| Literature DB >> 22608503 |
Bregje W M van Bon1, Christian Gilissen, Dorothy K Grange, Raoul C M Hennekam, Hülya Kayserili, Hartmut Engels, Heiko Reutter, John R Ostergaard, Eva Morava, Konstantinos Tsiakas, Bertrand Isidor, Martine Le Merrer, Metin Eser, Nienke Wieskamp, Petra de Vries, Marloes Steehouwer, Joris A Veltman, Stephen P Robertson, Han G Brunner, Bert B A de Vries, Alexander Hoischen.
Abstract
Cantú syndrome is a rare disorder characterized by congenital hypertrichosis, neonatal macrosomia, a distinct osteochondrodysplasia, and cardiomegaly. Using an exome-sequencing approach applied to one proband-parent trio and three unrelated single cases, we identified heterozygous mutations in ABCC9 in all probands. With the inclusion of the remaining cohort of ten individuals with Cantú syndrome, a total of eleven mutations in ABCC9 were found. The de novo occurrence in all six simplex cases in our cohort substantiates the presence of a dominant disease mechanism. All mutations were missense, and several mutations affect Arg1154. This mutation hot spot lies within the second type 1 transmembrane region of this ATP-binding cassette transporter protein, which may suggest an activating mutation. ABCC9 encodes the sulfonylurea receptor (SUR) that forms ATP-sensitive potassium channels (K(ATP) channels) originally shown in cardiac, skeletal, and smooth muscle. Previously, loss-of-function mutations in this gene have been associated with idiopathic dilated cardiomyopathy type 10 (CMD10). These findings identify the genetic basis of Cantú syndrome and suggest that this is a new member of the potassium channelopathies.Entities:
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Year: 2012 PMID: 22608503 PMCID: PMC3370286 DOI: 10.1016/j.ajhg.2012.04.014
Source DB: PubMed Journal: Am J Hum Genet ISSN: 0002-9297 Impact factor: 11.025