Project description:ChIP seq of endogenous Smad3 and JMJD3 proteins in mouse embryonic neural stem cells treated with TGFbeta during 30 minutes. Neural stem cells were treated with TGFbeta during 30 minutes, and then chromatin immunoprecipitation was carried out with specific JMJD3 or Smad3 antibodies. Positive and negative controls for each immunoprecipitation were checked before sequencing. Input was used to normalized the sequencing results.
Project description:Chromatin immunoprecipitation followed by deep sequencing (ChIP seq), using L4-staged animals that express an integrated construct of lir-3 fused to a GFP tag
Project description:Chromatin immunoprecipitation DNA-sequencing (ChIP-seq) for histone modifications, H3K27ac, H3K4me3, H3K27me3 and H3K9me3 in H460 (T/T) and H460 (C/C) cells
Project description:To define the activity of TFCP2L1 following CXCR2 perturbation, we performed chromatin immunoprecipitation and sequencing analysis (CHIPseq) on B16F0 tumorigenic melanoma cells following treatment with vehicle or SX-682.
Project description:During Arabidopsis (Arabidopsis thaliana) leaf epidermis development, precursor cells divide and differentiate to form distinct patterns of trichomes, pavement cells, and stomata. The mechanisms governing these developmental transitions remain unclear. We identified the homeodomain-like protein HDL, which is required for heterochromatin compaction through interactions with the histone deacetylase HDA6 and the methyltransferase KRYPTONITE during the cell cycle. Mutants of HDL showed a prolonged interphase, fewer cell divisions, and greater endoreduplication, resulting in fewer stomata and more trichomes. Chromatin immunoprecipitation and ATAC-sequencing revealed higher chromatin accessibility in HDL-bound regions and lower chromatin accessibility along the promoters of stomata-related genes, which also showed reduced expression in hdl mutants. These findings highlight the importance of chromatin organization in maintaining cell division potential and transcriptional control.
Project description:In order to identify direct gene targets and pathways regulated by MEIS1 in prostate cells and identify mechanisms of observed tumor suppression with MEIS1 expression, we performed Chromatin Immunoprecipitation and sequencing (ChIP-seq) of MEIS1 in the CWR22Rv1-LV-MEIS1 line. Also, given the dependence of HOXB13, and to enable determination of HOXB13-dependent vs. HOXB13-independent MEIS1 DNA binding, we performed parallel MEIS1 ChIP-seq in the CWR22Rv1-HOXB13ko-LV-MEIS1 line. LV-MEIS1 denotes cells with exogenous lentiviral expression of MEIS1, and they still express endogenous HOXB13. Knockout of HOXB13 was achieved by CRISPR and validated with western blotting. HOXB13ko-LV-MEIS1 denotes cells where the same lentiviral expression of MEIS1 was infected into the HOXB13ko cells, so these cells are positive for MEIS1 expression and negative for HOXB13.