ArticleCell death and differentiation2011
Roles of HAUSP-mediated p53 regulation in central nervous system development.
Article in Cell death and differentiation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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.
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Who cites it
50 citing papers in PubMed, 81 citations in OpenAlex.
- USP15 mutation associated with autism spectrum disorder alters progenitor fate and neuronal maturation in human brain organoids.Molecules and cells · 2026Article
- Proteome-wide Ubiquitinome Profiling Reveals Substrate-specific Dynamics Within the USP7 Network.Molecular & cellular proteomics : MCP · 2026Article
- Article
- Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025Review
- Small-molecule allosteric activator of ubiquitin-specific protease 7 (USP7).Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Hao-Fountain syndrome protein USP7 controls neuronal differentiation via BCOR-ncPRC1.1.Genes & development · 2025Article
- The Hao-Fountain syndrome protein USP7 regulates neuronal connectivity in the brain via a novel p53-independent ubiquitin signaling pathway.Cell reports · 2025Article
- Usp7 Regulates Glial Lineage Cell-Specific Transcription Factors by Modulating Histone H2B Monoubiquitination.International journal of stem cells · 2024Article
- The role of ubiquitination in health and disease.MedComm · 2024Review
- FOXL2 interaction with different binding partners regulates the dynamics of ovarian development.Science advances · 2024Article
- Molecular signatures in Mendelian neurodevelopment: a focus on ubiquitination driven DNA methylation aberrations.Frontiers in molecular neuroscience · 2024Review
- Inhibition of USP7 induces p53-independent tumor growth suppression in triple-negative breast cancers by destabilizing FOXM1.Cell death and differentiation · 2023Article
- USP7 controls NGN3 stability and pancreatic endocrine lineage development.Nature communications · 2023Article
- USP7 inactivation suppresses APC-mutant intestinal hyperproliferation and tumor development.Stem cell reports · 2023Article
- Organ defects of the Usp7Biomedical journal · 2023Article
- Oncogenic deubiquitination controls tyrosine kinase signaling and therapy response in acute lymphoblastic leukemia.Science advances · 2022Article
- The DUB Club: Deubiquitinating Enzymes and Neurodevelopmental Disorders.Biological psychiatry · 2022Review
- Neuroinflammation inhibition by small-molecule targeting USP7 noncatalytic domain for neurodegenerative disease therapy.Science advances · 2022Article
- Role of the DUB enzyme USP7 in dendritic arborization, neuronal migration, and autistic-like behaviors in mice.iScience · 2022Article
- Deubiquitinases in cell death and inflammation.The Biochemical journal · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The deubiquitinase HAUSP (herpesvirus-associated ubiquitin-specific protease; also called USP7) has a critical role in regulating the p53-Mdm2 (murine double minute 2) pathway. By using the conventional knockout approach, we previously showed that hausp inactivation leads to early embryonic lethality. To fully understand the physiological functions of hausp, we have generated mice lacking hausp specifically in the brain and examined the impacts of this manipulation on brain development. We found that deletion of hausp in neural cells resulted in neonatal lethality. The brains from these mice displayed hypoplasia and deficiencies in development, which were mainly caused by p53-mediated apoptosis. Detailed analysis also showed an increase of both p53 levels and p53-dependent transcriptional activation in hausp knockout brains. Notably, neural cell survival and brain development of hausp-mutant mice can largely be restored in the p53-null background. Nevertheless, in contrast to the case of mdm2- and mdm4 (murine double minute 4)-mutant mice, inactivation of p53 failed to completely rescue the neonatal lethality of these hausp-mutant mice. These results indicate that HAUSP-mediated p53 regulation is crucial for brain development, and also suggest that both the p53-dependent and the p53-independent functions of HAUSP contribute to the neonatal lethality of hausp-mutant mice.
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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.