ArticleBlood2013
Apc regulates the function of hematopoietic stem cells largely through β-catenin-dependent mechanisms.
Article in Blood, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Mechanism of APC truncation involved in colorectal cancer tumorigenesis (Review).Oncology letters · 2025Review
- Wnt regulation of hematopoietic stem cell development and disease.Current topics in developmental biology · 2023Review
- Extracellular Adenosine (eAdo) - AStem cell reviews and reports · 2022Article
- Hematopoietic stem cell regeneration through paracrine regulation of the Wnt5a/Prox1 signaling axis.The Journal of clinical investigation · 2022Article
- Therapeutic Vulnerabilities of Transcription Factors in AML.Molecular cancer therapeutics · 2021Review
- Cancer Stem Cells,Cells · 2020Review
- Microtubule plus-end tracking Adenopolyposis Coli negatively regulates proplatelet formation.Scientific reports · 2018Article
- β-Catenin Is a Candidate Therapeutic Target for Myeloid Neoplasms with del(5q).Cancer research · 2017Article
- Dickkopf-1 promotes hematopoietic regeneration via direct and niche-mediated mechanisms.Nature medicine · 2017Article
- High Levels of Canonical Wnt Signaling Lead to Loss of Stemness and Increased Differentiation in Hematopoietic Stem Cells.Stem cell reports · 2016Article
- Pre-clinical efficacy of combined therapy with novel β-catenin antagonist BC2059 and histone deacetylase inhibitor against AML cells.Leukemia · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Emerging evidence suggests that adenomatous polyposis coli (Apc) plays a critical role in the maintenance of hematopoietic stem/progenitor cells (HSCs/HPCs). The molecular pathways responsible for the function of Apc in HSCs/HPCs remain unclear. By genetic approach, we demonstrated that inactivation of β-catenin rescued the exhaustion of Apc-deficient HSCs/HPCs, thereby preventing bone marrow failure in Apc-deficient mice. β-catenin loss inhibited the excessive proliferation and apoptosis of Apc-deficient HSCs/HPCs, as well as their defects in myeloid and erythroid differentiation. In addition, loss of β-catenin reversed the down-regulation of Cdkn1a, Cdkn1b, and Mcl1 induced by Apc ablation in Lin(-)Sca(+)c-Kit(+). In assays of long-term stem cell function, the HSCs with deficiency of both Apc and β-catenin displayed a significantly enhanced self-renewal capacity compared with β-catenin-deficient and control HSCs. Our findings suggest that Apc regulates the survival, proliferation, and differentiation of HSCs/HPCs largely through a β-catenin-mediated pathway. They also indicate that multiple downstream targets of Apc including β-catenin may coordinately regulate HSC self-renewal.
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Registered trials
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.