ArticleSignal transduction and targeted therapy
USP7 deubiquitinates and stabilizes NOTCH1 in T-cell acute lymphoblastic leukemia.
Article in Signal transduction and targeted therapy. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 62 citations in OpenAlex.
- It takes two to tango: the intersection of deubiquitinases and mMolecular cancer · 2026Review
- MYC-induced USP10 stabilizes SOX4 to promote thymocyte proliferation and leukemia onset in mice.Nature communications · 2026Article
- T cell acute lymphoblastic leukemia exploits a neural proinflammatory pathway to colonize the meninges.The Journal of clinical investigation · 2026Article
- Emerging roles of USP7 in tumor immune evasion, metabolic reprogramming, and therapeutic resistance.Frontiers in immunology · 2026Review
- USP7 sustains hematopoietic stem cell homeostasis partially via PU.1 stabilization.International journal of biological sciences · 2026Article
- USP7 alterations are associated with a poor survival in pediatric T-cell acute lymphoblastic leukemia.Blood advances · 2025Article
- USP7 mutations are associated with adverse outcomes in pediatric T cell acute lymphoblastic leukemia and lymphoma.Annals of hematology · 2025Article
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- Cryptococcosis, tuberculosis, and a kidney cancer fail to fit the atherosclerosis paradigm for foam cell lipid content.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- USP24 promotes hepatocellular carcinoma progression by deubiquitinating and stabilizing YAP1.Cancer cell international · 2025Article
- Broad-spectrum ubiquitin-specific protease inhibition as a mechanism for the cytotoxicity of YM155 in cancers.Scientific reports · 2025Article
- USP7 reduces the level of nuclear DICER, impairing DNA damage response and promoting cancer progression.Molecular oncology · 2024Article
- Notch Partners in the Long Journey of T-ALL Pathogenesis.International journal of molecular sciences · 2023Review
- A review of deubiquitinases and thier roles in tumorigenesis and development.Frontiers in bioengineering and biotechnology · 2023Review
- Oncogenic deubiquitination controls tyrosine kinase signaling and therapy response in acute lymphoblastic leukemia.Science advances · 2022Article
- USP7 substrates identified by proteomics analysis reveal the specificity of USP7.Genes & development · 2022Article
- WISP1 induces ovarian cancer via the IGF1/αvβ3/Wnt axis.Journal of ovarian research · 2022Article
- Review
- Pharmacological Modulation of Ubiquitin-Proteasome Pathways in Oncogenic Signaling.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is a highly aggressive leukemia that is primarily caused by aberrant activation of the NOTCH1 signaling pathway. Recent studies have revealed that posttranslational modifications, such as ubiquitination, regulate NOTCH1 stability, activity, and localization. However, the specific deubiquitinase that affects NOTCH1 protein stability remains unestablished. Here, we report that ubiquitin-specific protease 7 (USP7) can stabilize NOTCH1. USP7 deubiquitinated NOTCH1 in vivo and in vitro, whereas knockdown of USP7 increased the ubiquitination of NOTCH1. USP7 interacted with NOTCH1 protein in T-ALL cells, and the MATH and UBL domains of USP7 were responsible for this interaction. Depletion of USP7 significantly suppressed the proliferation of T-ALL cells in vitro and in vivo, accompanied by downregulation of the NOTCH1 protein level. Similarly, pharmacologic inhibition of USP7 led to apoptosis of T-ALL cells. More importantly, we found that USP7 was significantly upregulated in human T-ALL cell lines and patient samples, and a USP7 inhibitor exhibited cell cytotoxicity toward primary T-ALL cells, indicating the clinical relevance of these findings. Overall, our results demonstrate that USP7 is a novel deubiquitinase that stabilizes NOTCH1. Therefore, USP7 may be a promising therapeutic target in the currently incurable T-ALL.
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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.