Project description:We performed genome-wide RNA-seq and ChrRNA-seq experiments in T47D cell lines after PADI2 knock down . Both the mRNA and chromatin RNA seq peformed in sicontrol and siPADI2 as in biological replicates . Also we performed mRNA seq in T47D cells expressing HA Tagged amanitin resistant wild type in comparison to R1810A mutant form of RNAP2.
Project description:We performed genome-wide PADI2 ChIP seq experiments in T47D cell lines and also RNP2 ChIP seq in T47D cells only expressing HA Tagged amanitin resistant wild type in comparison to R1810A mutant form of RNAP2.
Project description:We performed SMAD2 ChIP-seq analysis in T47D cells with/without Palbociclib treatment. To validate whether the changes in SMAD2 binding to the genome indeed resulted in changes in target gene expression, we performed RNA-seq transcriptome analyses in T47D with/without ActA stimulation and Palbo treatment.
Project description:We report the comprehensive genome-wide binding peaks for key factors inovled in oxygen sensing pathways, such as HIF1α, HIF1β and EglN2. In addition, we also report the genome-wide binding peaks for NRF1 in breast cancer cells We conducted HA-EglN2, HIF1α, HIF1β (ARNT) or NRF1 ChIP-Seq in the T47D cell line that overexpresses HA-EglN2 in the presence of hypoxia (1%) and DMOG treatment. T47D parental cells treated with the same condition followed by HA ChIP-seq served as the control to filter non-specific binding.
