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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE21574 | GEO | 2010/04/29

SECONDARY ACCESSION(S): PRJNA129313

REPOSITORIES: GEO

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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

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

Transcriptome-wide regulation of pre-mRNA splicing and expression by the RNA-binding protein Quaking during monocyte to macrophage differentiation [Microarray]

Project description:Expression levels of the RNA-binding protein Quaking (QKI) are low in monocytes of early, human atherosclerotic lesions, but abundant in macrophages of advanced plaques. Specific depletion of QKI protein impaired monocyte adhesion, migration, differentiation into macrophages, and foam cell formation in vitro and in vivo. RNA-seq and microarray analysis of human monocyte and macrophage transcriptomes, including those of a unique QKI haploinsufficient patient, revealed striking changes in QKI-dependent mRNA levels and splicing of RNA transcripts. Microarray analysis of gene expression and splicing in THP-1 cells transfected with shRNAs, with or without PMA treatment to induce differentiation. 12 total samples were analyzed: THP-1 monocytic cell line transfected with QKI or control shRNAs; samples taken at day 0 or day 3 of PMA-induced differentiation into macrophages.

2016-01-04 | E-GEOD-74887 | biostudies-arrayexpress

Identify QKI-bound transcripts via RIP-seq

Project description:N7-methylguanosine (m7G) modification, routinely occurring at the 5’ cap of mRNA or within tRNA and rRNA, also exists internally in mRNA. Although essential for mRNA translation as well as stress response, the “reader” protein for mRNA internal m7G modification is still unrevealed. Here, we reported that Quaking protein (QKI), especially QKI7, can selectively recognize the internal mRNA m7G decoration in the cytosol of various cell types. We identified over 1000 confident m7G-modified and QKI binding RNA targets with a conserved motif, “GANGAN (N=A/U/G)”. More strikingly, internal m7G reader QKI7 directly interacts with the SG core protein G3BP1 and can shuttle a subset of m7G-modified transcripts into SG mRNA pool under oxidative stress condition. Additionally, by sequestering mRNA within SGs, QKI7 modulates the translation efficiency of selected transcripts. Moreover, in line with the observation that doxorubicin triggers the assembly of SGs, QKI7 mediates the sensitivity of cancer cells to chemotherapy drug treatment.

2023-05-17 | GSE193036 | GEO

Recognition of internal mRNA N7-methylguanosine by QKI shuttles transcripts into stress granules and regulates translation

Project description:Recent studies reported that N7-methylguanosine (m7G) modification exists in internal mRNAs; however, the “reader” protein for mRNA internal m7G modification is still unrevealed. Here, by performing m7G MeRIP-seq and RIP-seq, we identified quaking protein (QKI) as a novel internal m7G modification reader. Internal mRNA m7G modification acts as a key player in mRNA translation under stress condition. To explore the mechanism underlying the function of QKI in translation regulation, we employed RNA-seq and Ribo-seq, and demonstrated that QKI7 regulates the translation efficiency of a subset of internal m7G-modified transcripts under stress condition.

2023-05-17 | GSE193039 | GEO

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

Transcriptome-wide regulation of pre-mRNA splicing and expression by the RNA-binding protein Quaking during monocyte to macrophage differentiation [Microarray]

2016-01-04 | GSE74887 | GEO

Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: IGF2BP data

Project description:To test the influence of IGF2BPs on the stability of their interacting mRNAs, as reported previously for some targets (Yisraeli, 2005), we simultaneously depleted all three IGF2BP family members using siRNAs and compared the cellular RNA from knockdown and mock-transfected cells on microarrays. The levels of transcripts identified by PAR-CLIP decreased in IGF2BP-depleted cells, indicating that IGF2BP proteins stabilize their target mRNAs. Moreover, transcripts that yielded clusters with the highest T to C mutation frequency were most destabilized (Figure 4G of PMID 20371350), indicating that the ranking criterion that we derived based on the analysis of PUM2 and QKI data generalizes to other RNA-binding proteins (RBPs). The RBPs IGF2BP1-3 were depleted by siRNAs and the expression level was compared to mock-transfected HEK 293 cells.

2010-05-27 | E-GEOD-21575 | biostudies-arrayexpress

Transcriptome-wide identification of RNA-binding protein and microRNA target sites by PAR-CLIP: IGF2BP data

2010-04-29 | GSE21575 | GEO

Transcriptome datasets of the Quaking (QKI) gene knock-down human oral squamous cell carcinoma (OSCC) cells

Project description:Here, we elucidated whether miR-200 family members control RNA-binding protein quaking (QKI), a newly identified tumor suppressor that is regulated during EMT. QKI expression was suppressed by miR-200 overexpression, and the 3'-UTR of QKI mRNA was directly targeted by miR-200 in luciferase reporter assays. ShRNA-mediated knockdown of QKI led to pronounced EMT and protumor effects in both in vitro and in vivo studies of oral squamous cell carcinoma. Furthermore, high expression of QKI protein is associated with favorable prognosis in surgically resected head and neck squamous cell carcinoma and lung adenocarcinoma. In conclusion, QKI increases during EMT and is targeted by miR-200; while, it suppresses EMT and tumorigenesis. We suggest that QKI and miR-200 form a negative feedback loop to maintain homeostatic responses to EMT-inducing signals.

2020-07-21 | GSE154730 | GEO

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