ArticleProceedings of the National Academy of Sciences of the United States of America2024
The Myc-associated zinc finger protein epigenetically controls expression of interferon-γ-stimulated genes by recruiting STAT1 to chromatin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- IFNγ shapes macrophage inflammatory responses by STAT1 isoform-specific epigenetic and transcriptional mechanisms.BMC genomics · 2026Article
- Zinc finger protein ZNF33B facilitates Japanese encephalitis virus replication by regulating mCell & bioscience · 2026Article
- Integrative single-cell transcriptomic analysis reveals immunomodulatory hub genes and candidate compounds for HIV-associated chronic inflammation.Virology journal · 2025Article
- Myc-associated zinc finger protein drives colorectal cancer metastasis through activating ubiquitin like with ring finger protein one.World journal of gastrointestinal oncology · 2025Article
- Injectable ECM-mimetic dynamic hydrogels abolish ferroptosis-induced post-discectomy herniation through delivering nucleus pulposus progenitor cell-derived exosomes.Nature communications · 2025Article
- Identification of novel mitophagy-related biomarkers for Kawasaki disease by integrated bioinformatics and machine-learning algorithms.Translational pediatrics · 2024Article
- Single-cell RNA sequencing and AlphaFold 3 insights into cytokine signaling and its role in uveal melanoma.Frontiers in immunology · 2024Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The MYC-Associated Zinc Finger Protein (MAZ) plays important roles in chromatin organization and gene transcription regulation. Dysregulated expression of MAZ causes diseases, such as glioblastoma, breast cancer, prostate cancer, and liposarcoma. Previously, it has been reported that MAZ controls the proinflammatory response in colitis and colon cancer via STAT3 signaling, suggesting that MAZ is involved in regulating immunity-related pathways. However, the molecular mechanism underlying this regulation remains elusive. Here, we investigate the regulatory effect of MAZ on interferon-gamma (IFN-γ)-stimulated genes via STAT1, a protein that plays an essential role in immune responses to viral, fungal, and mycobacterial pathogens. We demonstrate that about 80% of occupied STAT1-binding sites colocalize with occupied MAZ-binding sites in HAP1/K562 cells after IFN
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Registered trials
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