Project description:This SuperSeries is composed of the following subset Series: GSE11874: Chromatin Immunoprecipitation microarray data from antiHA IP in stable LNCaP cells expressing either YFP or HA-SOX4/YFP GSE11913: Illumina expression data from LNCaP cells overexpressing either SOX4 or GFP GSE11914: Expression data from LNCaP cells transfected with SOX4 cDNA, SOX4 siRNA or GFP cDNA Refer to individual Series
Project description:SOX4 is a critical developmental transcription factor in vertebrates and is required for precise differentiation and proliferation in multiple tissues. In addition, SOX4 is overexpressed in many human malignancies, but the precise role of SOX4 in cancer progression is not well understood. Here we have identified the direct transcriptional targets of SOX4 using a genome-wide localization ChIP-chip analysis. Keywords: ChIP-chip LNCaP prostate cancer cells were stably infected with a lentivirus containing either HA-SOX4-IRES-YFP or IRES-YFP alone. Cells were sorted for YFP expression and expanded in tissue culture before chromatin immunoprecipitation against the HA epitope tag was performed.
Project description:This data from co-immunoprecipitation (co-IP) using YFP-Trap magnetic beads followed by mass spectrometry, using protein extracts prepared from the chloroplast fraction of cells expressing YFP-ATG8or YFP-HA.
Project description:The transcription factor HOXC6 is upregulated in human prostate cancer. SiRNA knockdown of HOXC6 induces apoptosis in LNCaP cells while upregulation rescued LNCaP cells from siRNA-induced apoptosis. We used chromatin immunoprecipitaiton followed by microarray to identify the gene promoters that are bound by HOXC6 in LNCaP cells. Keywords: Stable expression and chromatin immunoprecipitation
Project description:Transcriptional profiling of Schneider 2 cells comparing control stable inducible HA-expressing cells with stable inducible HA-crc expressing cells after 6h of induction with 0.7mM copper sulphate.
Project description:Transcriptional profiling of Schneider 2 cells comparing control stable inducible HA-expressing cells with stable inducible HA-crc expressing cells after 3h of induction with 0.7mM copper sulphate.
Project description:To address whether expression of ALS/FTD-associated UBQLN2 mutant variants changes the cellular proteome, we performed label-free quantification-based global protein abundance profiling of patient-derived LCLs and CRISPR engineered HeLa cells. UBQLN2 mutant in both cell lines carried the mutation T487I or P497S both of which were reported to cause ALS (Deng et al., 2011; Williams et al, 2012). In addition, HeLa cells stably expressing HA-tagged MAP1B (HA-MAP1B) were subjected to HA immunoprecipitation (IP) followed by mass spectrometry to identify MAP1B interacting proteins.
Project description:Prostate stroma-specific TGF-beta signaling induces morphological changes in LNCaP cells. We have previously shown that stromal TGF-beta signaling regulates prostate tumor growth. To further delineate the underlying mechanisms, we generated LNCaP cells overexpressing an HA-tagged constitutively activate TGF-beta1 ligand (LNCaP-HA-TGF-β1(a)) and control LNCaP cells (LNCaP-Ctrl), and performed in vitro co-cultures of LNCaP-HA-TGF-β1(a) and LNCaP-Ctrl cells on top of the confluent HPS-19I cells, a human prostate stromal cell line. Since LNCaP cells are defective in TGF-beta receptor I (TbetaRI / ALK-5) that is essential for mediating TGF-beta signaling, only HPS19I cells are able to respond to TGF-beta ligand in these co-cultures. This provides a unique opportunity to study how prostate stromal cell-specific TGF-beta signaling regulates PCa biology. To identify the prostate epithelia-specific gene that was regulated by prostate stromal TGF-beta signaling, we also treated HPS19I cells using conditioned media collected from LNCaP- HA-TGF-β1(a) cells and LNCaP-Ctrl cells cultured in RPMI1640 supplemented with 0.2% FBS. After 6 days of treatment, we extracted total RNA from these HPS19I cells and performed microarray.
