ArticleImmunity & ageing : I & A2020
ARID3a expression in human hematopoietic stem cells is associated with distinct gene patterns in aged individuals.
Article in Immunity & ageing : I & A, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Unveiling the prognostic value of ARID3A in breast cancer through bioinformatic analysis.Heliyon · 2025Article
- Predicting the pro-longevity or anti-longevity effect of model organism genes with enhanced Gaussian noise augmentation-based contrastive learning on protein-protein interaction networks.NAR genomics and bioinformatics · 2024Article
- ARID3a from the ARID family: structure, role in autoimmune diseases and drug discovery.Acta pharmacologica Sinica · 2023Review
- Article
- Systems approaches to investigate the role of NF-κB signaling in aging.The Biochemical journal · 2022Review
- Deficiencies in the DNA Binding Protein ARID3a Alter Chromatin Structures Important for Early Human Erythropoiesis.ImmunoHorizons · 2021Article
- Reconstructing Boolean network ensembles from single-cell data for unraveling dynamics in the aging of human hematopoietic stem cells.Computational and structural biotechnology journal · 2021Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundImmunologic aging leads to immune dysfunction, significantly reducing the quality of life of the elderly. Aged-related defects in early hematopoiesis result in reduced lymphoid cell development, functionally defective mature immune cells, and poor protective responses to vaccines and pathogens. Despite considerable progress understanding the underlying causes of decreased immunity in the elderly, the mechanisms by which these occur are still poorly understood. The DNA-binding protein ARID3a is expressed in a subset of human hematopoietic progenitors. Inhibition of ARID3a in bulk human cord blood CD34
resultsOur data reveal decreased frequencies of ARID3a-expressing peripheral blood HSCs from aged healthy individuals compared with young donor HSCs. Inhibition of ARID3a in young donor-derived HSCs limits B lineage potential, suggesting a role for ARID3a in B lymphopoiesis in bone marrow-derived HSCs. Increasing ARID3a levels of HSCs from aged donors in vitro alters B lineage development and maturation. Finally, single cell analyses of ARID3a-expressing HSCs from young versus aged donors identify a number of differentially expressed genes in aged
conclusionsThese data suggest that ARID3a-expressing HSCs from aged individuals differ at both molecular and functional levels compared to ARID3a-expressing HSCs from young individuals.
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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.