Corrigendum: The genome sequence of the orchid Phalaenopsis equestris Jing Cai, Xin Liu, Kevin Vanneste, Sebastian Proost, Wen-Chieh Tsai, Ke-Wei Liu, Li-Jun Chen, Ying He, Qing Xu, Chao Bian, Zhijun Zheng, Fengming Sun, Weiqing Liu, Yu-Yun Hsiao, Zhao-Jun Pan, Chia-Chi Hsu, Ya-Ping Yang, Yi-Chin Hsu, Yu-Chen Chuang, Anne Dievart, Jean-Francois Dufayard, Xun Xu, Jun-Yi Wang, Jun Wang, Xin-Ju Xiao, Xue-Min Zhao, Rong Du, Guo-Qiang Zhang, Meina Wang, Yong-Yu Su, Gao-Chang Xie, Guo-Hui Liu, Li-Qiang Li, Lai-Qiang Huang, Yi-Bo Luo, Hong-Hwa Chen, Yves Van de Peer & Zhong-Jian Liu Nat. Genet. 47, 65–72 (2015); published online 24 November 2014; corrected after print 9 January 2015; corrected after print 6 February 2015 In the version of this article initially published, the legend for Figure 1b referred to red arrows indicating the inferred divergence dates. No arrows are depicted in the figure, so this sentence has been removed from the figure legend in the HTML and PDF versions of the article.
Corrigendum: Mutations in the voltage-gated potassium channel gene KCNH1 cause Temple-Baraitser syndrome and epilepsy
In the version of this article initially published, in Figure 2a, the order of the protein alterations for variants c.1465C>T and c.1480A>G was inverted. The correct protein alterations for these two variants are p.Leu489Phe and p.Ile494Val, respectively. This error has been corrected in the HTML and PDF versions of the article.
Cas Simons, Lachlan D Rash, Joanna Crawford, Linlin Ma, Ben Cristofori-Armstrong, David Miller, Kelin Ru, Gregory J Baillie, Yasemin Alanay, Adeline Jacquinet, François-Guillaume Debray, Alain Verloes, Joseph Shen, Gözde Yesil, Serhat Guler, Adnan Yuksel, John G Cleary, Sean M Grimmond, Julie McGaughran, Glenn F King, Michael T Gabbett & Ryan J Taft Nat. Genet. 47, 73–77 (2015); published online 24 November 2014; corrected after print 6 February 2015
volume 47 | number 3 | MARCH 2015 | nature genetics
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Temple-Baraitser syndrome (TBS) is a multisystem developmental disorder characterized by intellectual disability, epilepsy, and hypoplasia or aplasia of the nails of the thumb and great toe. Here we report damaging de novo mutations in KCNH1 (encodin
Zimmermann-Laband syndrome (ZLS) is a developmental disorder characterized by facial dysmorphism with gingival enlargement, intellectual disability, hypoplasia or aplasia of nails and terminal phalanges, and hypertrichosis. We report that heterozygou
Potassium channels are the targets of antiepileptic drugs (AEDs), which play important roles in the etiology of epilepsy. KCNA1 and KCNA2 encode mammalian Kv1.1 and Kv1.2 channels, which are essential roles in the initiation and shaping of action pot
Several potassium channel genes have been implicated in different neurological disorders including genetic and acquired epilepsy. Among them, KCNQ2 and KCNQ3, coding for KV7.2 and KV7.3 voltage-gated potassium channels, present an example how genetic
Using a feline model, erections caused by a new class of vasodilator agents that specifically activate potassium (K+-ATP) channels (lemakalim, nicorandil, and pinacidil) were compared to baseline and maximal erections induced by a standard drug combi
Molecular insights into monogenic idiopathic epilepsies have illustrated the central role of channelopathies in their etiology. Among ion channels, both high- and low-voltage-activated calcium channels and their ancillary subunits Cav2.1 (P/Q-type) c
A variety of genetic backgrounds cause the loss of function of thiazide-sensitive sodium chloride cotransporter, encoded by SLC12A3, responsible for the phenotypes in Gitelman syndrome. Recently, the phenomenon of exon skipping, in which exonic mutat
Filippi syndrome is a rare, presumably autosomal-recessive disorder characterized by microcephaly, pre- and postnatal growth failure, syndactyly, and distinctive facial features, including a broad nasal bridge and underdeveloped alae nasi. Some affec
Massively parallel sequencing has revealed many de novo mutations in the etiology of developmental and epileptic encephalopathies (EEs), highlighting their genetic heterogeneity. Additional candidate genes have been prioritized in silico by their co-