ArticleBrain research2010
Abnormal gene expression in cerebellum of Npc1-/- mice during postnatal development.
Article in Brain research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 32 citations in OpenAlex.
- Efficacy of N-acetylcysteine in phenotypic suppression of mouse models of Niemann-Pick disease, type C1.Human molecular genetics · 2013Trial
- Phytochemical alkaloids orchestrate immunometabolism against viral infections.National science review · 2025Article
- Neuraminidase 1 regulates neuropathogenesis by governing the cellular state of microglia via modulation of Trem2 sialylation.Cell reports · 2025Article
- Exploring Pro-Inflammatory Immunological Mediators: Unraveling the Mechanisms of Neuroinflammation in Lysosomal Storage Diseases.Biomedicines · 2023Review
- Article
- Do heterozygous mutations of Niemann-Pick type C predispose to late-onset neurodegeneration: a review of the literature.Journal of neurology · 2021Review
- Toll-like receptor mediated lysozyme expression in Niemann-pick disease, type C1.Molecular genetics and metabolism · 2020Article
- Single Cell Transcriptome Analysis of Niemann-Pick Disease, Type C1 Cerebella.International journal of molecular sciences · 2020Article
- Abnormal LAMP1 glycosylation may play a role in Niemann-Pick disease, type C pathology.PloS one · 2020Article
- Identification of Novel Pathways Associated with Patterned Cerebellar Purkinje Neuron Degeneration in Niemann-Pick Disease, Type C1.International journal of molecular sciences · 2019Article
- Increased interactions and engulfment of dendrites by microglia precede Purkinje cell degeneration in a mouse model of Niemann Pick Type-C.Scientific reports · 2019Article
- Proteomics of the corpus callosum to identify novel factors involved in hypomyelinated Niemann-Pick Type C disease mice.Molecular brain · 2019Article
- The Role of Geranylgeranyltransferase I-Mediated Protein Prenylation in the Brain.Molecular neurobiology · 2016Review
- Enhanced expression of matrix metalloproteinase-12 contributes to Npc1 deficiency-induced axonal degeneration.Experimental neurology · 2015Article
- Human and mouse neuroinflammation markers in Niemann-Pick disease, type C1.Journal of inherited metabolic disease · 2014Article
- Involvement of the N-methyl-D-aspartate receptor GluN2D subunit in phencyclidine-induced motor impairment, gene expression, and increased Fos immunoreactivity.Molecular brain · 2013Article
- Genetic dissection of a cell-autonomous neurodegenerative disorder: lessons learned from mouse models of Niemann-Pick disease type C.Disease models & mechanisms · 2013Review
- Complement is dispensable for neurodegeneration in Niemann-Pick disease type C.Journal of neuroinflammation · 2012Article
- Microarray expression analysis and identification of serum biomarkers for Niemann-Pick disease, type C1.Human molecular genetics · 2012Article
- Neuronal and epithelial cell rescue resolves chronic systemic inflammation in the lipid storage disorder Niemann-Pick C.Human molecular genetics · 2012Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Niemann-Pick Type C (NPC) disease is an autosomal recessive neurodegenerative disorder with abnormal lipid storage as the major cellular pathologic hallmark. Genetic analyses have identified mutations in NPC1 gene in the great majority of cases, while mutations in NPC2 account for the remainders. Yet little is known regarding the cellular mechanisms responsible for NPC pathogenesis, especially for neurodegeneration, which is the usual cause of death. To identify critical steps that could account for the pathological manifestations of the disease in one of the most affected brain structures, we performed global gene expression analysis in the cerebellum from 3-week old Npc1+/+ and Npc1-/- mice with two different microarray platforms (Agilent and Illumina). Differentially expressed genes identified by both microarray platforms were then subjected to KEGG pathway analysis. Expression of genes in six pathways was significantly altered in Npc1-/- mice; functionally, these signaling pathways belong to the following three categories: (1) steroid and terpenoid biosynthesis, (2) immune response, and (3) cell adhesion/motility. In addition, the expression of several proteins involved in lipid transport was significantly altered in Npc1-/- mice. Our results provide novel molecular insight regarding the mechanisms of pathogenesis in NPC disease and reveal potential new therapeutic targets.
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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.