Project description:mITP-induced transcriptional changes were measured in 48 hpf wild-type or ahr2hu3335 embryos exposed to 0 or 0.2 uM mITP from 6-48 hpf.
Project description:Herceptin (trastuzumab) is a humanized monoclonal antibody targeted to the Her2 receptor tyrosine kinase. Despite a robust response rate to Herceptin-based therapies in Her2-positive patients, resistance frequently arises within one year of the initial response. To address the mechanism of Herceptin resistance, we selected clonal variants of Her2-positive BT474 human breast cancer cells (BT/HerR) that are highly resistant to the anti-proliferative effects of Herceptin in the presence of 0.2 uM or 1.0 uM Herceptin. Our original report on these cell lines demonstrated sustained PI3K/Akt signaling and sensitivity to PI3K inhibitors in BT/HerR cells in the presence of Herceptin, suggesting dysregulation of that pathway as an essential component of Herceptin-resistant proliferation. To address the mechanism by which BT/HerR cells and their PI3K/Akt signaling pathway became resistant to Herceptin, we analyzed gene expression profiles of two clones (BT/HerR1.0C and BT/HerR 1.0E) that were selected in 1.0 uM Herceptin and two clones (BT/HerR0.2D and BT/HerR 0.2J) that were selected in 0.2 uM Herceptin, in comparison to the Herceptin sensitive BT474 parent cells.
Project description:The aim of this study was to identify differential gene expression resulting from the inhibition of RORgt in human CD4+ T cells. Human CD4+ T cells were cultured with anti-CD3/anti-CD28 mAb for 20 to 60 hours concurrent with exposure to Vehicle (DMSO), TMP778 (0.2 uM) or TMP776 (0.2 uM). All samples were then processed for RNA extraction, labeling, and hybridization to Affymetrix arrays.
