Project description:Identification of 2′–5′ OA binding proteins in human (HeLa), mouse (BMDM) and fly (Schneider S2) cells using affinity purification mass spectrometry (AP-MS). Pulsed SILAC-based translational profiling in HeLa and HeLa S3 cells treated with 2′–5′ OA or OH-2′–5′ OA.
Project description:We established HeLa cell lines stably expressing a short hairpin RNA against SIRT6 (S6 sh2), and then completed genome-wide microarray analysis in shSIRT6 knock-down and control pSR HeLa cells. Prior to RNA extraction, HeLa cells were treated with TNF-alpha (5 ng/ml) for the indicated times. Total RNA was extracted with TRIzol (Invitrogen) and amplified with Ambion MessageAmp RNA Amplification kit. Amplified human Universal Reference RNA (Stratagene) was used as reference RNA for analysis. Construction and array hybridization of human cDNA microarrays were performed as previously described (Perou et al., 2000). Groups of assays that are related as part of a time series. Compound Based Treatment: 5 ng/ml TNF-alpha Keywords: time_series_design
Project description:PolyA+ RNA from cytosol of HeLa and GM06990 cells using Affymetrix ENCODE tiling chip with NCBI build 35 annotation. Keywords: Expression profiling on tiling array
Project description:Gene profiling studies using RNA from HeLa cells overexpressing point mutants of SATB1 defective in phosphorylation or acetylation unequivocally demonstrated the importance of these modifications towards the ability of SATB1 to act as a global regulator of gene expression. HeLa cells were chosen as a representative of non-T cells, and do not express SATB1 endogenously. Keywords: cDNA array
Project description:Transcription profiling by array of HeLa cells after the knock-down of ASF1 (ASF1a & ASF1b) by siRNA compared to non-targeting control siRNA
Project description:Transcription profiling by array of mouse male retinas to investigate IGF-I-induced chronic gliosis and retinal stress IGF-I exert multiple effects in different retinal cell populations in both physiological and pathological conditions. Transgenic mice overexpressing IGF-I in the retina showed impaired electroretinographic responses at 6-7 months of age that worsen with age. This retinal neuronal dysfunction was correlated with the loss of rod photoreceptors, bipolar, ganglion and amacrines cells. Neuronal alterations were preceded by the overexpression of retinal stress markers, acute phase proteins and gliosis-related genes. IGF-I overexpression leads to chronic gliosis and microgliosis in TgIGF-I retinas, with mild oxidative stress, impaired recycling of glutamate and defective potassium buffering. These impaired supportive functions can contribute to neurodegeneration in TgIGF-I retinas, together with the increased production of pro-inflammatory cytokines, potential mediators of neuronal death.