Evidence map›Paper›PMID 41609415›Full record

ArticleThe FEBS journal2026

Anemia-associated mutations disrupt the CDIN1-Codanin1 complex in inherited congenital dyserythropoietic anemia I (CDA-I) disease.

Martin Stojaspal, Tomas Brom, Ivona Nečasová, Tomáš Janovič, Pavel Veverka, Naina Verma, Lukáš Uhrík, Lenka Hernychova, Ctirad Hofr

Abstract read
In one paragraph

Article in The FEBS journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Mechanism of ASF1 Inhibition by CDAN1.bioRxiv : the preprint server for biology · 2024
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Martin StojaspalLifeB, FGP - NCBR, Faculty of Science, Masaryk University, Brno, Czech Republic.ORCID https://orcid.org/0000-0003-4767-1285
Tomas BromLifeB, FGP - NCBR, Faculty of Science, Masaryk University, Brno, Czech Republic.ORCID https://orcid.org/0000-0003-1046-192X
Ivona NečasováLifeB, FGP - NCBR, Faculty of Science, Masaryk University, Brno, Czech Republic.
Tomáš JanovičLifeB, FGP - NCBR, Faculty of Science, Masaryk University, Brno, Czech Republic.ORCID https://orcid.org/0000-0003-4471-5756
Pavel VeverkaLifeB, FGP - NCBR, Faculty of Science, Masaryk University, Brno, Czech Republic.ORCID https://orcid.org/0000-0003-1803-9504
Naina VermaResearch Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.ORCID https://orcid.org/0009-0002-7959-6961
Lukáš UhríkResearch Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.ORCID https://orcid.org/0000-0002-6077-4249
Lenka HernychovaResearch Centre for Applied Molecular Oncology, Masaryk Memorial Cancer Institute, Brno, Czech Republic.ORCID https://orcid.org/0000-0002-4352-0626
Ctirad HofrLifeB, FGP - NCBR, Faculty of Science, Masaryk University, Brno, Czech Republic.ORCID https://orcid.org/0000-0001-6333-8023

Funding

Grantová Agentura České Republiky Ctirad Hofr GA23-05241S
6 · The paper itself

Abstract

Congenital dyserythropoietic anemia type I (CDA-I) is a rare hereditary disease marked by ineffective erythropoiesis, a characteristic spongy heterochromatin structure in erythroblasts, and mutations in the genes CDAN1 and CDIN1, which encode the proteins Codanin1 and CDIN1. Codanin1 regulates histone shuttling via the chaperone ASF1, yet the role of CDIN1 in CDA-I pathology remains unclear. Notably, CDIN1 is known to interact directly with the C-terminus of Codanin1. Although mutations in both genes are critical to the disease phenotype, their molecular-level effects have not been fully elucidated. Here, we present a comprehensive structural and functional analysis of the CDIN1-Codanin1 C-terminus complex. Using complementary biophysical techniques, we show that CDIN1 and Codanin1 C-terminus form a high-affinity heterodimeric complex with equimolar stoichiometry. We further delineate the essential interacting regions of CDIN1 and Codanin1. We demonstrate that CDA-I-associated mutations in either protein disrupt the CDIN1-Codanin1 interaction, suggesting a potential molecular mechanism underlying the disease.

Indexed as

Anemia, Dyserythropoietic, CongenitalMutationGlycoproteinsHumansNuclear ProteinsProtein BindingCDAN1 protein, humanGlycoproteinsNuclear ProteinsC15orf41CDIN1chromatinCodanin1congenital dyserythropoietic anemiaprotein–protein interactionquantitative biochemistry

Identifiers

PMID41609415
PMCPMC13370696

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.