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Stau2 RIP-Chip in Mouse E13-14 Cortex

ABSTRACT: The double-stranded RNA binding protein Staufen2 (Stau2) is asymmetrically localized and segregated during asymmetric cell divisions in the developing mouse cortex and promotes intermediate progenitor cell fate. We carry out RNA immunoprecipitation with a Stau2 specific antibody, followed by microarray analysis to identify Stau2 assoicated RNAs that may be shuttled asymmetrically into one daughter cell thus affecting cell fate. Cortex was dissected from E13-14 timed-pregnant Swiss Webster Mice (Taconic) and RNA immunoprecipitation followed by microarray analysis was carried out to identy Stau2 associated RNA cargos.

ORGANISM(S): Mus musculus

SUBMITTER: Sridar Chittur

PROVIDER: E-GEOD-38222 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Asymmetric segregation of the double-stranded RNA binding protein Staufen2 during mammalian neural stem cell divisions promotes lineage progression.

Kusek Gretchen G Campbell Melissa M Doyle Frank F Tenenbaum Scott A SA Kiebler Michael M Temple Sally S

Cell stem cell 20120816 4

Asymmetric cell divisions are a fundamental feature of neural development, and misregulation can lead to brain abnormalities or tumor formation. During an asymmetric cell division, molecular determinants are segregated preferentially into one daughter cell to specify its fate. An important goal is to identify the asymmetric determinants in neural progenitor cells, which could be tumor suppressors or inducers of specific neural fates. Here, we show that the double-stranded RNA-binding protein Sta ...[more]

PMID: 22902295

Similar Datasets

Stau2 RIP-Chip in Mouse E13-14 Cortex

Project description:The double-stranded RNA binding protein Staufen2 (Stau2) is asymmetrically localized and segregated during asymmetric cell divisions in the developing mouse cortex and promotes intermediate progenitor cell fate. We carry out RNA immunoprecipitation with a Stau2 specific antibody, followed by microarray analysis to identify Stau2 assoicated RNAs that may be shuttled asymmetrically into one daughter cell thus affecting cell fate.

2012-12-21 | GSE38222 | GEO

mRNA-seq and AGO2-RIP-seq of JURKAT T-cell acute lymphoblastic leukemia cell line upon overexpression of hsa-miR-143-3p

Project description:The aim of this study was to investigate the effect of hsa-miR-143-3p on global gene expression in T-cell acute lymphoblastic leukemia (T-ALL) and to unravel its direct target genes. For this purpose we selected Jurkat T-ALL cell line characterized by low expression of this miRNA. The cells were transduced either with pCDH-CMV-MCS-EF1_GFP_puro empty vector (System Biosciences) or pCDH-CMV-MCS-EF1_GFP pre-mir-143 vector, each variant in three biological replicates. Total RNA was isolated from each samples. Additionally, RISC complexes containing miRNAs bound to their target mRNAs were isolated by AGO2 immunoprecipitation and the obtained fraction of RISC-bound RNA was isolated from each sample. All 12 libraries (6 total RNA samples and 6 AGO2-RIP samples) were sequenced on Illumina NovaSeq6000 platform, in 2x150 mode, with a coverage of 60M paired reads/sample.

2024-08-31 | E-MTAB-13462 | biostudies-arrayexpress

Genome-wide identification of transcripts associated with lncRNA-ATB by RIP-seq

Project description:The role of TGF-β-induced epithelial-mesenchymal transition (EMT) in cancer cell dissemination is well established, but the involvement of lncRNAs in TGF-β signaling is still unknown. In this study, we observed that the lncRNA-Activated by TGF-β (lncRNA-ATB) was upregulated in hepatocellular carcinoma (HCC) metastases and associated with poor prognosis. lncRNA-ATB upregulated ZEB1 and ZEB2 by competitively binding the miR-200 family and then induced EMT and invasion. In addition, lncRNA-ATB promoted organ colonization of disseminated tumor cells by binding IL11 mRNA, inducing autocrine of IL11 and triggering STAT3 signaling. Globally, lncRNA-ATB promotes the invasion-metastasis cascade. Thus, these findings suggest that lncRNA-ATB, a mediator of TGF-β signaling, could predispose HCC patients to metastases and may serve as a potential target for anti-metastatic therapies. To identify mRNA species bound by lncRNA-ATB, we performed an RIP to pull down endogenous mRNAs associated with the lncRNA-ATB and sequenced the retrieved RNA.

