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Transcriptional profiling of hypoxic cells and identification of HEXIM1-dependent genes.

ABSTRACT: To identify primary response genes (PRGs) that were differently expressed within 1 hr of hypoxia exposure, we performed global transcriptional profiling using the Agilent Technologies SurePrint G3 Human GE Microarray . To identify Hexim1-dependent genes, we compare profiles of hypoxia PRGs in cells transfected with control or Hexim1 targeting double-strand siRNA HeLa cells were transfected with control and HEXIM1-targeted double-strand siRNA and 48 hr after treated with IL-1beta in combination with normoxia or hypoxia (5% CO2, 0.5% O2, balanced with N2) O for 1 hr.

ORGANISM(S): Homo sapiens

SUBMITTER: Olga Safronova

PROVIDER: E-GEOD-41023 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional profiling of hypoxic cells and identification of HEXIM1-dependent genes.

Project description:To identify primary response genes (PRGs) that were differently expressed within 1 hr of hypoxia exposure, we performed global transcriptional profiling using the Agilent Technologies SurePrint G3 Human GE Microarray . To identify Hexim1-dependent genes, we compare profiles of hypoxia PRGs in cells transfected with control or Hexim1 targeting double-strand siRNA

2012-09-21 | GSE41023 | GEO

Hela SPAG4 siRNA

Project description:In order to clarify the downstream target genes of SPAG4, we performed knockdown of SPAG4 using siRNA both under normoxia and hypoxia. Hela cells are cultured for 24 hours under normoxia and hypoxia after knocking down of SPAG4 using different sequences of siRNA.

2013-04-16 | E-GEOD-46054 | biostudies-arrayexpress

A module-based translational strategy shows a central role for S100A4 in allergy

Project description:The involvement of thousands of genes complicates the identification of clinically relevant candidate genes in common diseases. We hypothesized that genes co-regulated with a key gene in allergy, IL13, would form a module that could help to discover novel candidate genes. We identified a Th2 cell module by siRNA mediated knock down of 25 putative IL13-regulating transcription factors (TFs) followed by expression profiling. Human CD4+ T cells (hBP CD4+ T cells, 2W-200, Lonza, Vallensbak Strand, Denkmark) were nucleofected either with nucleofection buffer, 1 ÂµM human on target plus SMART pool siRNA against ELK1, GATA3, NFATC3, MAF, NFKB1, JUN, STAT3 (Dharmacon, Lafayette, CO) or non-targeting siRNA using the AMAXA nucleofection program U-014. Six hours after then nucleofection cells were washed, activated and polarized towards Th2. The CD4+ cells were activated with plate bound anti-CD3 (500ng / ml for coating of the plate), with soluble anti-CD28 (500ng / ml) and with IL-2 (17ng /ml, all purchased from R&D). Th2 polarization was induced with anti-IL-12 (5Âµg/ml) and IL-4 (10ng / ml). For RT-PCR and microarray analyisis the cells were harvested 12 hours of polarization and total RNA was extracted.

2014-02-05 | E-GEOD-46333 | biostudies-arrayexpress

Gene expression profiling of the cell death induced by heat stress in DNA-PK-knockdown human cervical carcinoma HeLa cells

Project description:The objective of the present study is to investigate the role of DNA-PK inhibition in cell death induced by heat stress (44M-BM-0C, 60 min). Comparative gene expression analysis was performed with mock cells, negative control siRNA-treated cells and DNA-PK siRNA-treated cells. The expression of DNA-PK was confirmed by Western blotting. Gene expression was analyzed using GeneChip oligonucleotide microarrays and computational gene expression analysis tools. DNA-PK-knockdown human cervical carcinoma HeLa cells were treated with heat (44M-BM-0C, 60 min) and then were cultured at 37M-BM-0C for 6 h. Total RNA samples were prepared from the cells. Gene expression was analyzed by an Affymetrix GeneChipM-BM-. system with GeneChip Human Gene 1.0 ST arrays. Sample preparation for array hybridization was carried out as described in the manufacturer's instructions.

2012-07-12 | E-GEOD-39063 | biostudies-arrayexpress

Integrative AUF1 PAR-CLIP analysis uncovers AUF1 roles in translation and genome integrity (Ribosome)

Project description:We report that AUF1 modulates global mRNA stability and translation, in turn promoting the maintenance of DNA integrity. Please see individual series. In short, For AUF1 PAR-CLIP, the four isoforms of AUF1 (p37, p40, p42, and p45) tagged with a Flag epitope were expressed in HEK293 cells. For total RNA-Seq HEK293 cells were transfected with Control siRNA, AUF1 siRNA, Empty Vector, Flag-AUF1 p37, p40, p42, or p45 as well as WI-38 cells were collected at PDL 15 and 55 and also transfected with Control siRNA, AUF1 siRNA, HuR siRNA. For Ribo-Seq HeLa cells were transfected with Control siRNA, AUF1 siRNA, or HuR siRNA.

2014-11-04 | E-GEOD-52976 | biostudies-arrayexpress

Expression data from HeLa cells after MBD2 and MBD3 knock down

Project description:The heterogeneous collection of NuRD complexes can be grouped into the MBD2 or MBD3 containing complexes MBD2-NuRD and MBD3-NuRD. MBD2 is known to bind to methylated CpG sequences in vitro in contrast to MBD3. Although functional differences have been described, a direct comparison of MBD2 and MBD3 in respect to genome-wide binding and function has been lacking. Here we show when depleting cells for MBD2, the MBD2 bound genes increase their activity, whereas MBD2 plus MBD3 bound genes reduce their activity. Most strikingly, MBD3 is enriched at active promoters, whereas MBD2 is bound at methylated promoters and enriched at exon sequences of active genes. This suggests a functional connection between MBD2 binding to chromatin and splicing. 9 Total samples were analysed. Three individual replicates for HeLa cells treated with siRNA against MBD2, MBD3 or scrambled siRNA were performed. We calculated the fold change of gene expression of cells treated with MBD2- or MBD3-siRNA over cells treated with scrambled siRNA.

