triplicate from: The following samples were analyzed in triplicate: wild-type HEK-293 cells, siTDP43-treated HEK-293 cells, siTDP43-treated HEK-293 cells overexpressing a flagged-wildtype TDP-43, siTDP43-treated HEK-293 cells overexpressing a RNA-binding deficient mutant.

2015-08-11 | E-GEOD-67195 | biostudies-arrayexpress

RNA sequencing of SRSF3 depleted pluripotent cells

Project description:RNA seqeuncing was performed to identifiy changes in genes expression and alternative splicing following SRSF3 depletion in pluripotent stem cells.

2018-05-10 | GSE113794 | GEO

SRSF3/AMOTL1 Splicing Axis Promotes the Tumorigenesis of Nasopharyngeal Carcinoma through Regulating the Nucleus Translocation of YAP1

Project description:Dysregulation of serine/arginine splicing factors (SRSFs) and thereby the abnormal alternative splicing (AS) has been widely implicated in the development of multiple cancers, but scarcely investigated in nasopharyngeal carcinoma (NPC). Here we examine the expression of 12 classical SRSFs between 87 NPC and 10 control samples, revealing a significant upregulation of SRSF3 and its association with worse prognosis in NPC. Functional assays demonstrate that SRSF3 knockdown markedly inhibits the proliferation, migration, tumorigenesis and induces apoptosis in NPC cells, suggesting its oncogenic role in NPC progression. Transcriptome analysis reveals 1 934 SRSF3-regulated AS events in genes involved in cell cycle and mRNA metabolism, among which the generation of a long isoform of AMOTL1 (AMOTL1-L) is further verified through a direct bond of SRSF3 RRM domain with the exon 12 of AMOTL1 to promote the exon inclusion. Functional studies reveal that AMOTL1-L could promote the proliferation and migration of NPC cells, nor did AMOTL1-S. Moreover, overexpression of AMOTL1-L significantly rescues the abovementioned inhibitory effects of SRSF3 knockdown, nor did AMOTL1-S. Furthermore, compared with AMOTL1-S, AMOTL1-L has a localization preference in the intracellular than the cell membrane, leading to a stronger interaction with YAP1 to promote its translocation to nucleus. Taken together, our findings identify SRSF3/AMOTL1 as a novel alternative splicing axis with pivotal roles in NPC development, which could be served as promising prognostic biomarkers and therapeutic targets of NPC.

2023-08-21 | GSE227503 | GEO

Analysis of gene expression and splicing after doxycycline-induced knockdown of SRSF3

Project description:SRSF3 is overexpressed in human invasive ovarian cancer and its overexpression is required for cancer cell growth and survival. To decipher the mechnisms behind the role of SRSF3 in ovarian cancer, we examined the gene expression and splicing in the ovarian cancer cell line that was engineered to express a doxycycline-induced SRSF3 siRNA, which was able to knockdown SRSF3 expression by 90% and induce apoptosis. Total RNAs extracted from A2780/SRSF3si2, a subline of ovarian cancer cell line A2780, treated with or without doxycycline at 0.1ug/ml for three days were analyzed using Affymetrix GeneChip® Human Exon 1.0 ST Array

2015-08-06 | E-GEOD-71745 | biostudies-arrayexpress

Srsf3 mediates alternative RNA splicing downstream of PDGFRα signaling.

Project description:Signaling through the platelet-derived growth factor receptor alpha (PDGFRa) is critical for mammalian craniofacial development, though the mechanisms by which the activity of downstream intracellular effectors is regulated to mediate gene expression changes have not been defined. We find that the RNA-binding protein Srsf3 is phosphorylated at Akt consensus sites downstream of PI3K-mediated PDGFRa signaling in palatal mesenchyme cells, leading to its nuclear translocation. We further demonstrate that ablation of Srsf3 in the neural crest lineage leads to facial clefting due to defective cranial neural crest cell specification and survival. Finally, we show that Srsf3 regulates the alternative RNA splicing of transcripts encoding protein kinases in the facial process mesenchyme to negatively regulate PDGFRa signaling. Collectively, our findings reveal that PI3K/Akt-mediated PDGFRa signaling primarily modulates gene expression through alternative RNA splicing in the facial mesenchyme and identify Srsf3 as a critical regulator of craniofacial development.

2021-06-30 | GSE161510 | GEO

Analysis of gene expression and splicing after doxycycline-induced knockdown of SRSF3

2015-08-06 | GSE71745 | GEO

SRSF3-mediated regulation of N6-methyladenosine modification-related lncRNA ANRIL splicing in promotion of pancreatic cancer resistance to gemcitabine I

Project description:Serine/arginine-rich splicing factor 3 (SRSF3) functions to regulate mRNA alternative splicing, a molecular mechanism to process more than 90% of the protein-coding genes and provides an essential source for the biological versatility and targeting of SRSF3 could be a novel approach for cancer therapy. This study identify that SRSF3 expression was upregulated in pancreatic cancer tissues and associated with drug resistance and poor prognosis. Thus, we found that SRSF3 regulated ANRIL splicing and modified m6A modification of ANRIL in pancreatic cancer cells. More importantly, we demonstrated that the m6A methylation on lncRNA-ANRIL was essential for splicing process. Meanwhile, we also found that the different isoforms of ANRIL were differentially expressed in drug-resistant pancreatic cancer cell lines, and SRSF3 promotes gemcitabine resistance by regulating the expression of ANRIL-208. In addition, ANRIL-208 regulated pancreatic cancer cell chemoresistance by forming a complex with Ring1b and EZH2 and enhanced DNA homologous recombination repair (HR) capacity. In conclusion, the current study first established the link among SRSF3, m6A modification, lncRNA splicing, and DNA HR repair in pancreatic cancer, and first demonstrated that abnormal alternative splicing and m6A modification are closely related to chemotherapy resistance in pancreatic cancer.

2022-05-11 | GSE197352 | 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