Project description:To investigate the effect on chromatin accessibility with reduced ERBB2 signalling in oesophageal adenocarcinoma, we performed ATAC-seq in OE19 cells treated with either siNT or siERBB2.
Project description:To investigate initial changes to chromatin accessibility associated with resistance to lapatinib, we performed ATAC-seq on WTSI-OESO_009 cells treated with 1000 nM lapatinib for 24 hours and vehicle control (DMSO) for 24 hours.
Project description:To investigate initial changes to chromatin accessibility associated with resistance to lapatinib, we performed ATAC-seq on KYAE1 cells treated with 500 nM lapatinib for 24 hours and vehicle control (DMSO) for 24 hours.
Project description:To investigate initial changes to chromatin accessibility associated with resistance to lapatinib, we performed ATAC-seq on NCI-N87 cells treated with 250nM lapatinib for 24 hours and vehicle control (DMSO) for 24 hours.
Project description:To investigate changes to chromatin accessibility associated with resistance to lapatinib, we performed ATAC-seq on OE19 cells treated with 500 nM lapatinib for 1, 7 and 35 days and vehicle control (DMSO) for 1 day.
Project description:To investigate initial changes to chromatin accessibility associated with resistance to lapatinib, we performed ATAC-seq on ESO26 cells treated with 500 nM lapatinib plus 1000 nM MK-2206 (an AKT inhibitor) for 24 hours and vehicle control (DMSO) for 24 hours.
Project description:To investigate whether changes to chromatin accessibility associated with resistance to lapatinib are a stable or a reversible state, we treated OE19 cells with 500 nM lapatinib for 35 days and then withdrew lapatinib for 1, 2, 3 and 14 days. Control cells treated with DMSO for 1 day and 'resistant' cells treated with 500 nM lapatinib for 35 days were also sequenced.
Project description:The glucocorticoid receptor (GR) is a nuclear hormone receptor critical to the regulation of energy metabolism and the inflammatory response. The actions of GR are highly dependent on cell type and environmental context. Here, we demonstrate the necessity for liver lineage-determining factor hepatocyte nuclear factor 4A (HNF4A) in defining liver-specificity of GR action. In normal mouse liver, the HNF4 motif lies adjacent to the glucocorticoid response element (GRE) at GR binding sites found within regions of open chromatin. In the absence of HNF4A, the liver GR cistrome is remodelled, with both loss and gain of GR recruitment evident. Loss of chromatin accessibility at HNF4A-marked sites leads to loss of GR binding at weak GRE motifs. GR binding is gained at sites characterised by strong GRE motifs, which typically show GR recruitment in non-liver tissues. The functional importance of these HNF4A-regulated GR sites is further demonstrated by evidence of an altered transcriptional response to glucocorticoid treatment in the Hnf4a-null liver.
Project description:A small dose of the anti-HIV drug efavirenz (EFV) was previously discovered to activate CYP46A1, a cholesterol-eliminating enzyme in the brain, and mitigate some of the manifestation of Alzheimer’s disease in 5XFAD mice(a mouse model foe Alzheimers disease. Herein, we investigated the retina of these animals, which were found to have genetically determined retinal vascular lesions associated with deposits within the retinal pigment epithelium and sub retinal space.. Thus gain an unbiased insight into the processes in the retina that could be to affected by efavirenz treatment, the proteomic approach was used to compare the retinas of efavirenz -treated and control 5XFAD mice.