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T47D Breast cancer cell line ChIP-seq data II

ABSTRACT: We performed genome-wide CDK9 ChIP seq experiments in T47D cells only expressing HA Tagged amanitin resistant wild type in comparison to R1810A mutant form of RNAP2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE113971 | GEO | 2018/11/21

REPOSITORIES: GEO

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T47D Breast cancer cell line ChIP-seq data

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.

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T47D RNA-seq and ChrRNA-seq data

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.

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Gene expression of T47D-MTVL human breast cancer cells upon H1.4 knock-down or overexpression

Project description:Gene expression of T47D-MTVL human breast cancer cells expressing Dox-inducible shRNAs against histone H1.4 (sh120) or multiple H1 variants (sh225), or overexpressing WT or K26A mutant HA-tagged H1.4. T47D-MTVL, breast cancer cell line carrying one stably integrated copy of luciferase reporter gene driven by the MMTV promoter, is stably infected with an inducible system for the expression of shRNAs.Cells stably express RedFP and KRAB repressor fused to Tet regulator.Upon Dox treatment, cells express RedFP and the cloned shRNA. Stable breast cancer-derived cell lines expressing an shRNA against one of each of the histone H1 isoforms in response to doxycycline (Dox) were grown for six days in the presence or absence of Dox, in duplicate, and RNA extracted for microarray hybridization. Cell lines used: inducible shRNA against H1.4 or multiple H1 variants, and random shRNA-expression vector. Stable breast cancer-derived cell lines expressing the histone H1.4 isoform, WT or K26A, HA-tagged, in duplicate, and RNA extracted for microarray hybridization. Cell lines used: overexpressing H1.4 WT or K26A mutant.

2014-05-16 | E-GEOD-55786 | biostudies-arrayexpress

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.

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T47D Breast cancer cell line ChIP-seq data II

Project description:T47D Breast cancer cell line ChIP-seq data II

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aCGH hybridization of breast cancer cell line T47D

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Project description:T47D shNT versus T47D shRON

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Convergence of distinct RNA-silencing pathways on GW182/Tnrc6 [RIP-seq II]

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