Evidence map›Paper›PMID 42726640›Full record

ArticleCell reports2026

Endothelial PERK restricts lymphoid regeneration by reducing DLL4-NOTCH3 signaling at the Pre-B niche.

Bingqing Zou, Qiuyun Chen, Junjun Zheng, Yimin Ma, Jay Myers, Yinghui Shang, Mofei Huang, Paul Christensen, Stanley Adoro, Chih-Hang Anthony Tang and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 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

5 · Who and what money

Authors and funding

18 authors.

Bingqing ZouDepartment of Pathology and Genomic Medicine, Houston Methodist Research Institute, Houston, TX 77030, USA; Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
Qiuyun ChenDepartment of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
Junjun ZhengCenter for Immunotherapy, Houston Methodist Neal Cancer Center, Houston Methodist Research Institute, Houston, TX 77030, USA.
Yimin MaDepartment of Pathology and Genomic Medicine, Houston Methodist Research Institute, Houston, TX 77030, USA; Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA.
Jay MyersDepartment of Pediatrics, Case Western Reserve University, Cleveland, OH 44106, USA.
Yinghui ShangDepartment of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Hematology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China.
Mofei HuangDepartment of Pathology and Genomic Medicine, Houston Methodist Research Institute, Houston, TX 77030, USA.
Paul ChristensenDepartment of Pathology and Genomic Medicine, Houston Methodist Research Institute, Houston, TX 77030, USA.
Stanley AdoroExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Chih-Hang Anthony TangHouston Methodist Neal Cancer Center, Houston Methodist Research Institute, Houston, TX 77030, USA.
Chih-Chi Andrew HuHouston Methodist Neal Cancer Center, Houston Methodist Research Institute, Houston, TX 77030, USA.
Sai Ravi Kiran PingaliDepartment of Medicine, Houston Methodist Research Institute, Houston, TX 77030, USA.
Wei XinDepartment of Pathology, University of South Alabama, Mobile, AL 36688, USA.
Keith Syson ChanHouston Methodist Neal Cancer Center, Houston Methodist Research Institute, Houston, TX 77030, USA; Department of Urology, Houston Methodist Research Institute, Houston, TX 77030, USA.
Stephen WongTranslational Biophotonics Laboratory, Department of Systems Medicine and Bioengineering, Houston Methodist Neal Cancer Center, Houston, TX 77030, USA.
Youli ZuDepartment of Pathology and Genomic Medicine, Houston Methodist Research Institute, Houston, TX 77030, USA; Department of Pathology and Laboratory Medicine and Microbiology and Immunology, Weill Medical College of Cornell University, New York City, NY 10021, USA.
Hamed Jafar-NejadDepartment of Molecular & Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA.
Lan ZhouDepartment of Pathology and Genomic Medicine, Houston Methodist Research Institute, Houston, TX 77030, USA; Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA; Department of Pathology and Laboratory Medicine and Microbiology and Immunology, Weill Medical College of Cornell University, New York City, NY 10021, USA. Electronic address: lzhou3@houstonmethodist.org.

Funding

Targeting Notch2 in Hematopoietic Cell Therapy.R01HL103827 · NHLBI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI ZHOU, LAN · 2012 to 2022
$4.3M
Roles of Glycosylation and Deglycosylation During Animal DevelopmentR35GM130317 · NIGMS · BAYLOR COLLEGE OF MEDICINE · PI Hamed Jafar-Nejad · 2019 to 2026
$3.7M
Hes1-loss promotes dysregulation of epithelial homeostasis and inflammation in a serrated adenocarcinoma modelR01CA222064 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI ZHOU, LAN · 2018 to 2022
$2.0M
NCI NIH HHS R01 CA222064NHLBI NIH HHS R01 HL103827NIGMS NIH HHS R35 GM130317
6 · The paper itself

Abstract

Delayed immune recovery after hematopoietic stem cell (HSC) transplantation is associated with a poor clinical outcome. We study the role of unfolded protein response (ER stress) in hematopoietic regeneration within the bone marrow (BM) microenvironment. We reveal that BM endothelium PERK activation is a prominent feature of patients with leukemia and is a hallmark response in mice following ionizing irradiation. Ablating endothelial Perk boosts NOTCH ligand DLL4 expression and promotes DLL4-dependent early HSC and B progenitor regeneration. Single-cell analysis reveals that endothelial DLL4 activates NOTCH3 expressed by mesenchymal stroma cells, and that the PERK-DLL4 axis coordinates the regulation of lymphoid commitment. NOTCH3 is critical for the upregulation of IL7 following irradiation and the expansion of lymphoid progenitors. These findings not only unveil an ER stress-controlled vascular-stroma signaling mechanism in regenerative hematopoiesis but also highlight PERK blockade as a promising strategy to improve immune recovery after myeloablative transplantation.

Indexed as

Adaptor Proteins, Signal TransducingCalcium-Binding ProteinseIF-2 KinaseReceptor, Notch3RegenerationStem Cell NicheAnimalsHematopoietic Stem CellsHumansIntracellular Signaling Peptides and ProteinsMiceMice, Inbred C57BLSignal TransductionAdaptor Proteins, Signal TransducingCalcium-Binding ProteinsDLL4 protein, mouseeIF-2 KinaseIntracellular Signaling Peptides and ProteinsNotch3 protein, mouseReceptor, Notch3bone marrow endotheliumCP: cell biologyCP: developmental biologyDLL4ER stressIL7MSCNOTCH3PERK

Identifiers

PMID42726640
PMCPMC13650770

What OpenQuestion holds

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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.