ArticleNature communications2016
DCAF1 controls T-cell function via p53-dependent and -independent mechanisms.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 34 citations in OpenAlex.
- SKI is critical to counter TGF-β signaling to promote T cell function and autoimmunity.Science advances · 2026Article
- Targeting PIM2 improves antitumor immunity through promoting effector function and persistence of CD8 T cells.The Journal of clinical investigation · 2026Article
- OICR-41103 as a chemical probe for the DCAF1 WD40 domain.Communications biology · 2025Article
- Review
- CRL4-DCAF1 Ubiquitin Ligase Dependent Functions of HIV Viral Protein R and Viral Protein X.Viruses · 2024Review
- CRL4Life science alliance · 2024Article
- Discovery of a Novel DCAF1 Ligand Using a Drug-Target Interaction Prediction Model: Generalizing Machine Learning to New Drug Targets.Journal of chemical information and modeling · 2023Article
- Targeting USP2 regulation of VPRBP-mediated degradation of p53 and PD-L1 for cancer therapy.Nature communications · 2023Article
- The cohesin modifier ESCO2 is stable during DNA replication.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Article
- Analysis of ceRNA Regulatory Mechanism of Rape Pollen Allergy Based on Whole-Transcriptome Sequencing of Peripheral Blood Mononuclear Cells.Journal of asthma and allergy · 2023Article
- The CRL4 E3 ligase Mahjong/DCAF1 controls cell competition through the transcription factor Xrp1, independently of polarity genes.Development (Cambridge, England) · 2022Article
- VPRBP Functions Downstream of the Androgen Receptor and OGT to Restrict p53 Activation in Prostate Cancer.Molecular cancer research : MCR · 2022Article
- Cinobufagin alleviates lipopolysaccharide-induced acute lung injury by regulating autophagy through activation of the p53/mTOR pathway.Frontiers in pharmacology · 2022Article
- The CRL4The EMBO journal · 2021Article
- The E3 ubiquitin ligase Cul4b promotes CD4+ T cell expansion by aiding the repair of damaged DNA.PLoS biology · 2021Article
- Ddb1 Is Essential for the Expansion of CD4Frontiers in immunology · 2021Article
- Ddb1-Cullin4-Associated-Factor 1 in Macrophages Restricts theJournal of inflammation research · 2021Article
- CRL4Science advances · 2020Article
- DCAF1 regulates Treg senescence via the ROS axis during immunological aging.The Journal of clinical investigation · 2020Article
- DCAF1 (VprBP): emerging physiological roles for a unique dual-service E3 ubiquitin ligase substrate receptor.Journal of molecular cell biology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
Abstract
On activation, naive T cells grow in size and enter cell cycle to mount immune response. How the fundamental processes of T-cell growth and cell cycle entry are regulated is poorly understood. Here we report that DCAF1 (Ddb1-cullin4-associated-factor 1) is essential for these processes. The deletion of DCAF1 in T cells impairs their peripheral homeostasis. DCAF1 is upregulated on T-cell receptor activation and critical for activation-induced T-cell growth, cell cycle entry and proliferation. In addition, DCAF1 is required for T-cell expansion and function during anti-viral and autoimmune responses in vivo. DCAF1 deletion leads to a drastic stabilization of p53 protein, which can be attributed to a requirement of DCAF1 for MDM2-mediated p53 poly-ubiquitination. Importantly, p53 deletion rescues the cell cycle entry defect but not the growth defect of DCAF1-deficient cells. Therefore, DCAF1 is vital for T-cell function through p53-dependent and -independent mechanisms.
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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.