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Two missense mutations in KCNQ1 cause pituitary hormone deficiency and maternally inherited gingival fibromatosis.

Johanna TommiskaJohanna KänsäkoskiLasse SkibsbyeKirsi VaaralahtiXiaonan LiuEmily J LodgeChuyi TangLei YuanRainer FagerholmJørgen K KantersPäivi LahermoMari KaunistoRiikka Keski-FilppulaSanna VuoristoKristiina PulliTapani EbelingLeena ValanneEeva-Marja SankilaSirpa KivirikkoMitja LääperiFilippo CasoniPaolo GiacobiniFranziska Phan-HugTal BukiManuel Tena-SempereNelly PitteloudRiitta VeijolaMarita Lipsanen-NymanKari KaunistoPatrice MollardCynthia Lilian AndoniadouJoel A HirschMarkku VarjosaloThomas JespersenTaneli Raivio
Published in: Nature communications (2017)
Familial growth hormone deficiency provides an opportunity to identify new genetic causes of short stature. Here we combine linkage analysis with whole-genome resequencing in patients with growth hormone deficiency and maternally inherited gingival fibromatosis. We report that patients from three unrelated families harbor either of two missense mutations, c.347G>T p.(Arg116Leu) or c.1106C>T p.(Pro369Leu), in KCNQ1, a gene previously implicated in the long QT interval syndrome. Kcnq1 is expressed in hypothalamic GHRH neurons and pituitary somatotropes. Co-expressing KCNQ1 with the KCNE2 β-subunit shows that both KCNQ1 mutants increase current levels in patch clamp analyses and are associated with reduced pituitary hormone secretion from AtT-20 cells. In conclusion, our results reveal a role for the KCNQ1 potassium channel in the regulation of human growth, and show that growth hormone deficiency associated with maternally inherited gingival fibromatosis is an allelic disorder with cardiac arrhythmia syndromes caused by KCNQ1 mutations.
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