ChIP-seq for H3K27ac in the GR18 cell line treated for 1.5 h with 1 µM dexamethasone
Ontology highlight
ABSTRACT: We performed ChIP-seq in the GR18 cell line (derived from U2OS ATTC:HTB-96, stably transfected with an expression construct for GR), upon glucocorticoid (dexamethasone)treatment for 90 minutes. Cells were cross-linked with 1% formaldehyde for 3 minutes.
Project description:To identify the genes regulated by the Glucocorticoid Receptor (GR), we performed RNA-seq in GR18 cell line (derived from U2OS ATTC:HTB-96, stably transfected with an expression construct for GR), upon glucocorticoid (dexamethasone) or vehicle (ethanol) treatment.
Project description:To identify the genes regulated by the Glucocorticoid Receptor (GR), we performed RNA-seq in GR18 cell line (derived from U2OS ATTC:HTB-96, stably transfected with an expression construct for GR), upon glucocorticoid (dexamethasone) or vehicle (ethanol) treatment for 24 hours.
Project description:We performed ATAC-seq in the GR18 cell line (derived from U2OS ATTC:HTB-96, stably transfected with an expression construct for GR), upon glucocorticoid (dexamethasone) or vehicle (ethanol) treatment for 90 minutes.
Project description:We performed ChIP-seq targeting the H3K27ac, H3K4me1, H3K27me3 and H3K9me3 in the U2OS-GR and U2OS-AR cell lines. The cell lines are derived from U2OS ATTC:HTB-96 and stably transfected with an expression construct for either rat GR or human AR, respectively. The U2OS-GR cells were treated with dexamethasone (1 µM) or vehicle (ethanol) for 90 minutes. The U2OS-AR cells were treated with R1881 (5 nM) or vehicle (DMSO) for 4 hours.
Project description:To identify the genes regulated by the androgen receptor (AR), we performed RNA-seq in the U2OS-AR cell line (derived from U2OS ATTC:HTB-96, stably transfected with an expression construct for human AR), upon androgen (R1881) or vehicle (DMSO) treatment for 24 hours.
Project description:Given that mice transplanted with glucocorticoid-resistant T cells display more severe disease symptoms, the idea was that an RNA-seq comparison between mice transplanted with either wildtype or glucocorticoid-resistant T cells could yield genes involved in disease progression and potential therapeutic targets.
Project description:We performed total RNA-seq in the A549 cell line. Cells were treated with either 100 nM dexamethasone or 0.1% ethanol. After 4 hours, cells were washed 2x with PBS and cultured in hormone-free medium for 24 hours, after which cells were treated again for 4 hours with either 100 nM dexamethasone or 0.1% ethanol.
Project description:We performed ChIP-seq targeting the glucocorticoid receptor (GR) in the U2OS-GR cell line and the androgen receptor (AR) in the U2OS-AR cell line. The cell lines are derived from U2OS ATTC:HTB-96 and stably transfected with an expression construct for either rat GR or human AR, respectively. The U2OS-GR cells were treated with dexamethasone (1 µM) for 90 minutes. The U2OS-AR cells were treated with R1881 (5 nM) for 4 hours.
Project description:We performed STARR-seq with synthetic libraries (synSTARR-seq) in GR18 cell line (derived from U2OS ATTC:HTB-96, stably transfected with an expression construct for GR), upon glucocorticoid (dexamethasone) or vehicle (ethanol) treatment. The synthetic libraries are variants of the glucocorticoid receptor binding sites (GBS). The "GBS half site" library contains 8 consecutive randomized nucleotides within the core binding sites, while the "Cgt/Sgk library" contains 5 consecutive randomized nucleotides on the flank of the GBS.
Project description:We aimed to compare CTCF binding patterns, chromatin states and 3D genome structure in the absence and after activation of Wnt signaling in HEK293T cells.