CDK7-dependent Transcriptional Addition in Basal-like Breast Cancer
收藏官方服务:
资源简介:
CDK7-dependent Transcriptional Addition in Basal-like Breast Cancer
应用场景:
创建时间:
2015-05-21
相关数据集
ChIP-Seq analysis to identify direct binding of ZNF165
We found that the cancer testis antigen, ZNF165, is required for viability and modulates TGFÃ-induced gene expression in mesenchymal, Claudin-Low, TNBC. To begin to define ZNF165''s role in TNBC tumo
NIAID Data Ecosystem120
Genome-wide maps of XBP1 binding sites in different breast cancer cell lines [ChIP-Seq]. Homo sapiens
We report the application of ChIP-seq, which combines chromatin immunoprecipitation (ChIP) with massively parallel DNA sequencing, to map genome-wide XBP1 binding sites in different breast cancer cell
NIAID Data Ecosystem40
Genome-wide profiling of inflammatory cistrome reveals AP-1/c-Jun as a key regulator of TNFalpha-mediated triple-negative breast cancer progression [microarray]
Triple-negative breast cancer (TNBC) represents a highly aggressive form of breast cancer with limited treatment options. Proinflammatory cytokines such as TNFalpha can facilitate tumor progression an
NIAID Data Ecosystem30
CDK7-dependent Transcriptional Addiction in Triple-Negative Breast Cancer (Microarray)
Triple-negative breast cancer (TNBC) is a highly aggressive form of breast cancer that exhibits extremely high levels of genetic complexity and yet a relatively uniform transcriptional program. We pos
NIAID Data Ecosystem70
EBF1 survive HIF1 activity
Genome-wide mapping of the EBF1 transcriptional regulatory network revealed that EBF1 drives TNBC tumorigenicity by assembling a transcriptional complex with HIF1 that fine-tunes the expression of HIF
NIAID Data Ecosystem30



