ArticleNature communications2019
ERAP1 promotes Hedgehog-dependent tumorigenesis by controlling USP47-mediated degradation of βTrCP.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
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Who cites it
34 citing papers in PubMed, 51 citations in OpenAlex.
- Targeting USP47 reprograms macrophage polarization to ameliorate septic peritonitis and promote cutaneous wound healing.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Review
- Hypoxic Endothelial-Cell-Derived Exosomal lnc-DKK3 Reprograms Tumor-Associated Macrophages via USP47/PD-L1/RelA Axis to Promote Glioma Progression.Research (Washington, D.C.) · 2026Article
- ERAP1 Activity Modulates the Immunopeptidome but Also Affects the Proteome, Metabolism, and Stress Responses in Cancer Cells.Molecular & cellular proteomics : MCP · 2025Article
- Single-cell eQTL mapping reveals cell-type-specific genes associated with the risk of gastric cancer.Cell genomics · 2025Article
- Unveiling the impact of ERAP1 and ERAP2 on migration, angiogenesis and ER stress response.Frontiers in cell and developmental biology · 2025Review
- Combining ERAP1 silencing and entinostat therapy to overcome resistance to cancer immunotherapy in neuroblastoma.Journal of experimental & clinical cancer research : CR · 2024Article
- Exploiting the potential of the ubiquitin-proteasome system in overcoming tyrosine kinase inhibitor resistance in chronic myeloid leukemia.Genes & diseases · 2024Review
- Article
- ERAP Inhibitors in Autoimmunity and Immuno-Oncology: Medicinal Chemistry Insights.Journal of medicinal chemistry · 2024Review
- Friend or foe? Reciprocal regulation between E3 ubiquitin ligases and deubiquitinases.Biochemical Society transactions · 2024Review
- SALL4 is a CRL3Cell death and differentiation · 2024Article
- Exploring the neuropharmacological properties of scopoletin-richAmerican journal of translational research · 2024Article
- Imperatorin Suppresses Aberrant Hedgehog Pathway and Overcomes Smoothened Antagonist Resistance via STAT3 Inhibition.Drug design, development and therapy · 2024Article
- The strategies to cure cancer patients by eradicating cancer stem-like cells.Molecular cancer · 2023Review
- Structural and functional characterization of USP47 reveals a hot spot for inhibitor design.Communications biology · 2023Article
- Review
- Expression of FBXW11 in normal and disease-associated osteogenic cells.Journal of cellular and molecular medicine · 2023Article
- All-Trans Retinoic Acid Promotes a Tumor Suppressive OTUD6B-β-TrCP-SNAIL Axis in Esophageal Squamous Cell Carcinoma and Enhances Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- USP47 deubiquitylates Groucho/TLE to promote Wnt-β-catenin signaling.Science signaling · 2023Article
Corrections and comments
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Authors and funding
27 authors at 12 institutions in 4 countries.
Funding
Abstract
The Hedgehog (Hh) pathway is essential for embryonic development and tissue homeostasis. Aberrant Hh signaling may occur in a wide range of human cancers, such as medulloblastoma, the most common brain malignancy in childhood. Here, we identify endoplasmic reticulum aminopeptidase 1 (ERAP1), a key regulator of innate and adaptive antitumor immune responses, as a previously unknown player in the Hh signaling pathway. We demonstrate that ERAP1 binds the deubiquitylase enzyme USP47, displaces the USP47-associated βTrCP, the substrate-receptor subunit of the SCF
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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.