A novel channelopathy in pulmonary arterial hypertension [1]

New England Journal of Medicine

Volumn 369, Issue 22, 2013, Pages 2161-2162

  Olschewski, Andrea ^a   Nagaraj, Chandran ^a   Olschewski, Horst ^b  

^a LUDWIG BOLTZMANN INSTITUTE FOR LUNG VASCULAR RESEARCH   (Austria)

^b MEDICAL UNIVERSITY OF GRAZ   (Austria)

Author keywords

[No Author keywords available]

Indexed keywords

2 (4 AMYLCINNAMIDO) 4 CHLOROBENZOIC ACID; DASATINIB; POTASSIUM CHANNEL;

CHANNELOPATHY; GENE MUTATION; HOMOZYGOTE; HUMAN; KCNK3 GENE; LETTER; LOSS OF FUNCTION MUTATION; LUNG VASCULAR RESISTANCE; MEMBRANE POTENTIAL; MEMBRANE TRANSPORT; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; PULMONARY HYPERTENSION; GENETIC ASSOCIATION; GENETIC VARIABILITY; PROTEIN FUNCTION;

EID: 84888374175     PISSN: 00284793     EISSN: 15334406     Source Type: Journal    
DOI: 10.1056/NEJMc1311060     Document Type: Letter

References (5)

1. Ma L, Roman-Campos D, Austin ED, et al. A novel channelopathy in pulmonary arterial hypertension. N Engl J Med 2013;369:351-61.
2. Olschewski A, Li Y, Tang B, et al. Impact of TASK-1 in human pulmonary artery smooth muscle cells. Circ Res 2006;98:1072-80.
3. Nagaraj C, Tang B, Bálint Z, et al. Src tyrosine kinase is crucial for potassium channel function in human pulmonary arteries. Eur Respir J 2013;41:85-95.
4. Montani D, Bergot E, Günther S, et al. Pulmonary arterial hypertension in patients treated by dasatinib. Circulation 2012;125:2128-37.
5. Zuzarte M, Heusser K, Renigunta V, et al. Intracellular traffic of the K+ channels TASK-1 and TASK-3: role of N- and C-terminal sorting signals and interaction with 14-3-3 proteins. J Physiol 2009;587:929-52.