<HashMap><database>ENA</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/002/SRR5927362/SRR5927362.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/004/SRR5927364/SRR5927364.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/009/SRR5927359/SRR5927359.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/001/SRR5927361/SRR5927361.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/007/SRR5927357/SRR5927357.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/006/SRR5927366/SRR5927366.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/005/SRR5927365/SRR5927365.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/008/SRR5927358/SRR5927358.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/008/SRR5927368/SRR5927368.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/000/SRR5927360/SRR5927360.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/007/SRR5927367/SRR5927367.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR592/003/SRR5927363/SRR5927363.fastq.gz</Fastqsanger.gz></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><center_name>GENE REGULATION, RESEARCH, PETER MACCALLUM CANCER CENTRE</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA397984</full_dataset_link><scientific_name>Homo sapiens</scientific_name><long_description>Gene expression profiling was performed to characterise transcriptional programs associated with response to type I JAK2 inhibitor ruxolitinib, type II JAK2 inhibitor CHZ868 or shRNA-mediated JAK2 knockdown in MHH-CALL4 cells. Overall design: CRLF2-rearranged/JAK2I682F-expressing MHH-CALL4 cells were treated with vehicle (DMSO), CHZ868 (300 nM) or ruxolitinib (1000 nM) for 24 hours in duplicate and total RNA was freshly extracted for 3'-RNA-Seq. MHH-CALL4 cells were transduced with constitutive (pLMS-GFP) retroviral vectors harbouring shRNAs targeting JAK2 (shJAK2.209 or shJAK2.2826) or scrambled (shSCR) in duplicate and GFP+ cells were harvested at day 5 post-transduction for 3'-RNA-Seq.</long_description><tag>xref:PubMed:29907650</tag><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>Homo sapiens</name><description>Comparative gene expression profiling of MHH-CALL4 cells subject to pharmacological JAK2 inhibitor treatment (ruxolitinib or CHZ868) or shRNA-mediated JAK2 depletion in vitro</description><dates><last_updated>2025-09-24</last_updated><first_public>2018-01-02</first_public></dates><accession>PRJNA397984</accession><cross_references><GEO>GSE102534</GEO><taxon>9606</taxon><PubMed>29907650</PubMed></cross_references></HashMap>