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Analysis of gene expression in QKI knockdown CG-4 cells

ABSTRACT: QKI is required for myelin formation in the verterbrate brain. It functions by binding RNA and regulating its stability, translation, and/or aternative splicing. We have used Affymetrix exon arrays to assess changes in gene expression in response to QKI knockdown on an exon level in rat CG-4 oligodendrocyte precursor cells.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE26716 | GEO | 2011/01/20

SECONDARY ACCESSION(S): PRJNA136361

REPOSITORIES: GEO

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Analysis of gene expression in QKI knockdown CG-4 cells

Project description:QKI is required for myelin formation in the verterbrate brain. It functions by binding RNA and regulating its stability, translation, and/or aternative splicing. We have used Affymetrix exon arrays to assess changes in gene expression in response to QKI knockdown on an exon level in rat CG-4 oligodendrocyte precursor cells. Knockdown cells were compared to control cells. Knockdown groups included QKI siRNA transfection, QKI shRNA stable transfection, and hnRNP A1 transient transfection. Control groups consisted of untransfected, control siRNA transfection, control shRNA stable transfection. Each group was analyzed in triplicate.

2011-01-20 | E-GEOD-26716 | biostudies-arrayexpress

Genome-wide maps of Qki-5, Srebp2, and Pol II in oligodendrocytes

Project description:We found the genome-wide co-localization of Qki-5 and Srebp2. Notably, the genomic distribution analysis revealed that Qki-5 and Srebp2 highly co-occupied the regions of the promoter/transcription start site (TSS), where active transcription was taken place in a oligodendrocyte-specific manner, which was indicated by Pol II binding events. GO analysis of the genes whose promoters were co-bound by Qki-5, Srebp2, and Pol II showed a significant enrichment of the Srebp2-mediated cholesterol biosynthesis pathway, and Qki depletion led to reduced recruitment of Srebp2 and Pol II on the promoters of the genes involved in cholesterol biosynthesis. These data suggest Qki-5 as a potential transcription co-activator of Srebp2-mediated cholesterol biosynthesis in oligodendrocytes.

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Project description:Comparison of microRNA expression profile of CG-4 oligodendrocyte progenitor cells and differentiated cells.

2009-02-01 | E-MEXP-1764 | biostudies-arrayexpress

QKI and miR-155 in inflammation and leukemogenesis

Project description:Transcription profiling by array of siRNA against Quaking (QKI) transcripts to identify transcripts that are modulated by QKI activity. MiR-155 is an oncogene and we report here that it targets QKI transcripts. Therefore, we believe that QKI acts as a tumor suppressor gene in different leukemias. We ablated the expression of QKI transcripts using siRNAs in order to further elucidate the effects of QKI in leukemogenesis, and how miR-155 and QKI functionally interact with each other.

2016-01-17 | E-MTAB-2375 | biostudies-arrayexpress

Genomewide analysis of QKI-dependent alternative splicing

Project description:To identify QKI targets, we performed QKI knockdown in BEAS2B cells and analyzed alternative splicing patterns by high-throughput RNA sequencing. The mRNA profiles of control- and QKI-knockdown BEAS2B cells were generated by deep sequencing using Illumina GAIIx sequencer.

2014-04-14 | E-GEOD-55215 | biostudies-arrayexpress

CRISPR-TRAPSeq identifies the QKI RNA binding protein as important for astrocytic maturation and control of thalamocortical synapses (TRAP-Seq dataset)

Project description:Quaking RNA binding protein(QKI) is essential for oligodendrocyte development as myelination requires MBP mRNA regulation and localization to distal processes by its cytoplasmic isoforms(e.g. QKI-6). QKI-6 is also highly expressed in astrocytes, which we and others recently demonstrated have regulated mRNA localization. Here, we show via CLIPseq that QKI-6 binds 3’UTRs of a subset of astrocytic mRNAs, including many enriched in peripheral processes. Binding is enriched near stop codons, which is mediated partially by QKI binding motifs(QBMs) yet spreads to adjacent sequences. We developed CRISPR TRAPseq: a viral approach for mosaic, cell-type specific gene mutation with simultaneous translational profiling. This enabled study of QKI-6 CLIP targets in QKI-deleted astrocytes in an otherwise normal brain. Astrocyte-targeted QKI deletion altered translation and maturation, while also increasing synaptic density within the astrocyte's territory. Overall, our data indicate QKI is required for astrocyte maturation and demonstrate an approach for a highly targeted translational assessment of gene knockout in specific cell-types in vivo.

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Nanostring miRNA expression profiling analysis for QKI-5 knockdown H1299 cells and control cells

Project description:We used the NanoString Human nCounter miRNA expression platform to compare the miRNA expression profiles of QKI-5 knockdown H1299 cells and control cells We found that QKI-5 knockdown significantly changed miRNA expression pattern in lung cancer cells

2021-08-01 | GSE135348 | GEO

Genomewide analysis of QKI-dependent alternative splicing

Project description:To identify QKI targets, we performed QKI knockdown in BEAS2B cells and analyzed alternative splicing patterns by high-throughput RNA sequencing.

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Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: QKI data

Project description:To assess whether the transcripts identified by PAR-CLIP are regulated by the RNA-binding protein (RBP) Quaking (QKI), we analyzed the mRNA levels of mock-transfected and QKI-specific siRNA-transfected cells with microarrays. Transcripts crosslinked to QKI were significantly upregulated upon siRNA transfection, indicating that QKI negatively regulates bound mRNAs (Figure 3H of PMID 20371350), consistent with previous reports of QKI being a repressor. The RBP QKI was depleted by siRNAs and the expression level was compared to mock-transfected HEK 293 cells.

2010-05-27 | E-GEOD-21574 | biostudies-arrayexpress

Expression data from mRNAs co-precipitated with QKI in SW480 cells

Project description:In CRC cells, lncRNA NONHSAT136151 can bind to protein QKI but does not affect the expression of QKI. The binding of NONHSAT136151 may change the interactino of QKI with its target genes. We used microarrays to detail the abundance of mRNAs enriched by QKI in NONHSAT136151 silenced group and control group in CRC cells.

2023-03-21 | GSE227471 | GEO

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