2014-02-08 | E-GEOD-54799 | biostudies-arrayexpress

An eIF4E1/4E-T complex determines the genesis of neurons from precursors by translationally repressing a proneurogenic transcription program

Project description:Here, we have addressed the mechanisms that determine genesis of the correct numbers of neurons during development, focusing upon the embryonic cortex. We identify in neural precursors a repressive complex involving eIF4E1 and its binding partner 4E-T that coordinately represses translation of proteins that determine neurogenesis. This eIF4E1/4E-T complex is present in granules with the processing body proteins Lsm1 and Rck, and disruption of this complex causes premature and enhanced neurogenesis and neural precursor depletion. Analysis of the 4E-T complex shows that it is highly enriched in mRNAs encoding transcription factors and differentiation-related proteins. These include the proneurogenic bHLH mRNAs, which colocalize with 4E-T in granules, and whose protein products are aberrantly upregulated following knockdown of eIF4E, 4E-T, or processing body proteins. Thus, neural precursors are transcriptionally primed to generate neurons, but an eIF4E/4E-T complex sequesters and represses translation of proneurogenic proteins to determine appropriate neurogenesis. We obtained 3 biological replicates of IgG-bound RNA, 4E-T-bound RNA, and cooresponding total RNA input from mouse E12-13 cortices. RNA samples were analyzed on the Affymetrix Mouse Gene 2.0 ST Arrays.

2014-09-25 | E-GEOD-61729 | biostudies-arrayexpress

Genome-wide distribution of Pbx1/2/3 in mouse cortex at embryonic day 12.5 [ChIP-seq]

Project description:We demonstrate using conditional mutagenesis that Pbx1, with and without Pbx2+/ sensitization, regulates regional identity and laminar patterning of the developing mouse neocortex in cortical progenitors (Emx1-Cre) and in newly generated neurons (Nex1-Cre). Pbx1/2 mutants have three salient molecular phenotypes of cortical regional and laminar organization: hypoplasia of the frontal cortex, ventral expansion of the dorsomedial cortex, and ventral expansion of Reelin expression in the cortical plate of the frontal cortex, concomitant with an inversion of cortical layering in the rostral cortex. Molecular analyses, including PBX ChIP-seq, provide evidence that PBX promotes frontal cortex identity by repressing genes that promote dorsocaudal fate. Chromatin immunoprecipitation was performed using antibody against Pbx1/2/3/ (sc-888, Santa Cruz). Wild type E12.5 mouse whole cortex was used for the analysis.

2016-02-27 | E-GEOD-78720 | biostudies-arrayexpress

Genome-wide distribution of Pbx1/2/3 in mouse cortex at embryonic day 15.5 [ChIP-seq]

Project description:We demonstrate using conditional mutagenesis that Pbx1, with and without Pbx2+/ sensitization, regulates regional identity and laminar patterning of the developing mouse neocortex in cortical progenitors (Emx1-Cre) and in newly generated neurons (Nex1-Cre). Pbx1/2 mutants have three salient molecular phenotypes of cortical regional and laminar organization: hypoplasia of the frontal cortex, ventral expansion of the dorsomedial cortex, and ventral expansion of Reelin expression in the cortical plate of the frontal cortex, concomitant with an inversion of cortical layering in the rostral cortex. Molecular analyses, including PBX ChIP-seq, provide evidence that PBX promotes frontal cortex identity by repressing genes that promote dorsocaudal fate. Chromatin immunoprecipitation was performed using antibody against Pbx1/2/3 (sc-888, Santa Cruz). Wild type E15.5 mouse whole cortex was used for the analysis.

2016-03-12 | E-GEOD-79152 | biostudies-arrayexpress

DEAD box RNA helicase 5 and 17 are novel host factors for Sindbis virus infection.

