Evidence map›Paper›PMID 40091041›Full record

ArticleNature communications2025

Mechanism of ASF1 engagement by CDAN1.

Samantha F Sedor, Sichen Shao

Abstract read
In one paragraph

Article in Nature communications, 2025. 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. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors.

Samantha F SedorDepartment of Cell Biology, Harvard Medical School, Boston, MA, USA.ORCID http://orcid.org/0000-0001-5337-3036
Sichen ShaoDepartment of Cell Biology, Harvard Medical School, Boston, MA, USA. sichen_shao@hms.harvard.edu.ORCID http://orcid.org/0000-0003-2679-5537

Funding

Decoding ribosome-triggered quality control mechanismsDP2GM137415 · NIGMS · HARVARD MEDICAL SCHOOL · PI SHAO, SICHEN · 2019 to 2019
$2.5M
Recognition of Orphan Ribosomal Subunit Proteins by the Ubiquitin-Proteasome SystemF31HL157976 · NHLBI · HARVARD MEDICAL SCHOOL · PI SEDOR, SAMANTHA · 2021 to 2023
$115k
NHLBI NIH HHS F31 HL157976NIGMS NIH HHS DP2 GM137415U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) F31HL157976U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) DP2GM137415
6 · The paper itself

Abstract

Codanin-1 (CDAN1) is an essential and ubiquitous protein named after congenital dyserythropoietic anemia type I, an autosomal recessive disease that manifests from mutations in CDAN1 or CDIN1 (CDAN1 interacting nuclease 1). CDAN1 interacts with CDIN1 and the paralogous histone H3-H4 chaperones ASF1A (Anti-Silencing Function 1 A) and ASF1B. However, CDAN1 function remains unclear. Here, we analyze CDAN1 complexes using biochemistry, single-particle cryo-EM, and structural predictions. We find that CDAN1 dimerizes and assembles into cytosolic complexes with CDIN1 and multiple copies of ASF1A/B. One CDAN1 can engage two ASF1 through two B-domains commonly found in ASF1 binding partners and two helices that mimic histone H3 binding. We additionally show that ASF1A and ASF1B have different requirements for CDAN1 engagement. Our findings explain how CDAN1 sequesters ASF1A/B by occupying all functional binding sites known to facilitate histone chaperoning and provide molecular-level insights into this enigmatic complex.

Indexed as

Cell Cycle ProteinsMolecular ChaperonesBinding SitesCryoelectron MicroscopyHistonesHumansModels, MolecularProtein BindingProtein MultimerizationASF1A protein, humanASF1B protein, humanCell Cycle ProteinsHistonesMolecular Chaperones

Identifiers

PMID40091041
PMCPMC11911400

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.