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Expression analysis of Reh cells after transfection with shRNA targeting CBFA2T3 and/or constitutively active IKKβ(EE)

ABSTRACT: Genome-wide gene expression analysis of Reh cells following transfection with shRNA targeting CBFA2T3, constitutively active IKKβ(EE), or both in combination.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20115 | GEO | 2010/04/23

SECONDARY ACCESSION(S): PRJNA124249

REPOSITORIES: GEO

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Expression analysis of Reh cells after transfection with shRNA targeting CBFA2T3 and/or constitutively active IKKÎ²(EE)

Project description:Genome-wide gene expression analysis of Reh cells following transfection with shRNA targeting CBFA2T3, constitutively active IKKÎ²(EE), or both in combination. Affymetrix U133 Plus 2.0 oligonucleotide arrays were hybridized to determine the gene expression profile of acute lymphoblastic leukemia-derived Reh cells following transfection with i) control shRNA construct, ii) shRNA construct targeting CBFA2T3, iii) a constitutively active variant of the IkB kinase Î² (IKKÎ²(EE)), or iv) shRNA targeting CBFA2T3 in combination with IKKÎ²(EE). All hybridizations were done in biological duplicates.

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Project description:Genome-wide gene expression analysis of Reh cells following transfection with constitutively active IRF5-4D, constitutively active IKKÎ²(EE), or both in combination. Affymetrix U133 Plus 2.0 oligonucleotide arrays were hybridized to determine the gene expression profile of acute lymphoblastic leukemia-derived Reh cells following transfection with i) control constructs, ii), a constitutively active variant of IRF5 (IRF5-4D), iii) a constitutively active variant of the IkB kinase Î² (IKKÎ²(EE)), or iv) IRF5-4D in combination with IKKÎ²(EE). All hybridizations were done in biological duplicates.

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Homo sapiens

Project description:Expression analysis of Reh cells after transfection with shRNA targeting CBFA2T3 and/or constitutively active IKKβ(EE)

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Project description:Genomic copy number profiling of hepatocellular carcinomas (HCC) from IKKβ(EE)Hep mice (C57BL/6) constitutively expressing IKKβ in the liver without and after treatment with DEN (diethylnitrosamine) and of HCCs that developed in wild type mice (C57BL/6) after DEN treatment.

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Project description:IKKβ-dependent NF-κB activation is associated with inflammation and tumorigenesis and is critical for innate immunity. Despite risk of immune suppression, pharmacological blockade of IKKβ/NF-κB has been considered as an attractive strategy for treatment of inflammatory diseases and cancer. Unexpectedly, treatment with IKKβ inhibitors caused neutrophilia, which also occurs in mice with inducible IKKβ deletion, termed IkkβΔ mice. IkkβΔ mice show hyperproliferation of granulocyte progenitors and increased neutrophil lifespan. Deletion of IL-1 receptor 1 in IkkβΔ mice restored normal blood cellularity and prevented neutrophil-driven inflammation. However, IkkβΔ/Il-1r1-/- mice, in contrast to IkkβΔ mice, are highly susceptible to bacterial infections indicating that either IKKβ/NF-κB or IL-1R signaling are sufficient for maintaining anti-microbial defenses, but inactivation of both pathways severely compromises innate immunity. Thioglycollate-elicited peritoneal neutrophils were purified from IkkβF/F and IkkβΔ mice using anti-Ly-6G magnetic beads and cultured. Ly-6G+ neutrophils were collected and total RNA was extracted with TRIzol® (Invitrogen) and was purified by RNA micro cleanup Kit (Qiagen). Biotinylated cRNA was synthesized using an RNA Amplification Kit (Ambion) following manufacturer's directions. Biotin-labeled cRNA was hybridized to Illumina Mouse-Ref8 BeadChips (Illumina) and the results were analyzed using BeadStudio v3.1 software. Data analysis and quality control were carried out using Partek® software.

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Gene expression changes in REH following CDC42 inhibition

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