ArticlePLoS genetics2009
HECTD2 is associated with susceptibility to mouse and human prion disease.
Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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
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.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Genome-wide association study in multiple human prion diseases suggests genetic risk factors additional to PRNP.Human molecular genetics · 2012Pooled it
- Population screening for variant Creutzfeldt-Jakob disease using a novel blood test: diagnostic accuracy and feasibility study.JAMA neurology · 2014Trial
- Lactylation-Driven HECTD2 Limits the Response of Hepatocellular Carcinoma to Lenvatinib.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- HECTD2 as a target for veratric acid in the regulation of ferroptosis in renal cell carcinoma.Amino acids · 2024Article
- Article
- Article
- How Do Yeast Cells Contend with Prions?International journal of molecular sciences · 2020Review
- Proteasomal Inhibition Redirects the PrP-Like Shadoo Protein to the Nucleus.Molecular neurobiology · 2019Article
- LTR retroelement expansion of the human cancer transcriptome and immunopeptidome revealed by de novo transcript assembly.Genome research · 2019Article
- Neurodegenerative Disease Transmission and Transgenesis in Mice.Cold Spring Harbor perspectives in biology · 2017Review
- What's next for genomics and prion diseases?Future science OA · 2017Article
- Deubiquitinating enzyme VCIP135 dictates the duration of botulinum neurotoxin type A intoxication.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Early Origin and Evolution of the Angelman Syndrome Ubiquitin Ligase GeneFrontiers in cellular neuroscience · 2017Review
- Misfolding leads the way to unraveling signaling pathways in the pathophysiology of prion diseases.Prion · 2016Review
- Inherited mtDNA variations are not strong risk factors in human prion disease.Neurobiology of aging · 2015Article
- The proinflammatory role of HECTD2 in innate immunity and experimental lung injury.Science translational medicine · 2015Article
- Contrasting genetic architectures in different mouse reference populations used for studying complex traits.Genome research · 2015Review
- In vitro screen of prion disease susceptibility genes using the scrapie cell assay.Human molecular genetics · 2014Article
- Identification of a gene regulatory network associated with prion replication.The EMBO journal · 2014Article
- Genetic studies in human prion diseases.Journal of Korean medical science · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 3 countries.
Funding
Abstract
Prion diseases are fatal transmissible neurodegenerative disorders, which include Scrapie, Bovine Spongiform Encephalopathy (BSE), Creutzfeldt-Jakob Disease (CJD), and kuru. They are characterised by a prolonged clinically silent incubation period, variation in which is determined by many factors, including genetic background. We have used a heterogeneous stock of mice to identify Hectd2, an E3 ubiquitin ligase, as a quantitative trait gene for prion disease incubation time in mice. Further, we report an association between HECTD2 haplotypes and susceptibility to the acquired human prion diseases, vCJD and kuru. We report a genotype-associated differential expression of Hectd2 mRNA in mouse brains and human lymphocytes and a significant up-regulation of transcript in mice at the terminal stage of prion disease. Although the substrate of HECTD2 is unknown, these data highlight the importance of proteosome-directed protein degradation in neurodegeneration. This is the first demonstration of a mouse quantitative trait gene that also influences susceptibility to human prion diseases. Characterisation of such genes is key to understanding human risk and the molecular basis of incubation periods.
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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.