Unknown,Transcriptomics,Genomics,Proteomics

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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. 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.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Sean Ryder

PROVIDER: E-GEOD-26716 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Quaking regulates Hnrnpa1 expression through its 3' UTR in oligodendrocyte precursor cells.

Zearfoss N Ruth NR Clingman Carina C CC Farley Brian M BM McCoig Lisa M LM Ryder Sean P SP

PLoS genetics 20110106 1

In mice, Quaking (Qk) is required for myelin formation; in humans, it has been associated with psychiatric disease. QK regulates the stability, subcellular localization, and alternative splicing of several myelin-related transcripts, yet little is known about how QK governs these activities. Here, we show that QK enhances Hnrnpa1 mRNA stability by binding a conserved 3' UTR sequence with high affinity and specificity. A single nucleotide mutation in the binding site eliminates QK-dependent regul ...[more]

PMID: 21253564

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Dataset Information

Analysis of gene expression in QKI knockdown CG-4 cells

Publications

Quaking regulates Hnrnpa1 expression through its 3' UTR in oligodendrocyte precursor cells.

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