ReviewRedox biology2013
Cullin 3 as a novel target in diverse pathologies.
Review in Redox biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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
35 citing papers in PubMed, 62 citations in OpenAlex.
- The kinesin motor Kif9 regulates centriolar satellite positioning during interphase.Current biology : CB · 2025Article
- Hepatoprotective and Nephroprotective Effects ofInternational journal of molecular sciences · 2025Article
- Ubiquitin-conjugating enzyme UBE2N modulates proteostasis in immunoproteasome-positive acute myeloid leukemia.The Journal of clinical investigation · 2025Article
- Advancements in the research of the structure, function, and disease-related roles of ARMC5.Frontiers of medicine · 2025Review
- Genome-Wide DNA Methylation in Early-Onset-Dementia Patients Brain Tissue and Lymphoblastoid Cell Lines.International journal of molecular sciences · 2024Article
- Cullin-3 proteins be a novel biomarkers and therapeutic targets for hyperchloremia induced by oral poisoning.Scientific reports · 2024Article
- Article
- ARMC5 controls the degradation of most Pol II subunits, and ARMC5 mutation increases neural tube defect risks in mice and humans.Genome biology · 2024Article
- Deficiency of Cullin 3, a Protein Encoded by a Schizophrenia and Autism Risk Gene, Impairs Behaviors by Enhancing the Excitability of Ventral Tegmental Area (VTA) DA Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Evaluation of the role of Sigma 1 receptor and Cullin3 in retinal photoreceptor cells.Free radical biology & medicine · 2023Article
- The Ubiquitin-like Proteins ofBiomolecules · 2023Review
- Toxicoproteomics of Mono(2-ethylhexyl) phthalate and Perfluorooctanesulfonic Acid in Models of Prostatic Diseases.Chemical research in toxicology · 2023Article
- ARMC5 is part of an RPB1-specific ubiquitin ligase implicated in adrenal hyperplasia.Nucleic acids research · 2022Article
- Sorting nexin 6 interacts with Cullin3 and regulates programmed death ligand 1 expression.FEBS letters · 2021Article
- Spatiotemporal 22q11.21 Protein Network Implicates DGCR8-Dependent MicroRNA Biogenesis as a Risk for Late-Fetal Cortical Development in Psychiatric Diseases.Life (Basel, Switzerland) · 2021Article
- Nuclear Factor Erythroid-2-Related Factor 2 Signaling in the Neuropathophysiology of Inherited Metabolic Disorders.Frontiers in cellular neuroscience · 2021Review
- A Selective Review of the Excitatory-Inhibitory Imbalance in Schizophrenia: Underlying Biology, Genetics, Microcircuits, and Symptoms.Frontiers in cell and developmental biology · 2021Review
- De novo variants in CUL3 are associated with global developmental delays with or without infantile spasms.Journal of human genetics · 2020Article
- KEAP1, a cysteine-based sensor and a drug target for the prevention and treatment of chronic disease.Open biology · 2020Review
- The CRL3Signal transduction and targeted therapy · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence suggests that the malfunctioning disposal system of cell protein called ubiquitin-proteasome system (UPS) plays an important role in the development of disorders, including cancer and neurodegenerative diseases. Accumulating evidence suggests that the abnormal regulation of the E3 ubiquitin ligases, essential components of the UPS, contributes to uncontrolled proliferation, genomic instability and cancer, since these ligases and their substrates are involved in the regulation of cell cycle progression, gene transcription, signal transduction, DNA replication and others. Through selective degradation of specific substrates, E3 ligases regulate different biological processes. Cullins are a family of proteins that confer substrate specificity to multimeric complex of E3 ligases acting as scaffold proteins. So far, seven members of the cullin family of proteins have been identified. Interestingly, the data generated by several groups indicate that cullin 3 (Cul3) has begun to emerge as a protein involved in the etiopathology of multiple diseases. In this paper we examine the latest advances in basic research on the biology of Cul3 and how it could help to direct drug discovery efforts on this target.
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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.