ArticleHuman molecular genetics2010
Expression analysis of novel striatal-enriched genes in Huntington disease.
Article in Human molecular genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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
25 citing papers in PubMed, 51 citations in OpenAlex.
- Molecular and imaging biomarker responses to brain mutant HTT lowering in a mouse model of Huntington disease.Molecular therapy. Nucleic acids · 2025Article
- Role of CYLD in brain physiology and pathology.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Neuroactive Kynurenines as Pharmacological Targets: New Experimental Tools and Exciting Therapeutic Opportunities.Pharmacological reviews · 2024Review
- Biocytin-Labeling in Whole-Cell Recording: Electrophysiological and Morphological Properties of Pyramidal Neurons in CYLD-Deficient Mice.Molecules (Basel, Switzerland) · 2023Article
- Neural mechanism underlies CYLD modulation of morphology and synaptic function of medium spiny neurons in dorsolateral striatum.Frontiers in molecular neuroscience · 2023Article
- Cerebrospinal fluid biomarkers for assessing Huntington disease onset and severity.Brain communications · 2022Article
- The K63 deubiquitinase CYLD modulates autism-like behaviors and hippocampal plasticity by regulating autophagy and mTOR signaling.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Neurodegeneration in Multiple Sclerosis: Symptoms of Silent Progression, Biomarkers and Neuroprotective Therapy-Kynurenines Are Important Players.Molecules (Basel, Switzerland) · 2021Review
- FACS-array-based cell purification yields a specific transcriptome of striatal medium spiny neurons in a murine Huntington disease model.The Journal of biological chemistry · 2020Article
- Striatal Projection Neurons Require Huntingtin for Synaptic Connectivity and Survival.Cell reports · 2020Article
- Cell-Autonomous and Non-cell-Autonomous Pathogenic Mechanisms in Huntington's Disease: Insights from In Vitro and In Vivo Models.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Review
- Functional roles of ST8SIA3-mediated sialylation of striatal dopamine DTranslational psychiatry · 2019Article
- Advancing a High Throughput Glycotope-centric Glycomics Workflow Based on nanoLC-MSMolecular & cellular proteomics : MCP · 2017Article
- Tryptophan-2,3-dioxygenase (TDO) inhibition ameliorates neurodegeneration by modulation of kynurenine pathway metabolites.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Combined serial analysis of gene expression and transcription factor binding site prediction identifies novel-candidate-target genes of Nr2e1 in neocortex development.BMC genomics · 2015Article
- Indoleamine 2,3 Dioxygenase as a Potential Therapeutic Target in Huntington's Disease.Journal of Huntington's disease · 2015Review
- Possible involvement of self-defense mechanisms in the preferential vulnerability of the striatum in Huntington's disease.Frontiers in cellular neuroscience · 2014Review
- Multiple Aspects of Gene Dysregulation in Huntington's Disease.Frontiers in neurology · 2013Review
- Genetic manipulations of mutant huntingtin in mice: new insights into Huntington's disease pathogenesis.The FEBS journal · 2013Review
- The causative role and therapeutic potential of the kynurenine pathway in neurodegenerative disease.Journal of molecular medicine (Berlin, Germany) · 2013Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Selective degeneration of striatal neurons is a pathologic hallmark of Huntington disease (HD). The exact mechanism(s) behind this specific neurodegeneration is still unknown. Expression studies of diseased human post-mortem brain, as well as different mouse models exhibiting striatal degeneration, have demonstrated changes in the expression of many important genes with a large proportion of changes being observed in the striatal-enriched genes. These investigations have raised questions about how enrichment of particular transcripts in the striatum can lead to its selective vulnerability to neurodegeneration. Monitoring the expression changes of striatal-enriched genes during the course of the disease may be informative about their potential involvement in selective degeneration. In this study, we analyzed a Serial Analysis of Gene Expression (SAGE) database (www.mouseatlas.org) and compared the mouse striatum to 18 other brain regions to generate a novel list of striatal-enriched transcripts. These novel striatal-enriched transcripts were subsequently evaluated for expression changes in the YAC128 mouse model of HD, and differentially expressed transcripts were further examined in human post-mortem caudate samples. We identified transcripts with altered expression in YAC128 mice, which also showed consistent expression changes in human post-mortem tissue. The identification of novel striatal-enriched genes with altered expression in HD offers new avenues of study, leading towards a better understanding of specific pathways involved in the selective degeneration of striatal neurons in HD.
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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.