2013-02-08 | E-GEOD-41003 | biostudies-arrayexpress

Influence of G0s2 gene knockdown on primary hepatocyte

Project description:Hepatocellular carcinoma is the third leading cause of cancer death worldwide, and it is necessary to elucidate the mechanism of hepatocarcinogenesis. Circadian clock systems have been related in cell cycle and carcinogenesis. In this study, hepatocarcinogenesis induced by DEN administration in mice was inhibited by knockdown of G0s2 at early stage in carcinogenesis. In addition, the circadian expression of G0s2 in mouse liver was regulated by RARM-NM-1 controlled by clock genes and ATRA. Moreover, mice administered both ATRA and DEN were not induced hepatocellular carcinoma, and decreased the expression of G0s2 at second day after the initiation of administration. These findings suggest that the control of G0s2 expression is important in carcinogenesis and G0s2 might be the novel target for prevention, diagnosis and treatment of hepatocellular carcinoma. Differential gene expression between G0s2 siRNA or Control siRNA transfected primary hepatocyte was measured after 24 hr of transfection.

2013-08-01 | E-GEOD-39288 | biostudies-arrayexpress

RNAi-mediated knockdown of Xist can rescue the impaired postimplantation development of cloned mouse embryo

Project description:Cloning mammals by somatic cell nuclear transfer (SCNT) is highly inefficient. Most SCNT-generated embryos die after implantation because of unidentified, complex epigenetic errors in the process of postimplantation embryonic development. Here, we identified the most upstream level of dysfunction leading to impaired development of clones by using RNA interference (RNAi) against Xist, a gene responsible for X chromosome inactivation (XCI). A prior injection of Xist-specific short interfering (si)RNA into reconstructed oocytes efficiently corrected the SCNT-specific aberrant Xist expression at the morula stage, but failed to do so thereafter at the blastocyst stage. However, we found that shortly after implantation this aberrant XCI status in cloned embryos had been corrected autonomously in both embryonic and extraembryonic tissues, probably through a newly established XCI control for postimplantation embryos. Embryo transfer experiments revealed that the siRNA-treated embryos showed 10 times higher survival than controls as early as embryonic day 5.5 and this high survival persisted until term, resulting in a remarkable improvement in cloning efficiency (12% vs. 1% in controls). Importantly, unlike control clones, these Xist-siRNA clones at birth showed only a limited dysregulation of their gene expression, indicating that correction of Xist expression in preimplantation embryos had a long-term effect on their postnatal normality. Thus, contrary to the general assumption, our results suggest that the fate of cloned embryos is determined almost exclusively before implantation by their XCI status. Furthermore, our strategy provides a promising breakthrough for mammalian SCNT cloning because RNAi treatment of oocytes is readily applicable to most mammal species. Gene expression were measured in mouse in vitro fertilized and somatic cell cloned embryos. Four biological replicates were performed in each group of Xist- or Control-siRNA.

2011-11-17 | E-GEOD-33208 | biostudies-arrayexpress

CTCF cooperates with CtIP to drive homologous recombination repair of double-strand breaks

Project description:The pleiotropic CCCTC-binding factor (CTCF) plays a role in homologous recombination (HR) repair of DNA double-strand breaks (DSBs). However, the precise mechanistic role of CTCF in HR remains largely unclear. Here, we show that CTCF engages in DNA end resection, which is the initial, crucial step in HR, through its interactions with MRE11 and CtIP. Depletion of CTCF profoundly impairs HR and attenuates CtIP recruitment at DSBs. CTCF physically interacts with MRE11 and CtIP and promotes CtIP recruitment to sites of DNA damage. Subsequently, CTCF facilitates DNA end resection to allow HR, in conjunction with MRE11-CtIP. Notably, the zinc finger domain of CTCF binds to both MRE11 and CtIP and enables proficient CtIP recruitment, DNA end resection, and HR. The N-terminus of CTCF is able to bind to only MRE11 and its C-terminus is incapable of binding to MRE11 and CtIP, thereby resulting in compromised CtIP recruitment, DSB resection, and HR. Overall, this suggests an important function of CTCF in DNA end resection through the recruitment of CtIP at DSBs. Collectively, our findings identify a critical role of CTCF at the first control point in selecting the HR repair pathway

2019-11-12 | PXD014441 | Pride

Exon array expression profiling: DYRK1A acts as transcriptional activator

Project description:Transcriptome analysis of depletion of DYRK1A in HeLa cells Global gene expression profiling has shown upregulation of many genes in the context of DYRK1A depletion in HeLa cells. Many of these genes deregulated by DYRK1A are involved in immune response system. Transcriptome analysis of siRNA against DYRK1A transfected in HeLa cells on GeneChipM-BM-. Human Exon 1.0 ST Arrays (Affimetrix). Control HeLa cells have been transfected with the same concentration of siRNA non-targeting (siNT). Experiment has been done experimental triplicates.

2014-05-01 | E-GEOD-43259 | biostudies-arrayexpress

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