ArticleThe Biochemical journal2020
A complex comprising C15ORF41 and Codanin-1: the products of two genes mutated in congenital dyserythropoietic anaemia type I (CDA-I).
Article in The Biochemical journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- CDIN1-Codanin-1 complex defective in congenital dyserythropoietic anaemia type I is an RNA nuclease.Nature communications · 2026Article
- Anemia-associated mutations disrupt the CDIN1-Codanin1 complex in inherited congenital dyserythropoietic anemia I (CDA-I) disease.The FEBS journal · 2026Article
- Codanin-1, defective in congenital dyserythropoietic anemia I (CDA-I), regulates erythroid differentiation.Annals of hematology · 2025Article
- Article
- Mechanism of ASF1 engagement by CDAN1.Nature communications · 2025Article
- CODANIN-1 sequesters ASF1 by using a histone H3 mimic helix to regulate the histone supply.Nature communications · 2025Article
- Hereditary disorders of ineffective erythropoiesis.Blood cells, molecules & diseases · 2025Review
- Mechanism of ASF1 Inhibition by CDAN1.bioRxiv : the preprint server for biology · 2024Article
- Molecular complex detection in protein interaction networks through reinforcement learning.BMC bioinformatics · 2023Article
- Recapitulation of erythropoiesis in congenital dyserythropoietic anaemia type I (CDA-I) identifies defects in differentiation and nucleolar abnormalities.Haematologica · 2021Article
- The EHA Research Roadmap: Anemias.HemaSphere · 2021Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
Congenital dyserythropoietic anaemia (CDA) type I is a rare blood disorder characterised by moderate to severe macrocytic anaemia and hepatomegaly, with spongy heterochromatin and inter-nuclear bridges seen in bone marrow erythroblasts. The vast majority of cases of CDA type I are caused by mutations in the CDAN1 gene. The product of CDAN1 is Codanin-1, which interacts the histone chaperone ASF1 in the cytoplasm. Codanin-1 is a negative regulator of chromatin replication, sequestering ASF1 in the cytoplasm, restraining histone deposition and thereby limiting DNA replication. The remainder of CDA-I cases are caused by mutations in the C15ORF41 gene, but very little is known about the product of this gene. Here, we report that C15ORF41 forms a tight, near-stoichiometric complex with Codanin1 in human cells, interacting with the C-terminal region of Codanin-1. We present the characterisation of the C15ORF41-Codanin-1 complex in humans in cells and in vitro, and demonstrate that Codanin-1 appears to sequester C15ORF41 in the cytoplasm as previously shown for ASF1. The findings in this study have major implications for understanding the functions of C15ORF41 and Codanin-1, and the aetiology of CDA-I.
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