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.
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.
Jeong-Ah Kim *Wisconsin Blood Cancer Research Institute, Department of Cell and Regenerative Biology, Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.ORCID http://orcid.org/0000-0001-6933-6053
Siqi Shen *Department of Biostatistics and Biomedical Informatics, Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.ORCID http://orcid.org/0000-0003-1661-1247
Christina M JurotichWisconsin Blood Cancer Research Institute, Department of Cell and Regenerative Biology, Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Jane E ChurpekDivision of Hematology, Oncology, and Palliative Care, Department of Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.
Sunduz KelesDepartment of Biostatistics and Biomedical Informatics, Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. keles@stat.wisc.edu.ORCID http://orcid.org/0000-0001-9048-0922
Emery H BresnickWisconsin Blood Cancer Research Institute, Department of Cell and Regenerative Biology, Carbone Cancer Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. ehbresni@wisc.edu.ORCID http://orcid.org/0000-0002-1151-5654
Funding
WNPRC Supplemental Request for Nonhuman Primate Enclosures to Equip HIV/AIDS-Related Research FacilitiesP51OD011106 · OD · UNIVERSITY OF WISCONSIN-MADISON · PI Dorota A. Grejner-Brzezinska · 2012 to 2026
$150.7M
UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Justine Yang Bruce · 1985 to 2026
$142.6M
Hematopoietic Regulation via GATA SwitchesR01DK068634 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI Emery H. Bresnick · 2006 to 2026
$7.5M
Statistical Methods for the Analysis of ChlP-chip DataR01HG003747 · NHGRI · UNIVERSITY OF WISCONSIN-MADISON · PI KELES, SUNDUZ · 2007 to 2024
$4.8M
Discriminating Pathogenic from Benign Alleles of Myelodysplastic Syndrome Predisposition GenesR21AI186406 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI BRESNICK, EMERY H. · 2024 to 2025
$428k
NCI NIH HHS P30 CA014520NHGRI NIH HHS R01 HG003747NIAID NIH HHS R21 AI186406NIDDK NIH HHS R01 DK068634NIH HHS P51 OD011106U.S. Department of Health & Human Services | National Institutes of Health (NIH) P30CA014520U.S. Department of Health & Human Services | National Institutes of Health (NIH) R01DK68634U.S. Department of Health & Human Services | National Institutes of Health (NIH) R21AI186405
6 · The paper itself
Abstract
Post-transcriptional diversification of RNA transcripts mediated by complex processing machinery, including DEAD-box ATPases, establishes and maintains cellular phenotypes. For example, DDX41 controls RNA splicing, innate immune signaling, and genome stability. Although heterozygous DDX41 germline genetic variation occurs in familial myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), the DDX41 contributions to splicing globally, biological processes, and pathogenic mechanisms are incompletely defined. Using a genetic rescue system with Ddx41
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.
Oncogenic DEAD-box ATPase DDX41 establishes transcript ensembles via CLK3-dependent and -independent mechanisms. · full record | OpenQuestion