M
Murray J. Cairns
Researcher at University of Newcastle
Publications - 201
Citations - 14007
Murray J. Cairns is an academic researcher from University of Newcastle. The author has contributed to research in topics: microRNA & Gene. The author has an hindex of 45, co-authored 175 publications receiving 10172 citations. Previous affiliations of Murray J. Cairns include Harvard University & Johnson & Johnson.
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Journal ArticleDOI
Do common genotypes of FK506 binding protein 5 (FKBP5) moderate the effects of childhood maltreatment on cognition in schizophrenia and healthy controls
Melissa J. Green,Alessandra Raudino,Murray J. Cairns,Jing Qin Wu,Paul A. Tooney,Rodney J. Scott,Vaughan J. Carr +6 more
TL;DR: The mechanisms of trauma-dependent effects of FKBP5 following early life trauma deserve further exploration in healthy and psychotic samples, in the context of epigenetic effects and perhaps epistasis with other genes.
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Pairwise common variant meta-analyses of schizophrenia with other psychiatric disorders reveals shared and distinct gene and gene-set associations
William R. Reay,Murray J. Cairns +1 more
TL;DR: Gene-based analysis of common variation revealed 67 schizophrenia-associated genes shared with other psychiatric phenotypes, including bipolar disorder, major depressive disorder, ADHD and autism-spectrum disorder, and uncovered several candidate pleiotropic genes which warrant further investigation.
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Alternative mRNA fates identified in microRNA-associated transcriptome analysis
TL;DR: These findings suggest that miRNA regulate target genes directly through interactions with both conserved and non-conserved target recognition elements, and can lead to both a decrease and increase in transcript abundance.
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E6AP gene suppression and characterization with in vitro selected hammerhead ribozymes.
TL;DR: Ribozyme-mediated reduction in E6AP expression was found to enhance the apoptotic response of HeLa cells to mitomycin C-induced DNA damage, suggesting that E 6AP has potential as a drug target, as its suppression can potentiate apoptosis in HPV-positive cells treated with a cytotoxic drug.
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Alteration of transcriptional networks in the entorhinal cortex after maternal immune activation and adolescent cannabinoid exposure.
TL;DR: It is suggested that a combination of environmental exposures during development leads to significant genomic remodeling that disrupts maturation of the EC and its associated circuitry with important implications as the potential antecedents of memory and learning deficits in schizophrenia and other neuropsychiatric disorders.