Project description:The DEAD-box ATP-dependent RNA helicases DDX5 and DDX17 play a role in many aspects of cellular RNA biology, including metabolism, translation, splicing, transcription regulation, ribosome biogenesis, mRNA nuclear export, and miRNA processing. Moreover, both RNA helicases were found to either promote or inhibit viral replication upon several RNA virus infections. Here we show that DDX5 depletion by siRNA or CRISPR/Cas9 has a negative impact on Sindbis virus (SINV) infection at the viral protein, RNA and infectious particle level. Moreover, we demonstrate that DDX5 which is predominately nuclear in uninfected conditions, re-localizes to the cytoplasm upon infection where it interacts with the viral RNA and with the SINV capsid protein. Furthermore, proteomic analysis of DDX5 interactome in mock and SINV infected HCT116 cells confirmed its interaction with DDX17 and identified PNPT1 as a new DDX5 partner. Of note, while PNPT1 localization remains mostly unchanged in mock and infected cells, DDX17 re-localizes to the cytoplasm with DDX5 upon SINV infection and interacts with SINV capsid protein. Finally, depletion of DDX17 further reduces SINV infection in a DDX5-depleted background suggesting a cumulative proviral effect of DDX5 and 17 proteins on SINV.

2024-05-22 | PXD044867 | Pride

Reduced expression of RBM47 enhances Nrf2 activity to promote tumor growth in A549 lung adenocarcinoma cells

Project description:We identified RNA binding motif protein 47 (RBM47) as a target gene of transforming growth factor (TGF)-beta in mammary gland epithelial cells (NMuMG cells) that have undergone the epithelial-to-mesenchymal transition (EMT). TGF-beta repressed RBM47 expression in NMuMG cells and lung cancer cell lines. Expression of RBM47 correlated with good prognosis in patients with lung, breast, and gastric cancer. RBM47 suppressed the expression of cell metabolism-related genes, which were the direct targets of nuclear factor erythroid 2-related factor 2 (Nrf2; also known as NFE2L2). RBM47 bound to KEAP1 and Cullin3 mRNAs, and knockdown of RBM47 inhibited their protein expression, which led to enhanced binding of Nrf2 to target genomic regions. Knockdown of RBM47 also enhanced the expression of some Nrf2 activators, p21/CDKN1A and MafK induced by TGF-beta. Both mitochondrial respiration rates and the side population cells in lung cancer cells increased in the absence of RBM47. Our findings, together with the enhanced tumor formation and metastasis of xenografted mice by knockdown of the RBM47 expression, suggested tumor suppressive roles for RBM47 through the inhibition of Nrf2 activity. Effect of shRNA for RBM47 and TGF-beta on gene expression was evaluated by RNA-seq and RBM47-bound RNAs were identified by RIP-seq in A549 cells.

2016-03-01 | E-GEOD-61910 | biostudies-arrayexpress

Nuclear mRNA quality control is bypassed for rapid export of stress responsive transcripts (Microarray)

Project description:Comparative analyses of Mex67 and Npl3 binding to mRNA at normal growth condition (25Â°C) and upon shift to heat stress (30 min, 42Â°C). Comparative analyses of mRNA binding of Mex67, Npl3 and no tag control at normal growth condition (25Â°C) and upon heat stress (30 min, 42Â°C) via RNA Co-IP experiments. Respective co-purified mRNAs were subjected to cDNA Microarray chips.

2016-06-14 | E-GEOD-83267 | biostudies-arrayexpress

HuR (ELAVL1) RIP-chip and knockdown exon array

Project description:Integrative regulatory mapping indicates that the RNA-binding protein HuR (ELAVL1) couples pre-mRNA processing and mRNA stability In this dataset, we employed two distinct experiments. 1) HuR RIP-chip to identify mRNA targets of HuR. 2) HuR knockdown to identify mRNAs whose expression are dependent on HuR. All 12 samples were normalized with PLIER using Affymetrix power tools. To identify RNA targets of HuR, HuR RIP samples were compared to Mock RIP samples. To identify RNA regulated by HuR, HuR knockdown samples were compared to mock knockdown samples.

2011-08-18 | E-GEOD-29778 | biostudies-arrayexpress

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