ArticleMolecular immunology2011
CLEC5A (MDL-1) is a novel PU.1 transcriptional target during myeloid differentiation.
Article in Molecular immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
30 citing papers in PubMed, 43 citations in OpenAlex.
- Epigenetic programming by H3K23ac defines lineage fate of Meg3Nature cell biology · 2026Article
- Downregulation of the Long Non-Coding RNACancers · 2026Article
- Big data analytics for CLEC5A dynamics based on single cell genomics and proteomics reveal its diverse functions in human diseases.Nanotheranostics · 2026Article
- Pathogenesis of psoriatic arthritis: new insights from a bone marrow perspective.Current opinion in rheumatology · 2025Review
- IL-23 induces CLEC5AJournal of autoimmunity · 2024Article
- Interleukin-23 Regulates Inflammatory Osteoclastogenesis via Activation of CLEC5A(+) Osteoclast Precursors.Arthritis & rheumatology (Hoboken, N.J.) · 2023Article
- [Overexpression of CLEC5A inhibits cell proliferation and metastasis and reverses epithelial-mesenchymal transition in hepatocellular carcinoma].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Regulation of immune response against third-stageFrontiers in immunology · 2023Article
- Interleukin-1 contributes to clonal expansion and progression of bone marrow fibrosis in JAK2V617F-induced myeloproliferative neoplasm.Nature communications · 2022Article
- Characterisation of the Circulating Transcriptomic Landscape in Inflammatory Bowel Disease Provides Evidence for Dysregulation of Multiple Transcription Factors Including NFE2, SPI1, CEBPB, and IRF2.Journal of Crohn's & colitis · 2022Article
- BCL11A promotes myeloid leukemogenesis by repressing PU.1 target genes.Blood advances · 2022Article
- Activation of the Innate Immune Checkpoint CLEC5A on Myeloid Cells in the Absence of Danger Signals Modulates Macrophages' Function but Does Not Trigger the Adaptive T Cell Immune Response.Journal of immunology research · 2022Article
- CLEC5A: A Promiscuous Pattern Recognition Receptor to Microbes and Beyond.Advances in experimental medicine and biology · 2020Review
- Elevated Expression of C-Type Lectin Domain Family 5-Member A (CLEC5A) and Its Relation to Inflammatory Parameters and Disease Course in Adult-Onset Still's Disease.Journal of immunology research · 2020Article
- Inflammasome Fuels Dengue Severity.Frontiers in cellular and infection microbiology · 2020Review
- Identification of a Specific Gene Module for Predicting Prognosis in Glioblastoma Patients.Frontiers in oncology · 2019Article
- Global Gene Expression Response in Peripheral Blood Cells of Petroleum Workers Exposed to Sub-Ppm Benzene Levels.International journal of environmental research and public health · 2018Article
- CRISPR/Cas9-mediated ASXL1 mutations in U937 cells disrupt myeloid differentiation.International journal of oncology · 2018Article
- Activation of Nrf2 by the dengue virus causes an increase in CLEC5A, which enhances TNF-α production by mononuclear phagocytes.Scientific reports · 2016Article
- Threshold Levels of Gfi1 Maintain E2A Activity for B Cell Commitment via Repression of Id1.PloS one · 2016Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
C-type lectin domain family 5, member A (CLEC5A), also known as myeloid DNAX activation protein 12 (DAP12)-associating lectin-1 (MDL-1), is a cell surface receptor strongly associated with the activation and differentiation of myeloid cells. CLEC5A associates with its adaptor protein DAP12 to activate a signaling cascade resulting in activation of downstream kinases in inflammatory responses. Currently, little is known about the transcriptional regulation of CLEC5A. We identified CLEC5A as one of the most highly induced genes in a microarray gene profiling experiment of PU.1 restored myeloid PU.1-null cells. We further report that CLEC5A expression is significantly reduced in several myeloid differentiation models upon PU.1 inhibition during monocyte/macrophage or granulocyte differentiation. In addition, CLEC5A mRNA expression was significantly lower in primary acute myeloid leukemia (AML) patient samples than in macrophages and granulocytes from healthy donors. Moreover, we found activation of a CLEC5A promoter reporter by PU.1 as well as in vivo binding of PU.1 to the CLEC5A promoter. Our findings indicate that CLEC5A expression in monocyte/macrophage and granulocytes is regulated by PU.1.
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Registered trials
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.