ArticleNature immunology2014
c-Myc-induced transcription factor AP4 is required for host protection mediated by CD8+ T cells.
Article in Nature immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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.
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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
62 citing papers in PubMed, 97 citations in OpenAlex.
- Single-cell gain-of-function mapping reveals latent regulatory programs governing CD8Research square · 2026Article
- c-MYC enhances transcription of the type 1 diabetes mellitus associated gene BATF3 via promoter binding.Scientific reports · 2026Article
- Latent Regulatory Programs Generate Synthetic T Cell States with Enhanced Therapeutic Potential.bioRxiv : the preprint server for biology · 2026Article
- MSI2 exerts antitumor effects by regulating T-cell function in kidney renal clear cell carcinoma.Translational andrology and urology · 2025Article
- Transcription factor activator protein 4 (AP4)-mediated intrinsic control of axon regeneration.Science advances · 2025Article
- The transcriptional repressor BLIMP1 enforces TCF-1-dependent and -independent restriction of the memory fate of CD8Immunity · 2025Article
- Enhancing the potency of CAR-T cells against solid tumors through transcription factor engineering.JCI insight · 2025Review
- Genome-wide CRISPR screen identifies IRF1 and TFAP4 as transcriptional regulators of Galectin-9 in T cell acute lymphoblastic leukemia.Science advances · 2025Article
- TRIM28 is an essential regulator of three-dimensional chromatin state underpinning CD8Nature communications · 2025Article
- Immunosenescence, Physical Exercise, and their Implications in Tumor Immunity and Immunotherapy.International journal of biological sciences · 2025Review
- c-Myc uses Cul4b to preserve genome integrity and promote antiviral CD8Nature communications · 2023Article
- Metabolic diversity of tumor-infiltrating T cells as target for anti-immune therapeutics.Cancer immunology, immunotherapy : CII · 2023Review
- Modular pooled discovery of synthetic knockin sequences to program durable cell therapies.Cell · 2023Article
- Immunosenescence: molecular mechanisms and diseases.Signal transduction and targeted therapy · 2023Review
- Application of ATAC-seq in tumor-specific T cell exhaustion.Cancer gene therapy · 2023Review
- tRNA-mNature immunology · 2022Article
- The MITF regulatory network in melanoma.Pigment cell & melanoma research · 2022Article
- AP4 suppresses DNA damage, chromosomal instability and senescence via inducing MDC1/Mediator of DNA damage Checkpoint 1 and repressing MIR22HG/miR-22-3p.Molecular cancer · 2022Article
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- Review
2 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Although the transcription factor c-Myc is essential for the establishment of a metabolically active and proliferative state in T cells after priming, its expression is transient. It remains unknown how T cell activation is maintained after c-Myc expression is downregulated. Here we identified AP4 as the transcription factor that was induced by c-Myc and sustained activation of antigen-specific CD8+ T cells. Despite normal priming, AP4-deficient CD8+ T cells failed to continue transcription of a broad range of c-Myc-dependent targets. Mice lacking AP4 specifically in CD8+ T cells showed enhanced susceptibility to infection with West Nile virus. Genome-wide analysis suggested that many activation-induced genes encoding molecules involved in metabolism were shared targets of c-Myc and AP4. Thus, AP4 maintains c-Myc-initiated cellular activation programs in CD8+ T cells to control microbial infection.
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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.