ArticleMolecular biology of the cell2012
The RNA-binding protein QKI5 is a direct target of C/EBPα and delays macrophage differentiation.
Article in Molecular biology of the cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
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- The multifaceted role of quaking protein in neuropsychiatric disorders and tumor progression.Frontiers in neuroscience · 2024Review
- The Quaking RNA-binding proteins as regulators of cell differentiation.Wiley interdisciplinary reviews. RNA · 2022Review
- QKI degradation in macrophage by RNF6 protects mice from MRSA infection via enhancing PI3K p110β dependent autophagy.Cell & bioscience · 2022Article
- Downregulation of miR-145 alleviates ox-LDL-induced inflammation by targeting QKI in macrophages.American journal of translational research · 2022Article
- A global screening identifies chromatin-enriched RNA-binding proteins and the transcriptional regulatory activity of QKI5 during monocytic differentiation.Genome biology · 2021Article
- Article
- Loss of QKI in macrophage aggravates inflammatory bowel disease through amplified ROS signaling and microbiota disproportion.Cell death discovery · 2021Article
- Qki is an essential regulator of microglial phagocytosis in demyelination.The Journal of experimental medicine · 2021Article
- MiR-486 promotes proliferation and suppresses apoptosis in myeloid cells by targeting Cebpa in vitro.Cancer medicine · 2018Article
- Matrix-Bound Nanovesicles Recapitulate Extracellular Matrix Effects on Macrophage Phenotype.Tissue engineering. Part A · 2017Article
- Quaking Deficiency Amplifies Inflammation in Experimental EndotoxemiaFrontiers in immunology · 2017Article
- Predicting RTS,S Vaccine-Mediated Protection from Transcriptomes in a Malaria-Challenge Clinical Trial.Frontiers in immunology · 2017Article
- Cross-talk between macrophages and atrial myocytes in atrial fibrillation.Basic research in cardiology · 2016Article
- Quaking and miR-155 interactions in inflammation and leukemogenesis.Oncotarget · 2015Article
- Evolutionary Dynamics of GLD-1-mRNA complexes in Caenorhabditis nematodes.Genome biology and evolution · 2014Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Differentiated macrophages are essential for the innate immune system; however, the molecular mechanisms underlying the generation of macrophages remain largely unknown. Here we show that the RNA-binding protein QKI, mainly QKI-5, is transcriptionally activated in the early differentiated monocytic progenitors when CCAAT/enhancer-binding protein (C/EBP) α is expressed. The forced expression of C/EBPα increases the endogenous expression of QKI. Chromatin immunoprecipitation analysis and reporter assays further confirm that C/EBPα activates the transcription of QKI, primarily by binding to the distal C/EBPα-binding site. Blocking the induction of QKI using RNA interference enhances the expression of endogenous CSF1R and facilitates macrophage differentiation. Further study of the mechanism reveals that QKI-5 facilitates the degradation of CSF1R mRNA by interacting with the distal QRE in the 3' untranslated region. In summary, we show that in committed macrophage progenitors, C/EBPα-activated QKI-5 negatively regulates macrophage differentiation by down-regulating CSF1R expression, forming a negative feedback loop during macrophage differentiation.
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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.