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8 results on '"Logan, John G."'

1. IGSF1 Deficiency Results in Human and Murine Somatotrope Neurosecretory Hyperfunction

Author

Joustra, Sjoerd D, Roelfsema, Ferdinand, van Trotsenburg, A S Paul, Schneider, Harald J, Kosilek, Robert P, Kroon, Herman M, Logan, John G, Butterfield, Natalie C, Zhou, Xiang, Toufaily, Chirine, Bak, Beata, Turgeon, Marc-Olivier, Brûlé, Emilie, Steyn, Frederik J, Gurnell, Mark, Koulouri, Olympia, Le Tissier, Paul, Fontanaud, Pierre, Duncan Bassett, J H, Williams, Graham R, Oostdijk, Wilma, Wit, Jan M, Pereira, Alberto M, Biermasz, Nienke R, Bernard, Daniel J, and Schoenmakers, Nadia

Published
2020
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2. An atlas of genetic influences on osteoporosis in humans and mice

Author

Morris, John A., Kemp, John P., Youlten, Scott E., Laurent, Laetitia, Logan, John G., Chai, Ryan C., Vulpescu, Nicholas A., Forgetta, Vincenzo, Kleinman, Aaron, Mohanty, Sindhu T., Sergio, C. Marcelo, Quinn, Julian, Nguyen-Yamamoto, Loan, Luco, Aimee-Lee, Vijay, Jinchu, Simon, Marie-Michelle, Pramatarova, Albena, Medina-Gomez, Carolina, Trajanoska, Katerina, Ghirardello, Elena J., Butterfield, Natalie C., Curry, Katharine F., Leitch, Victoria D., Sparkes, Penny C., Adoum, Anne-Tounsia, Mannan, Naila S., Komla-Ebri, Davide S. K., Pollard, Andrea S., Dewhurst, Hannah F., Hassall, Thomas A. D., Beltejar, Michael-John G., Adams, Douglas J., Vaillancourt, Suzanne M., Kaptoge, Stephen, Baldock, Paul, Cooper, Cyrus, Reeve, Jonathan, Ntzani, Evangelia E., Evangelou, Evangelos, Ohlsson, Claes, Karasik, David, Rivadeneira, Fernando, Kiel, Douglas P., Tobias, Jonathan H., Gregson, Celia L., Harvey, Nicholas C., Grundberg, Elin, Goltzman, David, Adams, David J., Lelliott, Christopher J., Hinds, David A., Ackert-Bicknell, Cheryl L., Hsu, Yi-Hsiang, Maurano, Matthew T., Croucher, Peter I., Williams, Graham R., Bassett, J. H. Duncan, Evans, David M., and Richards, J. Brent

Abstract

Osteoporosis is a common aging-related disease diagnosed primarily using bone mineral density (BMD). We assessed genetic determinants of BMD as estimated by heel quantitative ultrasound in 426,824 individuals, identifying 518 genome-wide significant loci (301 novel), explaining 20% of its variance. We identified 13 bone fracture loci, all associated with estimated BMD (eBMD), in ~1.2 million individuals. We then identified target genes enriched for genes known to influence bone density and strength (maximum odds ratio (OR) = 58, P= 1 × 10−75) from cell-specific features, including chromatin conformation and accessible chromatin sites. We next performed rapid-throughput skeletal phenotyping of 126 knockout mice with disruptions in predicted target genes and found an increased abnormal skeletal phenotype frequency compared to 526 unselected lines (P< 0.0001). In-depth analysis of one gene, DAAM2, showed a disproportionate decrease in bone strength relative to mineralization. This genetic atlas provides evidence linking associated SNPs to causal genes, offers new insight into osteoporosis pathophysiology, and highlights opportunities for drug development.

Published
2019
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3. Identification of 153 new loci associated with heel bone mineral density and functional involvement of GPC6 in osteoporosis

Author

Kemp, John P, Morris, John A, Medina-Gomez, Carolina, Forgetta, Vincenzo, Warrington, Nicole M, Youlten, Scott E, Zheng, Jie, Gregson, Celia L, Grundberg, Elin, Trajanoska, Katerina, Logan, John G, Pollard, Andrea S, Sparkes, Penny C, Ghirardello, Elena J, Allen, Rebecca, Leitch, Victoria D, Butterfield, Natalie C, Komla-Ebri, Davide, Adoum, Anne-Tounsia, Curry, Katharine F, White, Jacqueline K, Kussy, Fiona, Greenlaw, Keelin M, Xu, Changjiang, Harvey, Nicholas C, Cooper, Cyrus, Adams, David J, Greenwood, Celia M T, Maurano, Matthew T, Kaptoge, Stephen, Rivadeneira, Fernando, Tobias, Jonathan H, Croucher, Peter I, Ackert-Bicknell, Cheryl L, Bassett, J H Duncan, Williams, Graham R, Richards, J Brent, and Evans, David M

Abstract

Osteoporosis is a common disease diagnosed primarily by measurement of bone mineral density (BMD). We undertook a genome-wide association study (GWAS) in 142,487 individuals from the UK Biobank to identify loci associated with BMD as estimated by quantitative ultrasound of the heel. We identified 307 conditionally independent single-nucleotide polymorphisms (SNPs) that attained genome-wide significance at 203 loci, explaining approximately 12% of the phenotypic variance. These included 153 previously unreported loci, and several rare variants with large effect sizes. To investigate the underlying mechanisms, we undertook (1) bioinformatic, functional genomic annotation and human osteoblast expression studies; (2) gene-function prediction; (3) skeletal phenotyping of 120 knockout mice with deletions of genes adjacent to lead independent SNPs; and (4) analysis of gene expression in mouse osteoblasts, osteocytes and osteoclasts. The results implicate GPC6 as a novel determinant of BMD, and also identify abnormal skeletal phenotypes in knockout mice associated with a further 100 prioritized genes.

