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Targeting ZNF410 as a potential β-hemoglobinopathy therapy

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The nucleosome remodeling and deacetylase (NuRD) complex is a chromatin modifier with a key role in the switch from fetal to adult hemoglobin. In a new study, Vinjamur et al. identify a fetal hemoglobin repressor, ZNF410, which does not directly bind the γ-globin promoter but acts through highly specific regulation of CHD4, a protein subunit of the NuRD complex, thus presenting a potential approach for therapeutic reactivation of fetal hemoglobin.

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Fig. 1: ZNF410 transactivation of CHD4 through 27 evolutionarily conserved DNA-binding motifs.

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Authors and Affiliations

  1. National Heart, Lung and Blood Institute/NIH, Sickle Cell Branch, Bethesda, MD, USA

    Laxminath Tumburu & Swee Lay Thein

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  1. Laxminath Tumburu
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  2. Swee Lay Thein
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Correspondence to Swee Lay Thein.

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The authors declare no competing interests.

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Tumburu, L., Thein, S.L. Targeting ZNF410 as a potential β-hemoglobinopathy therapy. Nat Genet 53, 589–590 (2021). https://doi.org/10.1038/s41588-021-00817-y

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