Project description:Mouse WT129 ESCs and differentiated from them within 12 days glutamatergic neurons were used for the ChiP-seq experiment with an antibody against Sox2 protein. ES stands for mESCs, NP for neurons, inputs are provided for both cell types.
Project description:Mouse WT129 ESCs were differentiated into glutamatergic neurons and samples were collected at days 0 (mESCs), 4 (embryoid bodies), 8 (neuronal precursors) and 12 (neurons). ATAC-seq experiment in 4 biological replicates was performed at 4 indicated above time points to profile chromatin structure changes during differentiation.
Project description:Mouse WT129 ESCs were differentiated into glutamatergic neurons and samples were collected at days 0 (mESCs), 4 (embryoid bodies), 8 (neuronal precursors) and 12 (neurons). These are RNA-seq data to profile RNA expression during differentiation.
Project description:We compared the transcriptome of the Sox2+ cells in forming incisor (E14.5) to the Sox2+ cells in renewing incisor (P30), using the MTA Affymetrix array. We used mouse embryonic stem cells (mESCs) as naïve cell reference.
Project description:Purpose: Sox2 expression marks gastric stem and progenitor cells, raising important questions regarding the genes regulated by Sox2 and the role of Sox2 itself during stomach homeostasis and disease. The goal of this study is to determine the function of and the genes regulated by Sox2 in the stomach. Methods: Sox2 ChIP-enriched DNA and input DNA was isolated from gastric glands of adult antrum from Sox2 KO and Sox2 WT mice. DNA was purified and genomic libraries were prepared as described (Sulahian et al., 2014), using four micrograms of goat anti-SOX2 (AF2018, R&D). Libraries were sequenced (50 bp, single-end reads) on an Illumina Hi-Seq 2000 instrument. Results: Sox2 is dispensiable for gastric stem cell self-renewal and epithelial homeostasis, however modulates the expression of wnt, intestinal and cancer related genes Examination of Sox2 targets in the stomachs of Sox2 WT and Sox2 KO mice.
Project description:Estrogen Receptor alpha (ERα) is a key driver of most breast cancers, and it is the target of endocrine therapies used in the clinic to treat women with ERα positive (ER+) breast cancer. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ERα function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used to pull down the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ERα have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ERα in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.
