ArticleLeukemia2024
In vivo CRISPR/Cas9-mediated screen reveals a critical function of TFDP1 and E2F4 transcription factors in hematopoiesis.
Article in Leukemia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Mechanosensitive Stanniocalcin-1 Suppresses Smooth Muscle Cell Proliferation and Attenuates Experimental Pulmonary Hypertension.Circulation research · 2026Article
- A cholinergic checkpoint controls autoantibody selection via somatic hypermutation in lupus germinal centers.Cellular & molecular immunology · 2026Article
- RNA Helicase DDX21 Controls CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting USP10/SCD1 axis by RAF265 suppresses lipogenesis and induced ferroptosis in head and neck squamous cell carcinoma.Cell death discovery · 2026Article
- Sequential in vivo CRISPR screens identify the clonal dominance ofBlood science (Baltimore, Md.) · 2026Article
- Microbiome-derived bile acids as endogenous regenerative mediators in liver repair.Regenerative therapy · 2025Review
- Methods and applications of in vivo CRISPR screening.Nature reviews. Genetics · 2025Review
- Upregulation ofCanadian respiratory journal · 2025Article
- Omega-3 fatty acid synergy with glucocorticoid in mouse lupus macrophage model: targeting pathogenic pathways to reduce steroid dependence.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Hematopoiesis is a continuous process of blood cell production driven by hematopoietic stem and progenitor cells (HSPCs) in the bone marrow. Proliferation and differentiation of HSPCs are regulated by complex transcriptional networks. In order to identify transcription factors with key roles in HSPC-mediated hematopoietic reconstitution, we developed an efficient and robust CRISPR/Cas9-based in vivo genetic screen. Using this experimental system, we identified the TFDP1 transcription factor to be essential for HSPC proliferation and post-transplant hematopoiesis. We further discovered that E2F4, an E2F transcription factor, serves as a binding partner of TFDP1 and is required for HSPC proliferation. Deletion of TFDP1 caused downregulation of genes associated with the cell cycle, with around 50% of these genes being identified as direct targets of TFDP1 and E2F4. Thus, our study expands the transcriptional network governing hematopoietic development through an in vivo CRISPR/Cas9-based genetic screen and identifies TFDP1/E2F4 as positive regulators of cell cycle genes in HSPCs.
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Registered trials
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