Dataset Information


ChIP-seq analysis of androgen receptor binding in epididymis of ArKI mice

ABSTRACT: To analyze how SUMOylation of AR affects its chromatin binding, we generated a mouse model (ArKI) in which the two conserved SUMO acceptor lysines of androgen receptor (AR) were permanently abolished by converting them to arginines (ArK381R, K500R). ChIP-seq was used to analyse how the lack of AR SUMOylation affects the chromatin binding of AR in epididymis. Overall design: For each sample, caput epididymides (containing initial segments) from three wild type (WT) or ArKI (KI) mice were combined, chromatin binding of AR was analyzed using ChIP and sequenced using Illumina HiSeq 3000 system. We generated two replicates from WT and ArKI mice.

INSTRUMENT(S): Illumina HiSeq 2500 (Mus musculus)

ORGANISM(S): Mus musculus  

SUBMITTER: Einari Niskanen  

PROVIDER: GSE121151 | GEO | 2019-01-09


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GSE121151_AR-ChIP-seq_ArKI-Cap.bed.gz Bed
GSE121151_AR-ChIP-seq_WT-Cap.bed.gz Bed
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Androgen receptor (AR) is regulated by SUMOylation at its transactivation domain. In vitro, the SUMOylation is linked to transcriptional repression and/or target gene-selective regulation. Here, we generated a mouse model (ArKI) in which the conserved SUMO acceptor lysines of AR are permanently abolished (Ar<sup>K381R, K500R</sup>). ArKI males develop normally, without apparent defects in their systemic androgen action in reproductive tissues. However, the ArKI males are infertile. Their spermat  ...[more]

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