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: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: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:HeLa cells were treated with 100 mM NaCl during 2h versus untreated. HeLa cells treated with 100 mM NaCl during 2h versus HeLa cells treated with 100 mM NaCl during 2h after pre-treatment with 10 μM SB203580 for 30 min. Alternative splicing is a crucial mechanism for gene regulation that is modulated in response to a wide range of extracellular stimuli. Stress-activated protein kinases (SAPKs) play a key role in controlling several steps of mRNA biogenesis. Here, we show that osmostress has a major impact on the regulation of alternative splicing (AS), which is partly mediated through the action of the p38 SAPK.