ArticlebioRxiv : the preprint server for biology2026
Inhibition of Dot1L Histone Methyltransferase Expands Bone Injury-Responsive CXCL12
Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
The regenerative capacity of adult bone relies on the rapid activation and lineage engagement of skeletal stromal and progenitor cells (SSPCs). While signaling pathways that regulate these processes have been extensively studied, the epigenetic mechanisms that constrain progenitor activation and lineage permissiveness during adult bone repair remain poorly defined. Disruptor of telomeric silencing 1 like (Dot1L), the sole histone methyltransferase responsible for H3K79 methylation, is essential for skeletal development, yet its function in adult skeletal regeneration has not been established. Here, we identify Dot1L as a key epigenetic regulator that limits the early regenerative response to bone injury. Genetic reduction of Dot1L activity in the Prrx1
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