http://researchonline.federation.edu.au/vital/access/manager/Index ${session.getAttribute("locale")} 5 http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10862 Wed 07 Apr 2021 13:56:13 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:10714 Wed 07 Apr 2021 13:56:04 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:5239 Wed 07 Apr 2021 13:44:53 AEST ]]> http://researchonline.federation.edu.au/vital/access/manager/Repository/vital:14938 0.05). In a meta-analysis of up to ~1.3 million participants, we discovered 106 new BP-associated genomic regions and 87 rare (minor allele frequency ≤ 0.01) variant BP associations (P < 5 × 10−8), of which 32 were in new BP-associated loci and 55 were independent BP-associated single-nucleotide variants within known BP-associated regions. Average effects of rare variants (44% coding) were ~8 times larger than common variant effects and indicate potential candidate causal genes at new and known loci (for example, GATA5 and PLCB3). BP-associated variants (including rare and common) were enriched in regions of active chromatin in fetal tissues, potentially linking fetal development with BP regulation in later life. Multivariable Mendelian randomization suggested possible inverse effects of elevated systolic and diastolic BP on large artery stroke. Our study demonstrates the utility of rare-variant analyses for identifying candidate genes and the results highlight potential therapeutic targets. © 2020, The Author(s), under exclusive licence to Springer Nature America, Inc. There are 286 authors of this articles not all are listed in this record.]]> Thu 25 Nov 2021 11:48:02 AEDT ]]>