Evidence map›Paper›PMID 34561772›Full record

ArticleStem cell reviews and reports2021

Bmi1 Regulates Wnt Signaling in Hematopoietic Stem and Progenitor Cells.

Hao Yu, Rui Gao, Sisi Chen, Xicheng Liu, Qiang Wang, Wenjie Cai, Sasidhar Vemula, Aidan C Fahey, Danielle Henley, Michihiro Kobayashi and 7 more

Open access · greenAbstract read
In one paragraph

Article in Stem cell reviews and reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% of its field
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

14 citing papers in PubMed, 15 citations in OpenAlex.

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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

17 authors at 6 institutions in 2 countries.

Hao Yu *Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Rui Gao *Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Sisi Chen *Department of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Xicheng LiuNational Institute of Biological Science, Beijing, China.
Qiang WangDepartment of Biochemistry and Molecular Biology, College of Medicine, Pennsylvania State University, Hershey, PA, 17033, USA.
Wenjie CaiDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Sasidhar VemulaDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Aidan C FaheyDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Danielle HenleyDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Michihiro KobayashiDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Stephen Z LiuDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Zhijian QianDepartment of Medicine, University of Florida, Gainesville, FL, 32610, USA.
Reuben KapurDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Hal E BroxmeyerDepartment of Microbiology and Immunology, Indiana University, Indianapolis, IN, 46202, USA.
Zhonghua GaoDepartment of Biochemistry and Molecular Biology, College of Medicine, Pennsylvania State University, Hershey, PA, 17033, USA.
Rongwen XiNational Institute of Biological Science, Beijing, China. xirongwen@nibs.ac.cn.
Yan LiuDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, 46202, USA. yan.liu@northwestern.edu.ORCID http://orcid.org/0000-0003-4878-9111
Indiana University School of MedicineNational Institute of Biological Sciences, Beijing · CNPennsylvania State University · USIndiana University – Purdue University Indianapolis · USNorthwestern University · USUniversity of Florida · US

Funding

Indiana Clinical and Translational Sciences InstituteUL1TR001108 · NCATS · INDIANA UNIVERSITY INDIANAPOLIS · PI DENNE, SCOTT C., SHEKHAR, ANANTHA · 2013 to 2017
$23.3M
Project-005U54DK106846 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI Reuben Kapur, Karen Elizabeth Pollok · 2015 to 2026
$9.7M
Molecular mechanism underlying clonal expansion of hematopoietic stem cellsR01HL150624 · NHLBI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Yan Liu · 2019 to 2026
$3.8M
Role of p21 activated kinase in LeukemogenesisR01CA173852 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2014 to 2025
$3.4M
Hyperglycemia mediated myeloproliferative diseaseR01HL140961 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2019 to 2022
$2.3M
Targeting Novel Pathways in JMMLR01HL146137 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2019 to 2022
$2.2M
Mutant p53 rejuvenates aged stem cells through modulating epigenetic regulatorsR56AG052501 · NIA · INDIANA UNIVERSITY INDIANAPOLIS · PI LIU, YAN · 2017 to 2017
$255k
Molecular mechanisms underlying clonal expansion of hematopoietic stem cellsR56DK119524 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI LIU, YAN · 2018 to 2018
$150k
NCATS NIH HHS UL1 TR001108NCI NIH HHS R01 CA173852NHLBI NIH HHS R01 HL140961NHLBI NIH HHS R01 HL146137NHLBI NIH HHS R01 HL150624NIA NIH HHS R56 AG052501NIDDK NIH HHS R56 DK119524NIDDK NIH HHS U54 DK106846
6 · The paper itself

Abstract

Polycomb group protein Bmi1 is essential for hematopoietic stem cell (HSC) self-renewal and terminal differentiation. However, its target genes in hematopoietic stem and progenitor cells are largely unknown. We performed gene expression profiling assays and found that genes of the Wnt signaling pathway are significantly elevated in Bmi1 null hematopoietic stem and progenitor cells (HSPCs). Bmi1 is associated with several genes of the Wnt signaling pathway in hematopoietic cells. Further, we found that Bmi1 represses Wnt gene expression in HSPCs. Importantly, loss of β-catenin, which reduces Wnt activation, partially rescues the HSC self-renewal and differentiation defects seen in the Bmi1 null mice. Thus, we have identified Bmi1 as a novel regulator of Wnt signaling pathway in HSPCs. Given that Wnt signaling pathway plays an important role in hematopoiesis, our studies suggest that modulating Wnt signaling may hold potential for enhancing HSC self-renewal, thereby improving the outcomes of HSC transplantation.

Indexed as

Hematopoietic Stem Cell TransplantationWnt Signaling PathwayAnimalsHematopoiesisHematopoietic Stem CellsMicePolycomb Repressive Complex 1Proto-Oncogene ProteinsBmi1 protein, mousePolycomb Repressive Complex 1Proto-Oncogene ProteinsAnd β-cateninBmi1DifferentiationHSCSelf-renewalWnt

Identifiers

PMID34561772
PMCPMC9097559
OpenAlexW3199474346

What OpenQuestion holds

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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 OpenQuestion graph.