<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>18(1)</volume><submitter>Yang B</submitter><pubmed_abstract>&lt;i>Alkbh5&lt;/i> is one of the primary demethylases responsible for reversing N6-methyladenosine (m&lt;sup>6&lt;/sup>A) modifications on mRNAs, and it plays a crucial role in many physiological and pathological processes. Previous studies have shown that &lt;i>Alkbh5&lt;/i> is required for maintaining the function of leukemia stem cells but is dispensable for normal hematopoiesis. In this study, we found that &lt;i>Alkbh5&lt;/i> deletion led to a moderate increase in the number of multiple progenitor cell populations while compromising the long-term self-renewal capacity of hematopoietic stem cells (HSCs). Here, we used RNA-seq and m&lt;sup>6&lt;/sup>A-seq strategies to explore the underlying molecular mechanism. At the molecular level, &lt;i>Alkbh5&lt;/i> may regulate hematopoiesis by reducing m&lt;sup>6&lt;/sup>A modification</pubmed_abstract><journal>Open medicine (Warsaw, Poland)</journal><pagination>20230766</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10426271</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>&lt;i>Alkbh5&lt;/i> plays indispensable roles in maintaining self-renewal of hematopoietic stem cells.</pubmed_title><pmcid>PMC10426271</pmcid><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Liu Z</pubmed_authors><pubmed_authors>Li Z</pubmed_authors><pubmed_authors>Zou L</pubmed_authors><pubmed_authors>Chen Z</pubmed_authors><pubmed_authors>Zhou C</pubmed_authors><pubmed_authors>Kuang M</pubmed_authors><pubmed_authors>Yang B</pubmed_authors><pubmed_authors>Xiao F</pubmed_authors><pubmed_authors>Shu Y</pubmed_authors><pubmed_authors>Liu S</pubmed_authors></additional><is_claimable>false</is_claimable><name>&lt;i>Alkbh5&lt;/i> plays indispensable roles in maintaining self-renewal of hematopoietic stem cells.</name><description>&lt;i>Alkbh5&lt;/i> is one of the primary demethylases responsible for reversing N6-methyladenosine (m&lt;sup>6&lt;/sup>A) modifications on mRNAs, and it plays a crucial role in many physiological and pathological processes. Previous studies have shown that &lt;i>Alkbh5&lt;/i> is required for maintaining the function of leukemia stem cells but is dispensable for normal hematopoiesis. In this study, we found that &lt;i>Alkbh5&lt;/i> deletion led to a moderate increase in the number of multiple progenitor cell populations while compromising the long-term self-renewal capacity of hematopoietic stem cells (HSCs). Here, we used RNA-seq and m&lt;sup>6&lt;/sup>A-seq strategies to explore the underlying molecular mechanism. At the molecular level, &lt;i>Alkbh5&lt;/i> may regulate hematopoiesis by reducing m&lt;sup>6&lt;/sup>A modification</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023</publication><modification>2025-04-19T06:49:38.821Z</modification><creation>2025-04-19T06:49:38.821Z</creation></dates><accession>S-EPMC10426271</accession><cross_references><pubmed>37588656</pubmed><doi>10.1515/med-2023-0766</doi></cross_references></HashMap>