Evidence map›Paper›PMID 42226444›Full record

ArticleThe FEBS journal2026

A quantitative dissection of the DNA-binding properties of pathogenic GATA1 mutants.

Kaoru Takasaki

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. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Kaoru TakasakiDivision of Hematology, Children's Hospital of Philadelphia, Philadelphia, PA, USA.ORCID https://orcid.org/0000-0002-2081-9692

Funding

Dysregulation of transcription factors and chromatin architecture in Trisomy 21 hematopoietic disordersK08HL177281 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI Kaoru Takasaki · 2025 to 2026
$318k
Miuzno Fund in HematologyNHLBI NIH HHS K08 HL177281
6 · The paper itself

Abstract

Transcription factors are modulated by a precisely coordinated set of conditions, including cell context, target sequences and their accessibility, and co-factor recruitment. Disruption to any of these conditions can dramatically affect transcription factor activity, but quantitatively characterizing the consequences of individual mutations-either in the transcription factors themselves or in their target sequences-has remained a technical challenge. Zambo et al. present an innovation on their native holdup assay that measures DNA-protein binding activity under physiologic or near-physiologic conditions and use mutant GATA1-ATP2B4 binding as an illustrative example. This technique holds promise for uncovering the molecular mechanisms underlying genetically-driven diseases.

Indexed as

DNAGATA1 Transcription FactorMutationAnimalsHumansProtein BindingDNAGATA1 protein, humanGATA1 Transcription FactorDNA–protein bindingerythropoiesisGATA1GATA1snative holdup assay

Identifiers

PMID42226444
PMCPMC13534873

What Socratic holds

Textmetadata
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 Socratic graph.