ArticleNucleic acids research2026
Leukemia risk factor ARID5B coordinates HDAC-mediated transcriptional repression.
Article in Nucleic acids research, 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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Abstract
Multiple genetic association studies linked variants at ARID5B with predisposition to B-cell-derived acute lymphoblastic leukemia (B-ALL) in children. Still, the molecular function of ARID5B remains largely uncharacterized. Here, we employ a combination of proteomics, genomics, and transcriptomics to describe the molecular mechanisms of ARID5B. We identify that ARID5B interacts with MIER1, C16ORF87, HDAC1, and HDAC2 forming a chromatin repressor complex. By CUT&RUN, we mapped ARID5B binding in active regions of the genome, tethering HDAC1 and HDAC2 to distal regulatory elements and promoters. Genes actively repressed by the ARID5B repressor complex are involved in B-cell proliferation and B-cell-specific signaling. Together, we describe how ARID5B assembles into a repressor complex and regulates B-cell-specific processes. Understanding its molecular mechanism will help elucidating how noncoding germline variants at ARID5B predispose to B-ALL.
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