ArticleScience (New York, N.Y.)2015
Control of signaling-mediated clearance of apoptotic cells by the tumor suppressor p53.
Article in Science (New York, N.Y.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
153 citing papers in PubMed, 1 synthesis or guideline pooled it, 231 citations in OpenAlex.
- Large-Scale Exome-wide Association Analysis Identifies Loci for White Blood Cell Traits and Pleiotropy with Immune-Mediated Diseases.American journal of human genetics · 2016Pooled it
- Ineffectiveness of immune checkpoint inhibitors in prostate cancer: is it just a question of '-mabs'?The Journal of pathology · 2026Review
- VISTA Deficiency Exacerbates Autoimmune Uveitis by Promoting Microglial Activation via the TLR4/MyD88/NF-κB Pathway.Investigative ophthalmology & visual science · 2026Article
- Whole transcriptome sequencing and ceRNA regulatory network in diabetic peripheral neuropathy.Scientific reports · 2026Article
- Homeobox A10 in gastrointestinal malignancies: unraveling metastatic mechanisms and novel therapeutic opportunities.Cancer metastasis reviews · 2026Review
- T cell-intrinsic VISTA expression promotes resistance to CTLA-4 blockade by restricting CD8+ T cell responses.The Journal of clinical investigation · 2026Article
- IGSF11-VISTA is a critical and targetable immune checkpoint axis in diffuse midline glioma.Cancer cell · 2026Article
- Microglial phagocytosis in epilepsy: Mechanisms and impact.The Journal of physiology · 2026Review
- Near Infrared Photoimmunotherapy for Lung Cancer: Recent Development and Perspective.ImmunoTargets and therapy · 2026Review
- On the same side: VISTA and its ligands interact in cis on the cell surface.Protein science : a publication of the Protein Society · 2026Article
- Destruction of VISTA by TRIM25 ablation in T cells potentiates cancer immunotherapy.Cell research · 2025Article
- Targeted destruction of VISTA boosts anti-tumor immunotherapy.Cell research · 2025Article
- VISTA: An Emerging Immune Checkpoint With Clinical Relevance Across Diverse Malignancies.Immune network · 2025Review
- A Four Amino Acid Intracellular Motif of VISTA Blocks Growth Receptor Signaling in Cancer Cells to Induce Tumor Suppression.Cancer research · 2025Article
- The role of VISTA engagement in limiting neutrophil-mediated inflammation.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Emerging new immune checkpoint inhibitors in solid tumor immunotherapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Elucidating the Role ofCurrent issues in molecular biology · 2025Review
- Cancer network pharmacology: multi-network regulatory mechanisms and future directions.Medical oncology (Northwood, London, England) · 2025Review
- Negative Immune Checkpoint Inhibitors.Pharmaceutics · 2025Review
- Tumor-associated macrophages (TAMs): Constructing an immunosuppressive microenvironment bridge for pancreatic ductal adenocarcinoma (PDAC).Cancer pathogenesis and therapy · 2025Review
93 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
Authors and funding
16 authors at 3 institutions in 1 country.
Funding
Abstract
The inefficient clearance of dying cells can lead to abnormal immune responses, such as unresolved inflammation and autoimmune conditions. We show that tumor suppressor p53 controls signaling-mediated phagocytosis of apoptotic cells through its target, Death Domain1α (DD1α), which suggests that p53 promotes both the proapoptotic pathway and postapoptotic events. DD1α appears to function as an engulfment ligand or receptor that engages in homophilic intermolecular interaction at intercellular junctions of apoptotic cells and macrophages, unlike other typical scavenger receptors that recognize phosphatidylserine on the surface of dead cells. DD1α-deficient mice showed in vivo defects in clearing dying cells, which led to multiple organ damage indicative of immune dysfunction. p53-induced expression of DD1α thus prevents persistence of cell corpses and ensures efficient generation of precise immune responses.
Indexed as
Identifiers
What OpenQuestion holds
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.