<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/SRR473/001/SRR4733871/SRR4733871.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR473/000/SRR4733870/SRR4733870.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR473/007/SRR4733867/SRR4733867.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR473/006/SRR4733866/SRR4733866.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR473/003/SRR4733873/SRR4733873.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR473/009/SRR4733869/SRR4733869.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR473/002/SRR4733872/SRR4733872.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR473/005/SRR4733875/SRR4733875.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR473/004/SRR4733874/SRR4733874.fastq.gz</Fastqsanger.gz><Fastqsanger.gz>ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR473/008/SRR4733868/SRR4733868.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>Department of Medicine, Hem/Onc Division, The Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research, University of California San Francisco</center_name><full_dataset_link>https://www.ebi.ac.uk/ena/browser/view/PRJNA351841</full_dataset_link><scientific_name>Mus musculus</scientific_name><long_description>Autophagy is critical for protecting HSCs from metabolic stress. Here, we used a genetic approach to inactivate autophagy in adult HSCs by deleting the Atg12 gene. We show that loss of autophagy causes accumulation of mitochondria and an oxidative phosphorylation (OXPHOS)-activated metabolic state, which drives accelerated myeloid differentiation likely through epigenetic deregulations rather than transcriptional changes, and impairs HSC self-renewal activity and regenerative potential. Overall design: Quiescent HSCs HSCs (Lin-/c-Kit+/Sca-1+/Flk2-/CD150+/CD48-) were isolated from BL6 WT mice and activated HSCs were cultured 21 hours in cytokine+ media as described. DNA was extracted from -5 mice per group, and ERRBS was conducted as described in the methods. For cultured HSCs, HSCs were grown in StemPro34 medium (Invitrogen) supplemented with penicillin (50 U/ml)/streptomycin (50 μg/ml) and L-glutamine (2 mM), and with or without the following cytokines (±cyt): SCF (25 ng/ml), Flt3L (25 ng/ml), IL-11 (25 ng/ml), IL-3 (10 ng/ml), GM-CSF (10 ng/ml), Epo (4 U/ml) and Tpo (25 ng/ml) (Peprotech).</long_description><tag>xref:PubMed:28241143</tag><repository>ENA</repository></additional><is_claimable>false</is_claimable><name>Mus musculus</name><description>Autophagy maintains metabolism and functional activity of a subset of aged hematopoietic stem cells [ERRBS]</description><dates><last_updated>2025-09-24</last_updated><first_public>2017-04-19</first_public></dates><accession>PRJNA351841</accession><cross_references><GEO>GSE89338</GEO><taxon>10090</taxon><PubMed>28241143</PubMed></cross_references></HashMap>