ArticleFrontiers in cell and developmental biology2020
The Transcriptional Network That Controls Growth Arrest and Macrophage Differentiation in the Human Myeloid Leukemia Cell Line THP-1.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
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- Hypermethylation of microRNA-34c CpG Island predicts unfavorable prognosis in acute myeloid leukemia.Scientific reports · 2025Article
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- Molecular Mechanisms of Biochanin A in AML Cells: Apoptosis Induction and Pathway-Specific Regulation in U937 and THP-1.International journal of molecular sciences · 2025Article
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- Elf1 Deficiency Impairs Macrophage Development in Zebrafish Model Organism.International journal of molecular sciences · 2025Article
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- The alternative polyadenylation regulator CFIm25 promotes macrophage differentiation and activates the NF-κB pathway.Cell communication and signaling : CCS · 2025Article
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- The Bisdioxopiperazine ICRF-193 Attenuates LPS-induced IL-1β Secretion by Macrophages.Inflammation · 2024Article
- Human CD34Cellular and molecular life sciences : CMLS · 2023Article
- Aberrant APOBEC3B Expression in Breast Cancer Is Linked to Proliferation and Cell Cycle Phase.Cells · 2023Article
- Article
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- Size-tuneable and immunocompatible polymer nanocarriers for drug delivery in pancreatic cancer.Nanoscale · 2022Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The response of the human acute myeloid leukemia cell line THP-1 to phorbol esters has been widely studied to test candidate leukemia therapies and as a model of cell cycle arrest and monocyte-macrophage differentiation. Here we have employed Cap Analysis of Gene Expression (CAGE) to analyze a dense time course of transcriptional regulation in THP-1 cells treated with phorbol myristate acetate (PMA) over 96 h. PMA treatment greatly reduced the numbers of cells entering S phase and also blocked cells exiting G2/M. The PMA-treated cells became adherent and expression of mature macrophage-specific genes increased progressively over the duration of the time course. Within 1-2 h PMA induced known targets of tumor protein p53 (TP53), notably
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