
Caroline Hayward
Articles
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Dec 5, 2024 |
nature.com | Elias Allara |Steven Bell |Dipender Gill |Liam Gaziano |Feiyi Wang |Vinicius Tragante | +30 more
AbstractIron homoeostasis is tightly regulated, with hepcidin and soluble transferrin receptor (sTfR) playing significant roles. However, the genetic determinants of these traits and the biomedical consequences of iron homoeostasis variation are unclear. In a meta-analysis of 12 cohorts involving 91,675 participants, we found 43 genomic loci associated with either hepcidin or sTfR concentration, of which 15 previously unreported.
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Dec 5, 2024 |
nature.com | Elias Allara |Steven Bell |Dipender Gill |Liam Gaziano |Feiyi Wang |Vinicius Tragante | +30 more
AbstractIron homoeostasis is tightly regulated, with hepcidin and soluble transferrin receptor (sTfR) playing significant roles. However, the genetic determinants of these traits and the biomedical consequences of iron homoeostasis variation are unclear. In a meta-analysis of 12 cohorts involving 91,675 participants, we found 43 genomic loci associated with either hepcidin or sTfR concentration, of which 15 previously unreported.
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Dec 5, 2024 |
nature.com | Elias Allara |Steven Bell |Dipender Gill |Liam Gaziano |Feiyi Wang |Vinicius Tragante | +30 more
AbstractIron homoeostasis is tightly regulated, with hepcidin and soluble transferrin receptor (sTfR) playing significant roles. However, the genetic determinants of these traits and the biomedical consequences of iron homoeostasis variation are unclear. In a meta-analysis of 12 cohorts involving 91,675 participants, we found 43 genomic loci associated with either hepcidin or sTfR concentration, of which 15 previously unreported.
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Nov 5, 2024 |
nature.com | Tanya J. Major |Riku Takei |Yuya Shirai |Wei Qing Wang |Murray Cadzow |Amanda Phipps-Green | +35 more
Correction to: Nature Genetics https://doi.org/10.1038/s41588-024-01921-5. Published online 15 October 2024. In the version of the article originally published, there were errors in the consortium lists at the end of the paper. Maureen Rischmueller, Hyon K. Choi, Masahiro Nakatochi, Jeff N. Miner, Daniel H. Solomon, Kathleen M. Giacomini and Deanna J. Brackman were erroneously listed as members of the Japan Gout Genomics Consortium.
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Oct 15, 2024 |
nature.com | Tanya J. Major |Riku Takei |Yuya Shirai |Wei Qing Wang |Murray Cadzow |Amanda Phipps-Green | +35 more
AbstractGout is a chronic disease that is caused by an innate immune response to deposited monosodium urate crystals in the setting of hyperuricemia. Here, we provide insights into the molecular mechanism of the poorly understood inflammatory component of gout from a genome-wide association study (GWAS) of 2.6 million people, including 120,295 people with prevalent gout. We detected 377 loci and 410 genetically independent signals (149 previously unreported loci in urate and gout).
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