Published
2017
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4. Thyrostimulin Regulates Osteoblastic Bone Formation During Early Skeletal Development

Author

Bassett, J. H. Duncan, van der Spek, Anne, Logan, John G., Gogakos, Apostolos, Bagchi-Chakraborty, Jayashree, Murphy, Elaine, van Zeijl, Clementine, Down, Jenny, Croucher, Peter I., Boyde, Alan, Boelen, Anita, and Williams, Graham R.

Abstract

The ancestral glycoprotein hormone thyrostimulin is a heterodimer of unique glycoprotein hormone subunit alpha (GPA)2 and glycoprotein hormone subunit beta (GPB)5 subunits with high affinity for the TSH receptor. Transgenic overexpression of GPB5 in mice results in cranial abnormalities, but the role of thyrostimulin in bone remains unknown. We hypothesized that thyrostimulin exerts paracrine actions in bone and determined: 1) GPA2and GPB5expression in osteoblasts and osteoclasts, 2) the skeletal consequences of thyrostimulin deficiency in GPB5 knockout (KO) mice, and 3) osteoblast and osteoclast responses to thyrostimulin treatment. Gpa2and Gpb5expression was identified in the newborn skeleton but declined rapidly thereafter. GPA2and GPB5mRNAs were also expressed in primary osteoblasts and osteoclasts at varying concentrations. Juvenile thyrostimulin-deficient mice had increased bone volume and mineralization as a result of increased osteoblastic bone formation. However, thyrostimulin failed to induce a canonical cAMP response or activate the noncanonical Akt, ERK, or mitogen-activated protein kinase (P38) signaling pathways in primary calvarial or bone marrow stromal cell-derived osteoblasts. Furthermore, thyrostimulin did not directly inhibit osteoblast proliferation, differentiation or mineralization in vitro. These studies identify thyrostimulin as a negative but indirect regulator of osteoblastic bone formation during skeletal development.

Published
2015
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5. Response to Letter to the Editor: “IGSF1 Deficiency Results in Human and Murine Somatotrope Neurosecretory Hyperfunction”

Author

Joustra, Sjoerd D, Roelfsema, Ferdinand, van Trotsenburg, A S Paul, Schneider, Harald J, Kosilek, Robert P, Kroon, Herman M, Logan, John G, Butterfield, Natalie C, Zhou, Xiang, Toufaily, Chirine, Bak, Beata, Turgeon, Marc-Olivier, Brûlé, Emilie, Steyn, Frederik J, Gurnell, Mark, Koulouri, Olympia, Le Tissier, Paul, Fontanaud, Pierre, Bassett, J H Duncan, Williams, Graham R, Oostdijk, Wilma, Wit, Jan M, Pereira, Alberto M, Biermasz, Nienke R, Bernard, Daniel J, and Schoenmakers, Nadia

Published
2020
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8. Author Correction: An atlas of genetic influences on osteoporosis in humans and mice

Author

Morris, John A., Kemp, John P., Youlten, Scott E., Laurent, Laetitia, Logan, John G., Chai, Ryan C., Vulpescu, Nicholas A., Forgetta, Vincenzo, Kleinman, Aaron, Mohanty, Sindhu T., Sergio, C. Marcelo, Quinn, Julian, Nguyen-Yamamoto, Loan, Luco, Aimee-Lee, Vijay, Jinchu, Simon, Marie-Michelle, Pramatarova, Albena, Medina-Gomez, Carolina, Trajanoska, Katerina, Ghirardello, Elena J., Butterfield, Natalie C., Curry, Katharine F., Leitch, Victoria D., Sparkes, Penny C., Adoum, Anne-Tounsia, Mannan, Naila S., Komla-Ebri, Davide S. K., Pollard, Andrea S., Dewhurst, Hannah F., Hassall, Thomas A. D., Beltejar, Michael-John G., Adams, Douglas J., Vaillancourt, Suzanne M., Kaptoge, Stephen, Baldock, Paul, Cooper, Cyrus, Reeve, Jonathan, Ntzani, Evangelia E., Evangelou, Evangelos, Ohlsson, Claes, Karasik, David, Rivadeneira, Fernando, Kiel, Douglas P., Tobias, Jonathan H., Gregson, Celia L., Harvey, Nicholas C., Grundberg, Elin, Goltzman, David, Adams, David J., Lelliott, Christopher J., Hinds, David A., Ackert-Bicknell, Cheryl L., Hsu, Yi-Hsiang, Maurano, Matthew T., Croucher, Peter I., Williams, Graham R., Bassett, J. H. Duncan, Evans, David M., and Richards, J. Brent

Abstract

In the version of this article initially published, in Fig. 5a, the data in the right column of ‘DAAM2 gRNA1’ were incorrectly plotted as circles indicating ‘untreated’ rather than as squares indicating ‘treated’. The error has been corrected in the HTML and PDF versions of the article.

Published
2019
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