<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/SRR161/067/SRR16132067/SRR16132067_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/056/SRR16157056/SRR16157056_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/054/SRR16157054/SRR16157054_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/053/SRR16157053/SRR16157053_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/053/SRR16157053/SRR16157053_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/055/SRR16157055/SRR16157055_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/067/SRR16132067/SRR16132067_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/056/SRR16157056/SRR16157056_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/066/SRR16132066/SRR16132066_1.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/066/SRR16132066/SRR16132066_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/055/SRR16157055/SRR16157055_2.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR161/054/SRR16157054/SRR16157054_1.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>The first affiliated hospital of USTC</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA767433</full_dataset_link><tag>xref:EuropePMC:PMC8565356</tag><long_description>Evidence suggests that histone modification disorders are involved in leukemia pathogenesis. We previously reported that LukS-PV, a component of Panton-Valentine leukocidin (PVL), has anti-leukemia activities that can induce differentiation, increase apoptosis, and inhibit proliferation of acute myeloid leukemia (AML) cells. Furthermore, LukS-PV inhibited hepatoma progression by regulating histone deacetylation, speculating that LukS-PV may exert anti-leukemia activity by targeting histone modification regulators. In this study, the results showed that LukS-PV induced apoptosis by downregulating the methyltransferase SET8 and its target histone H4 monomethylated at Lys 20 (H4K20me1)</long_description><repository>ENA</repository></additional><is_claimable>false</is_claimable><name></name><description>LukS-PV induces AML cell apoptosis by targeting SET8.</description><dates><last_updated>2023-05-19</last_updated><first_public>2021-10-18</first_public></dates><accession>PRJNA767433</accession><cross_references/></HashMap>