Collaborative genome-wide association analysis supports a role for ANK3 and CACNA1C in bipolar disorder

Manuel A. R. Ferreira, Michael C. O'Donovan, Yan A. Meng, Ian R. Jones, Douglas M. Ruderfer, Lisa Jones, Jinbo Fan, George Kirov, Roy H. Perlis, Elaine K. Green, Jordan W. Smoller, Detelina Grozeva, Jennifer Stone, Ivan Nikolov, Kimberly Chambert, Marian L. Hamshere, Vishwajit L. Nimgaonkar, Valentina Moskvina, Michael E. Thase, Sian CaesarGary S. Sachs, Jennifer Franklin, Katherine Gordon-Smith, Kristin G. Ardlie, Stacey B. Gabriel, Christine Fraser, Brendan Blumenstiel, Matthew Defelice, Gerome Breen, Michael Gill, Derek W. Morris, Amanda Elkin, Walter J. Muir, Kevin A. McGhee, Richard Williamson, Donald J. MacIntyre, Alan W. MacLean, David St Clair, Michelle Robinson, Margaret Van Beck, Ana C. P. Pereira, Radhika Kandaswamy, Andrew McQuillin, David A. Collier, Nicholas J. Bass, Allan H. Young, Jacob Lawrence, I. Nicol Ferrier, Adebayo Anjorin, Anne Farmer, Wellcome Trust Case Control Consortium

Research output: Contribution to journalArticlepeer-review

983 Citations (Scopus)


To identify susceptibility loci for bipolar disorder, we tested 1.8 million variants in 4,387 cases and 6,209 controls and identified a region of strong association (rs10994336, P = 9.1 x 10(-9)) in ANK3 (ankyrin G). We also found further support for the previously reported CACNA1C (alpha 1C subunit of the L-type voltage-gated calcium channel; combined P = 7.0 x 10(-8), rs1006737). Our results suggest that ion channelopathies may be involved in the pathogenesis of bipolar disorder.

Original languageEnglish
Pages (from-to)1056-1058
Number of pages3
JournalNature Genetics
Issue number9
Early online date17 Aug 2008
Publication statusPublished - Sept 2008


  • loci
  • diseases
  • ranvier
  • genes


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