ArticleInternational journal of hematology2022
The acidic domain of Hmga2 and the domain's linker region are critical for driving self-renewal of hematopoietic stem cell.
Article in International journal of hematology, 2022. 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.
- Inhibition of HMGA2 binding to AT-rich DNA by its negatively charged C-terminus.Nucleic acids research · 2025Article
- 3' UTR-truncated HMGA2 promotes erythroblasts production from human embryonic stem cells.Stem cells translational medicine · 2025Article
- Regulation of HSC development and function by Lin28b.Frontiers in cell and developmental biology · 2025Review
- Chromatin modifier Hmga2 promotes adult hematopoietic stem cell function and blood regeneration in stress conditions.The EMBO journal · 2024Article
- Cellular carcinogenesis in preleukemic conditions:drivers and defenses.Fukushima journal of medical science · 2024Review
- Identification of Cellular Compositions in Different Microenvironments and Their Potential Impacts on Hematopoietic Stem Cells HSCs Using Single-Cell RNA Sequencing with Systematical Confirmation.Life (Basel, Switzerland) · 2023Article
- Animal models for COVID-19: advances, gaps and perspectives.Signal transduction and targeted therapy · 2022Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
High mobility group AT-hook 2 (Hmga2) is a chromatin modifier protein that plays a critical role in fetal development and leukemia propagation by binding to chromatin and DNA via its AT-hook domains. However, the molecular mechanisms by which Hmga2 activates the expression of target genes to drive the self-renewal of hematopoietic stem cells (HSCs) remain unclear. We generated Rosa26 locus Hmga2 conditional knock-in mice and found that overexpression of Hmga2 promoted self-renewal of normal HSCs, but maintained their fitness in bone marrow, and consequently was not sufficient to initiate malignancy. This result is consistent with previous findings showing that Hmga2 is a proto-oncogene. We also assessed the cellular functions of Hmga2 mutants lacking functional domains and demonstrated that the C-terminus acidic domain of Hmga2 and the domain's linker region were critical for activating genes involved in stem cell signatures, such as the Igf2bp2 gene, to drive proliferation of HSCs. In contrast, overexpression of Hmga1, a member of the Hmga family with a different linker region, did not drive proliferation of HSCs. Our results reveal a critical role for the acidic domain of Hmga2 and the domain's linker region in modulating the transcription and self-renewal functions of HSCs.
Indexed as
Identifiers
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Registered trials
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