ArticleJournal of human genetics2004
Down-regulation of Bcl-2 in the fetal brain of the Gaucher disease mouse model: a possible role in the neuronal loss.
Article in Journal of human genetics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 28 citations in OpenAlex.
- Gene expression profile in patients with Gaucher disease indicates activation of inflammatory processes.Scientific reports · 2019Article
- Induced Pluripotent Stem Cell Modeling of Gaucher's Disease: What Have We Learned?International journal of molecular sciences · 2017Review
- A Review of Gaucher Disease Pathophysiology, Clinical Presentation and Treatments.International journal of molecular sciences · 2017Review
- Neuronopathic Gaucher disease: dysregulated mRNAs and miRNAs in brain pathogenesis and effects of pharmacologic chaperone treatment in a mouse model.Human molecular genetics · 2015Article
- Article
- Animal models for Gaucher disease research.Disease models & mechanisms · 2011Review
- Global gene expression profile progression in Gaucher disease mouse models.BMC genomics · 2011Article
- Upregulation of proinflammatory cytokines in the fetal brain of the Gaucher mouse.Journal of Korean medical science · 2006Article
- Glycosphingolipidoses: beyond the enzymatic defect.Glycoconjugate journal · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gaucher disease is a lysosomal storage disorder resulting from an inborn deficiency of glucocerebrosidase. To investigate the genes responsible for the neuronal symptoms of Gaucher disease, gene expression profiles were analyzed in brains of the Gaucher disease mouse model using a cDNA microarray, and it was found that the bcl-2 gene is down-regulated. Immunoblotting and apoptosis assay were performed to study the relationship between the decreased expression of Bcl-2 and neuronal death on the brains of Gaucher mice fetuses at embryonic day 17.5 (E17.5) and E19.5. Decreased expression of Bcl-2 was observed in the brain stem and cerebellum but not in cortex by immunoblotting. In situ labeling of DNA fragmentation using terminal transferase-mediated dUTP nick-end-labeling (TUNEL) assay confirmed that apoptosis occurred in the brain stem and cerebellum. More apoptotic cells were detected in the brains of Gaucher mice fetuses at E19.5 than at E17.5. These results suggest that the accumulation of either glucocerebroside or glucosylsphingosine, as a result of glucocerebrosidase deficiency, affects gene expression and could be responsible for neuronal cell death.
Indexed as
Identifiers
What OpenQuestion holds
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.