Alkbh5是主要的去甲基酶之一，负责逆转mRNA上N6-甲基腺苷（m6A）修饰，它在许多生理和病理过程中发挥着关键作用。先前的研究表明，Alkbh5在维持白血病干细胞功能方面是必需的，但对于正常造血过程是可有可无的。在本研究中，我们发现Alkbh5的缺失导致多个祖细胞群体数量的中度增加，同时损害了造血干细胞（HSCs）的长期自我更新能力。我们使用RNA-seq和m6A-seq策略来探索其潜在的分子机制。在分子水平上，Alkbh5可能通过减少Cebpa的m6A修饰并维持基因表达水平来调节造血过程。总体而言，我们的研究揭示了Alkbh5在调节HSCs稳态中的关键作用，并为该领域的未来研究提供了参考。 © 2023作者，由De Gruyter出版

Alkbh5 is one of the primary demethylases responsible for reversing N6-methyladenosine (m6A) modifications on mRNAs, and it plays a crucial role in many physiological and pathological processes. Previous studies have shown that Alkbh5 is required for maintaining the function of leukemia stem cells but is dispensable for normal hematopoiesis. In this study, we found that Alkbh5 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 m6A-seq strategies to explore the underlying molecular mechanism. At the molecular level, Alkbh5 may regulate hematopoiesis by reducing m6A modification of Cebpa and maintaining gene expression levels. Overall, our study unveiled an essential role for Alkbh5 in regulating HSC homeostasis and provides a reference for future research in this area.© 2023 the author(s), published by De Gruyter.