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Your search keyword '"Shanley, L."' showing total 3 results
Start Over Author "Shanley, L." Publisher nature publishing group
3 results on '"Shanley, L."'

1. Citizen science and the United Nations Sustainable Development Goals

Author

Fritz, S., See, L., Carlson, T., Haklay, M., Oliver, J.L., Fraisl, D., Mondardini, R., Brocklehurst, M., Shanley, L., Schade, S., Wehn, U., Abrate, T., Anstee, J., Arnold, S., Billot, M., Campbell, J., Espey, J., Gold, M., Hager, G., He, S., Hepburn, L., Hsu, A., Long, D., Masó, J., McCallum, I., Muniafu, M., Moorthy, I., Obersteiner, M., Parker, A., Weissplug, M., West, S., Fritz, S., See, L., Carlson, T., Haklay, M., Oliver, J.L., Fraisl, D., Mondardini, R., Brocklehurst, M., Shanley, L., Schade, S., Wehn, U., Abrate, T., Anstee, J., Arnold, S., Billot, M., Campbell, J., Espey, J., Gold, M., Hager, G., He, S., Hepburn, L., Hsu, A., Long, D., Masó, J., McCallum, I., Muniafu, M., Moorthy, I., Obersteiner, M., Parker, A., Weissplug, M., and West, S.

Abstract

Traditional data sources are not sufficient for measuring the United Nations Sustainable Development Goals. New and non-traditional sources of data are required. Citizen science is an emerging example of a non-traditional data source that is already making a contribution. In this Perspective, we present a roadmap that outlines how citizen science can be integrated into the formal Sustainable Development Goals reporting mechanisms. Success will require leadership from the United Nations, innovation from National Statistical Offices and focus from the citizen-science community to identify the indicators for which citizen science can make a real contribution.

Published
2019

2. Analysis of the effects of depression associated polymorphisms on the activity of the BICC1 promoter in amygdala neurones

Author

Davidson, S, Shanley, L, Cowie, P, Lear, M, McGuffin, P, Quinn, J P, Barrett, P, and MacKenzie, A

Subjects
Transcription, Genetic, Mice, Transgenic, Transfection, Polymorphism, Single Nucleotide, Linkage Disequilibrium, Animals, Humans, RNA, Messenger, Promoter Regions, Genetic, Cells, Cultured, Neurons, Depressive Disorder, Major, Binding Sites, Computational Biology, RNA-Binding Proteins, Amygdala, Cyclic AMP-Dependent Protein Kinases, Introns, Rats, Up-Regulation, Enzyme Activation, Mice, Inbred C57BL, Affect, nervous system, Mice, Inbred CBA, Original Article, Signal Transduction
Abstract

The Bicaudal C Homolog 1 (BICC1) gene, which encodes an RNA binding protein, has been identified by genome wide association studies (GWAS) as a candidate gene associated with major depressive disorder (MDD). We explored the hypothesis that MDD associated single-nucleotide polymorphisms (SNPs) affected the ability of cis-regulatory elements within intron 3 of the BICC1 gene to modulate the activity of the BICC1 promoter region. We initially established that the BICC1 promoter drove BICC1 mRNA expression in amygdala, hippocampus and hypothalamus. Intriguingly, we provide evidence that MDD associated polymorphisms alter the ability of the BICC1 promoter to respond to PKA signalling within amygdala neurones. Considering the known role of amygdala PKA pathways in fear learning and mood these observations suggest a possible mechanism through which allelic changes in the regulation of the BICC1 gene in amygdala neurones may contribute to mood disorders. Our findings also suggest a novel direction for the identification of novel drug targets and the design of future personalised therapeutics.The Pharmacogenomics Journal advance online publication, 6 October 2015; doi:10.1038/tpj.2015.62.

Published
2015

3. Differential activity by polymorphic variants of a remote enhancer that supports galanin expression in the hypothalamus and amygdala: implications for obesity, depression and alcoholism.

Author

Davidson S, Lear M, Shanley L, Hing B, Baizan-Edge A, Herwig A, Quinn JP, Breen G, McGuffin P, Starkey A, Barrett P, and MacKenzie A

Subjects
Animals, Base Sequence, Cell Line, Tumor, Cells, Cultured, Enhancer Elements, Genetic physiology, Galanin biosynthesis, Gene Expression Regulation, Genetic Variation genetics, Humans, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Transgenic, Molecular Sequence Data, Neuroblastoma genetics, Polymorphism, Single Nucleotide physiology, Rats, Alcoholism genetics, Amygdala metabolism, Depression genetics, Galanin genetics, Hypothalamus metabolism, Obesity genetics
Abstract

The expression of the galanin gene (GAL) in the paraventricular nucleus (PVN) and in the amygdala of higher vertebrates suggests the requirement for highly conserved, but unidentified, regulatory sequences that are critical to allow the galanin gene to control alcohol and fat intake and modulate mood. We used comparative genomics to identify a highly conserved sequence that lay 42 kb 5' of the human GAL transcriptional start site that we called GAL5.1. GAL5.1 activated promoter activity in neurones of the PVN, arcuate nucleus and amygdala that also expressed the galanin peptide. Analysis in neuroblastoma cells demonstrated that GAL5.1 acted as an enhancer of promoter activity after PKC activation. GAL5.1 contained two polymorphisms; rs2513280(C/G) and rs2513281(A/G), that occurred in two allelic combinations (GG or CA) where the dominant GG alelle occurred in 70-83 % of the human population. Intriguingly, both SNPs were found to be in LD (R(2) of 0.687) with another SNP (rs2156464) previously associated with major depressive disorder (MDD). Recreation of these alleles in reporter constructs and subsequent magnetofection into primary rat hypothalamic neurones showed that the CA allele was 40 % less active than the GG allele. This is consistent with the hypothesis that the weaker allele may affect food and alcohol preference. The linkage of the SNPs analysed in this study with a SNP previously associated with MDD together with the functioning of GAL5.1 as a PVN and amygdala specific enhancer represent a significant advance in our ability to understand alcoholism, obesity and major depressive disorder.

Published
2011
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