Dataset Information


Genomic alterations activating KLF5 [ChIP-Seq]

ABSTRACT: We used ChIP-seq to map the binding sites of wild-type and mutant KLF5. In addition, by performing H3K27ac ChIP-seq, we mapped the enhancer regions in cell lines of head and neck squamous cell carcinomas, esophageal carcinomas, and stomach adenocarcinomas. Overall design: ChIP-seq of H3K27ac in head and neck squamous cell carcinoma cell lines (BHY, BICR6, BICR16, BICR31, CAL33, Detroit562, HSC4, YD8), esophagel carcinoma cell lines (TE6, TE10, TT) and stomach adenocarcinoma cell lines (AGS, GSU, KATOIII). ChIP-seq of KLF5 and p300 in BICR31 cells. ChIP-seq of V5 in HEK293T cells over-expressing, V5-Empty, V5-KLF5-WT and V5-KLF5-mutants. ChIP-seq of V5 and H3K27ac in HCC95 cells over-expressing V5-Empty, V5-KLF5-WT and V5-KLF5-E419Q.

INSTRUMENT(S): Illumina MiSeq (Homo sapiens)

SUBMITTER: Xiaoyang Zhang 

PROVIDER: GSE88976 | GEO | 2017-10-05



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The Krüppel-like family of transcription factors plays critical roles in human development and is associated with cancer pathogenesis. Krüppel-like factor 5 gene (KLF5) has been shown to promote cancer cell proliferation and tumorigenesis and to be genomically amplified in cancer cells. We recently reported that the KLF5 gene is also subject to other types of somatic coding and noncoding genomic alterations in diverse cancer types. Here, we show that these alterations activate KLF5 by three dist  ...[more]

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