ArticleLeukemia2019
Reduced expression but not deficiency of GFI1 causes a fatal myeloproliferative disease in mice.
Article in Leukemia, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- Temporally segregated functions for Gfi1 in the development and maintenance of direction selectivity in the vertebrate retina.Current biology : CB · 2026Article
- Base-resolution DNA methylome of human MDS hematopoietic stem cell reveals TET2-GFI1 epigenetic axis repressing MDS.Immunity & inflammation · 2026Article
- Bcl-xL is important for the antiapoptotic activity of Gfi1 and is upregulated by Gfi1 through hemgn.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Article
- Dose-dependent effect of GFI1 expression in the reconstitution and the differentiation capacity of HSCs.Frontiers in cell and developmental biology · 2023Article
- LSD1 inhibition modulates transcription factor networks in myeloid malignancies.Frontiers in oncology · 2023Review
- Curcumin as an Epigenetic Therapeutic Agent in Myelodysplastic Syndromes (MDS).International journal of molecular sciences · 2021Article
- Review
- A PML/RARα direct target atlas redefines transcriptional deregulation in acute promyelocytic leukemia.Blood · 2021Article
- Prevalence of the GFI1-36N SNP in Multiple Myeloma Patients and Its Impact on the Prognosis.Frontiers in oncology · 2021Article
- IGFBP7 activates retinoid acid-induced responses in acute myeloid leukemia stem and progenitor cells.Blood advances · 2020Article
- Article
- A novel regulatory circuit between p53 and GFI1 controls induction of apoptosis in T cells.Scientific reports · 2019Article
- Targeting the GFI1/1B-CoREST Complex in Acute Myeloid Leukemia.Frontiers in oncology · 2019Review
- Role of GFI1 in Epigenetic Regulation of MDS and AML Pathogenesis: Mechanisms and Therapeutic Implications.Frontiers in oncology · 2019Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Growth factor independent 1 (Gfi1) controls myeloid differentiation by regulating gene expression and limits the activation of p53 by facilitating its de-methylation at Lysine 372. In human myeloid leukemia, low GFI1 levels correlate with an inferior prognosis. Here, we show that knockdown (KD) of Gfi1 in mice causes a fatal myeloproliferative disease (MPN) that could progress to leukemia after additional mutations. Both KO and KD mice accumulate myeloid cells that show signs of metabolic stress and high levels of reactive oxygen species. However, only KO cells have elevated levels of Lysine 372 methylated p53. This suggests that in contrast to absence of GFI1, KD of GFI1 leads to the accumulation of myeloid cells because sufficient amount of GFI1 is present to impede p53-mediated cell death, leading to a fatal MPN. The combination of myeloid accumulation and the ability to counteract p53 activity under metabolic stress could explain the role of reduced GF1 expression in human myeloid leukemia.
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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.