ArticlePloS one2010
Analysis of chaperone mRNA expression in the adult mouse brain by meta analysis of the Allen Brain Atlas.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
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- Praja1 ubiquitin ligase facilitates degradation of polyglutamine proteins and suppresses polyglutamine-mediated toxicity.Molecular biology of the cell · 2021Article
- Quantitative analysis of global protein stability rates in tissues.Scientific reports · 2020Article
- A pantothenate kinase-deficient mouse model reveals a gene expression program associated with brain coenzyme a reduction.Biochimica et biophysica acta. Molecular basis of disease · 2020Article
- Multivariate association between single-nucleotide polymorphisms in Alzgene linkage regions and structural changes in the brain: discovery, refinement and validation.Statistical applications in genetics and molecular biology · 2017Article
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- Reciprocal Control of Thyroid Binding and the Pipecolate Pathway in the Brain.Neurochemical research · 2017Review
- Protein misfolding in neurodegenerative diseases: implications and strategies.Translational neurodegeneration · 2017Review
- Analysis of spatial-temporal gene expression patterns reveals dynamics and regionalization in developing mouse brain.Scientific reports · 2016Article
- The biology of proteostasis in aging and disease.Annual review of biochemistry · 2015Review
- Targeting Hsp90 and its co-chaperones to treat Alzheimer's disease.Expert opinion on therapeutic targets · 2014Review
- Selective vulnerability to neurodegenerative disease: the curious case of Prion Protein.Disease models & mechanisms · 2014Review
- Proteostasis in striatal cells and selective neurodegeneration in Huntington's disease.Frontiers in cellular neuroscience · 2014Review
- Lysine metabolism in mammalian brain: an update on the importance of recent discoveries.Amino acids · 2013Review
- Interactions between the neuromodulatory systems and the amygdala: exploratory survey using the Allen Mouse Brain Atlas.Brain structure & function · 2013Article
- Impaired heat shock response in cells expressing full-length polyglutamine-expanded huntingtin.PloS one · 2012Article
- Crystal structure of R120G disease mutant of human αB-crystallin domain dimer shows closure of a groove.Journal of molecular biology · 2011Article
- Expression profiling of autism candidate genes during human brain development implicates central immune signaling pathways.PloS one · 2011Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The pathology of many neurodegenerative diseases is characterized by the accumulation of misfolded and aggregated proteins in various cell types and regional substructures throughout the central and peripheral nervous systems. The accumulation of these aggregated proteins signals dysfunction of cellular protein homeostatic mechanisms such as the ubiquitin/proteasome system, autophagy, and the chaperone network. Although there are several published studies in which transcriptional profiling has been used to examine gene expression in various tissues, including tissues of neurodegenerative disease models, there has not been a report that focuses exclusively on expression of the chaperone network. In the present study, we used the Allen Brain Atlas online database to analyze chaperone expression levels. This database utilizes a quantitative in situ hybridization approach and provides data on 270 chaperone genes within many substructures of the adult mouse brain. We determined that 256 of these chaperone genes are expressed at some level. Surprisingly, relatively few genes, only 30, showed significant variations in levels of mRNA across different substructures of the brain. The greatest degree of variability was exhibited by genes of the DnaJ co-chaperone, Tetratricopeptide repeat, and the HSPH families. Our analysis provides a valuable resource towards determining how variations in chaperone gene expression may modulate the vulnerability of specific neuronal populations of mammalian brain.
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