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Alternative splicing signatures in apoptosis related genes of human HeLa cells with RNAi targeting p68 RNA helicase-DDX5

ABSTRACT: Alternative splicing profiling of apopotosis related genes in human HeLa cells (cervical cancer cell line) transfected with a plasmid expressing shRNAs targetting p68 helicase (DDX5, DEAD (Asp-Glu-Ala-Asp) box polypeptide 5) cloned into the pSuper expression vector compared to empty vector. Keywords: treated vs. untreated comparison; alternative splicing

ORGANISM(S): Homo sapiens

PROVIDER: GSE20010 | GEO | 2011/01/21

SECONDARY ACCESSION(S): PRJNA124079

REPOSITORIES: GEO

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Alternative splicing signatures in apoptosis related genes of human HeLa cells with RNAi targeting p68 RNA helicase-DDX5

Project description:Alternative splicing profiling of apopotosis related genes in human HeLa cells (cervical cancer cell line) transfected with a plasmid expressing shRNAs targetting p68 helicase (DDX5, DEAD (Asp-Glu-Ala-Asp) box polypeptide 5) cloned into the pSuper expression vector compared to empty vector. Keywords: treated vs. untreated comparison; alternative splicing Two-condition experiment, where the p68 DDX5 gene product levels was inhibited by siRNA transfection and compared to transfection with the negative control (scrambled siRNA). Biological replicates: 2, all independently grown and harvested. A dye swapping technical duplicate was performed for each biological replicate. Samples were hybridized onto a 44290 feature array designed by ExonHit to detect splicing events in apopotosis related genes and manufactured by Agilent using in situ synthesis of oligonucleotides by SurePrint technology.

2011-01-21 | E-GEOD-20010 | biostudies-arrayexpress

Expression signatures of human HeLa cells with RNAi targetting A1 hnRNP, FUS, H hnRNP and p68-DDX5

2008-08-20 | GSE12058 | GEO

Expression signatures of human HeLa cells with RNAi targetting A1 hnRNP, FUS, H hnRNP and p68-DDX5

Project description:Transcription profiling of human HeLa cells (cervical cancer cell line) transfected with a plasmid expressing shRNAs cloned into the pSuper expression vector compared to emprty vector negative controls for transfection. Four different RNA interference treatments targetted: A1 hnRNP (HNRNPA1, Heterogeneous nuclear ribonucleoprotein A1); FUS (fusion gene, involved in t(12;16) in malignant liposarcoma); H hnRNP (HNRNPH1); and p68 helicase (DDX5, DEAD (Asp-Glu-Ala-Asp) box polypeptide 5). Keywords: genetic modification Five-condition experiment, where HNRNPA1, FUS, HNRNPH1 and DDX5 gene product levels were inhibited by siRNA transfection and compared to transfection with the negative control (scrambled siRNA). Biological replicates: 2 of each of the first three treatments and 3 of the treatment against DDX5, all independently grown and harvested. No technical replicates were performed.

2008-08-20 | E-GEOD-12058 | biostudies-arrayexpress

p68 SMC differentiation

Project description:This project investigates the function of p68/p72 in muscle gene expression and skeletal C2C12 cell differentiation. p68/p72 in C2C12 cells cultured in either growth medium (GM) or differentiation medium (DM) was knocked down using shRNA p68/p72 retrovirus, and globle gene expression was profiled using Affymetrix MOE 430A and 430B GeneChip. Keywords: Time-Series

2006-07-13 | GSE5305 | GEO

Transcription profiling of p68/72 deficient C2C12 cells cultured in either growth medium or differentiation medium to investigate the function of p68/p72 in muscle gene expression and skeletal C2C12 cell differentiation.

2007-11-29 | E-GEOD-5305 | biostudies-arrayexpress

P68 protein inhibited the growth and invasion of glioma cells by adjusting the DUSP5

Project description:Preliminary research shows that,The P68 protein was highly expressed in the glioma tissue specimen and was associated with the patient's survival.Inhibition of P68 protein expression in glioma cell lines inhibits the growth, invasion and appreciation of tumor cells.In this study, gene chip was used to search for new downstream genes DUSP5 that affect the growth of glioma.The expression of inhibition or overexpression of P68 protein in glioma cell lines was consistent with the expression of expression DUSP5 and the effect of reduction DUSP5 on the growth of the tumor.The ability of the tumor to recover after the expression of DUSP5 expression in glioma cells was reduced,This indicates that P68 regulates the growth, increment and invasion of glioma cells.Through affymetrix gene chip, we use 3 biological specimens.That is three SIP68 , control of the glioma cells that infect NC.Try to get P68 protein regulated downstream gene by knocking down P68 protein.

2017-09-20 | GSE103981 | GEO

Clostridioides difficile P68

Project description:Clostridioides difficile P68 Genome sequencing and assembly

| PRJNA86041 | ENA

Mediation of CTCF transcriptional insulation by DEAD-box RNA-binding protein p68 and steroid receptor RNA activator SRA

Project description:CCCTC-binding factor (CTCF) is a DNA-binding protein that plays important roles in chromatin organization, though the mechanism by which CTCF carries out these functions is not fully understood. Recent studies show that CTCF recruits the cohesin complex to insulator sites and that cohesin is required for insulator activity. Here we have shown that the DEAD box RNA helicase p68 (DDX5) and its associated noncoding RNA, steroid receptor RNA activator (SRA), form a complex with CTCF that is essential for insulator function. p68 was detected at CTCF sites in the IGF2/H19 imprinted control region (ICR) as well as other genomic CTCF sites. In vivo depletion of SRA or p68 reduced CTCF-mediated insulator activity at the IGF2/H19 ICR, increased levels of IGF2 expression, and increased interactions between the endodermal enhancer and IGF2 promoter. p68/SRA also interacts with members of the cohesin complex. Depletion of either p68 or SRA does not affect CTCF binding to its genomic sites, but it does reduce cohesin binding. The results suggest that p68/SRA stabilizes the interaction of cohesin with CTCF, by binding to both, and is required for proper insulator function. Identification of p68-binding sites in Hela cells using ChIP-Seq.

2010-11-16 | E-GEOD-24126 | biostudies-arrayexpress

Mediation of CTCF transcriptional insulation by DEAD-box RNA-binding protein p68 and steroid receptor RNA activator SRA

2010-11-16 | GSE24126 | GEO

Genome-wide map of long non-coding RNA steroid receptor RNA activator (SRA) and its associated RNA heliase p68 in human pluripotent stem cells NTERA2

Project description:We performed Chromatin Isolation by RNA Purification (ChIRP) of SRA and ChIP of p68 following by high-throughput sequencing in NTERA2 cell line. We find that SRA localizes with p68 genome-wide at genes whose function is involved in embryonic development. SRA ChIRP and p68 ChIP of triplicate samples.

2014-06-18 | E-GEOD-58641 | biostudies-arrayexpress

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