ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR131/025/SRR13178325/SRR13178325.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR131/021/SRR13178321/SRR13178321.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR131/022/SRR13178322/SRR13178322.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR131/024/SRR13178324/SRR13178324.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR131/019/SRR13178319/SRR13178319.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR131/023/SRR13178323/SRR13178323.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR131/020/SRR13178320/SRR13178320.fastq.gzprimaryOK200GenomicsState key laboratories of Agrobiotechnology, College of biological sciences, China Agricutural Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA681928Mus musculusChIPseq experiments identify that ASPSCR1-TFE3 defines active enhancers across the genome and co-distributes with VCP/p97. RNAseq after knock-down of ASPSCR1-TFE3 or VCP, inhibition of VCP, or overexpression of each in alveolar soft part sarcoma cell lines demonstrates their co-dependence. HiChIP defines chromatin conformations that surround ASPSCR1-TFE3 targets and are lost on VCP knock-down. Overall design: ASPS cell lines, tumors from ASPS mouse model and tumors from ASPS patients are used for ChIP-seq with antibodies against ASPSCR1, VCP, POLII and various histone modifications. RNAseq in ASPS cell lines after application of siRNA against control, ASPSCR1-TFE3, or VCP, or application of VCP inhibitor CB-5083. H3K27ac-HiChIP in the FU-UR-1 cell line at baseline and after 6 days of siRNA against VCP.xref:PubMed:38326311ENAfalseASPSCR1-TFE3 reprograms transcription by organizing enhancers around hexameric VCP [mASPS_ChIP, ASPL_VCP_Pol2]ASPSCR1-TFE3 reprograms transcription by organizing enhancers around hexameric VCP [mASPS_ChIP, ASPL_VCP_Pol2]2025-09-242023-01-27PRJNA681928GSE1624761009038326311