ArticleProceedings of the National Academy of Sciences of the United States of America2001
Identification of two residues in MCM5 critical for the assembly of MCM complexes and Stat1-mediated transcription activation in response to IFN-gamma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 88 citations in OpenAlex.
- MCM2-7 proteins promote NF-κB transcriptional activity through cooperative promoter recruitment.Bioscience reports · 2026Article
- IFNγ shapes macrophage inflammatory responses by STAT1 isoform-specific epigenetic and transcriptional mechanisms.BMC genomics · 2026Article
- MAP-X reveals distinct protein complex dynamics across Plasmodium falciparum blood stages.Nature microbiology · 2025Article
- Mcm5 mutation leads to silencing of Stat1-bcl2 which accelerating apoptosis of immature T lymphocytes with DNA damage.Cell death & disease · 2025Article
- Review
- The MCM2-7 Complex: Roles beyond DNA Unwinding.Biology · 2024Review
- Quantity and quality of minichromosome maintenance protein complexes couple replication licensing to genome integrity.Communications biology · 2024Review
- Mutant p53 gains oncogenic functions through a chromosomal instability-induced cytosolic DNA response.Nature communications · 2024Article
- IFN-γ-STAT1-ERK Pathway Mediates Protective Effects of Invariant Natural Killer T Cells Against Doxorubicin-Induced Cardiomyocyte Death.JACC. Basic to translational science · 2023Article
- Unwinding the Role of the CMG Helicase in Inborn Errors of Immunity.Journal of clinical immunology · 2023Article
- Towards unravelling biological mechanisms behind radiation-induced oral mucositis via mass spectrometry-based proteomics.Frontiers in oncology · 2023Article
- Novel protein contact points among TP53 and minichromosome maintenance complex proteins 2, 3, and 5.Cancer medicine · 2022Article
- STAT1 and Its Crucial Role in the Control of Viral Infections.International journal of molecular sciences · 2022Review
- Mcm5 Represses Endodermal Migration through Cxcr4a-itgb1b Cascade Instead of Cell Cycle Control.Biomolecules · 2022Article
- Article
- Gene expression profiling revealed MCM3 to be a better marker than Ki67 in prognosis of invasive ductal breast carcinoma patients.Clinical and experimental medicine · 2020Article
- Assembly of a parts list of the human mitotic cell cycle machinery.Journal of molecular cell biology · 2019Article
- Interferon-stimulated genes: new platforms and computational approaches.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- Expression of Minichromosome Maintenance Proteins (MCM) and Cancer Prognosis: A meta-analysis.Journal of Cancer · 2018Article
- The C-Terminal Transactivation Domain of STAT1 Has a Gene-Specific Role in Transactivation and Cofactor Recruitment.Frontiers in immunology · 2018Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
In response to IFN-gamma, the latent cytoplasmic Stat1 (signal transducer and activator of transcription) proteins translocate into the nucleus and activate transcription. We showed previously that Stat1 recruits a group of nuclear proteins, among them MCM5 (minichromosome maintenance) and MCM3, for transcription activation. MCM5 directly interacts with the transcription activation domain (TAD) of Stat1 and enhances Stat1-mediated transcription activation. In this report, we identified two specific residues (R732, K734) in MCM5 that are required for the direct interaction between Stat1 and MCM5 both in vitro and in vivo. MCM5 containing mutations of R732/K734 did not enhance Stat1-mediated transcription activation in response to IFN-gamma. In addition, it also failed to form complexes with other MCM proteins in vivo, suggesting that these two residues may be important for an interaction domain in MCM5. Furthermore, MCM5 bearing mutations in its ATPase and helicase domains did not enhance Stat1 activity. In vitro binding assays indicate that MCM3 does not interact directly with Stat1, suggesting that the presence of MCM3 in the group of Stat1TAD-interacting proteins is due to the association of MCM3 with MCM5. Finally, gel filtration analyses of nuclear extracts from INF-gamma-treated cells demonstrate that there is a MCM5/3 subcomplex coeluting with Stat1. Together, these results strongly suggest that Stat1 recruits a MCM5/3 subcomplex through direct interaction with MCM5 in the process of IFN-gamma-induced gene activation.
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