ArticleFrontiers in immunology2023
Macrophage differentiation is marked by increased abundance of the mRNA 3' end processing machinery, altered poly(A) site usage, and sensitivity to the level of CstF64.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- LPS stimulation reveals male and female dimorphism in human iPSC-derived macrophages.iScience · 2026Article
- The alternative polyadenylation factor CFIm25 orchestrates macrophage antibacterial activity againstInfection and immunity · 2026Article
- Alternative polyadenylation releases PCBP1-mediated suppression of CFIm25 during macrophage differentiation.FEBS letters · 2026Article
- A Novel Role of Neutrophil Elastase in Podocyte Dysfunction Induced by High Glucose, PMA, and MDP.Journal of cellular physiology · 2025Article
- RNA Alternative Splicing and Polyadenylation and Regulation of the Glomerular Filtration Barrier.Journal of the American Society of Nephrology : JASN · 2025Article
- Bioactive compounds in the modulation of oxidative stress in monocytes and macrophages.Scientific reports · 2025Article
- RNA processing in innate immunity: regulation by RNA-binding proteins.Trends in biochemical sciences · 2025Review
- The alternative polyadenylation regulator CFIm25 promotes macrophage differentiation and activates the NF-κB pathway.Cell communication and signaling : CCS · 2025Article
- Mycobacterium tuberculosis modulates NUDT21-mediated alternative polyadenylation to enhance FTH1 expression in macrophages and promotes intracellular growth.Frontiers in cellular and infection microbiology · 2025Article
- Inhibition of Mac-1 allows human macrophages to migrate against the direction of shear flow on ICAM-1.Molecular biology of the cell · 2024Article
- Cleavage and polyadenylation factors are potential regulators of adipogenesis.BMC research notes · 2024Article
- Downregulation of CPSF6 leads to global mRNA 3' UTR shortening and enhanced antiviral immune responses.PLoS pathogens · 2024Article
- Elevated pre-mRNA 3' end processing activity in cancer cells renders vulnerability to inhibition of cleavage and polyadenylation.Nature communications · 2023Article
- The emerging theme of 3'UTR mRNA isoform regulation in reprogramming of cell metabolism.Biochemical Society transactions · 2023Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Regulation of mRNA polyadenylation is important for response to external signals and differentiation in several cell types, and results in mRNA isoforms that vary in the amount of coding sequence or 3' UTR regulatory elements. However, its role in differentiation of monocytes to macrophages has not been investigated. Macrophages are key effectors of the innate immune system that help control infection and promote tissue-repair. However, overactivity of macrophages contributes to pathogenesis of many diseases. In this study, we show that macrophage differentiation is characterized by shortening and lengthening of mRNAs in relevant cellular pathways. The cleavage/polyadenylation (C/P) proteins increase during differentiation, suggesting a possible mechanism for the observed changes in poly(A) site usage. This was surprising since higher C/P protein levels correlate with higher proliferation rates in other systems, but monocytes stop dividing after induction of differentiation. Depletion of CstF64, a C/P protein and known regulator of polyadenylation efficiency, delayed macrophage marker expression, cell cycle exit, attachment, and acquisition of structural complexity, and impeded shortening of mRNAs with functions relevant to macrophage biology. Conversely, CstF64 overexpression increased use of promoter-proximal poly(A) sites and caused the appearance of differentiated phenotypes in the absence of induction. Our findings indicate that regulation of polyadenylation plays an important role in macrophage differentiation.
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