Wang:Research: Difference between revisions
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<center><font face="lucida fax" style= "color:yellow" size="+2">'''Laboratory of Cancer Epigenomics'''</font></center> | <center><font face="lucida fax" style= "color:yellow" size="+2">'''Laboratory of Cancer Epigenomics'''</font></center> | ||
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<center><font face="lucida fax" style= "color:yellow" size="+1">'''Department of | <center><font face="lucida fax" style= "color:yellow" size="+1">'''Department of Cancer Biology and Genetics, The Ohio State University'''</font> | ||
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[[Wang | <font face="lucida fax" style="color:#ffffff" size="+1"> '''Home''' </font>]] | [[Wang | <font face="lucida fax" style="color:#ffffff" size="+1"> '''Home''' </font>]] |
Latest revision as of 09:02, 1 July 2016
My laboratory is primarily interested in understanding the genomic function of androgen receptor (AR) in the development and progression of prostate cancer. AR is a ligand-dependent transcription factor belonging to the nuclear hormone receptor (NR) superfamily. Recently, we have utilized high-throughput techniques such as ChIP-exo (chromatin immunoprecipitation-exonuclease combined with high-throughput sequencing) and ChIP-seq (ChIP combined with high-throughput sequencing) to globally identify AR-bound genomic sites and precisely define AR binding motifs leading to target gene expression at various stages of prostate cancer, including androgen-dependent prostate cancer (ADPC) and castration-resistant prostate cancer (CRPC). By combining AR binding maps with gene expression profiles, we have begun to understand how AR regulates target gene networks in ADPC and CRPC.
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