Channelopathies: Kir2.1 mutations jeopardize many cell functions

Current Biology

Volumn 11, Issue 18, 2001, Pages

  Jongsma, Habo J ^a,b   Wilders, Ronald ^a,b  

^a UNIVERSITY MEDICAL CENTER UTRECHT   (Netherlands)

^b UNIVERSITY OF AMSTERDAM   (Netherlands)

Author keywords

[No Author keywords available]

Indexed keywords

ANIMALIA;

EID: 0035908917     PISSN: 09609822     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0960-9822(01)00437-7     Document Type: Review

References (14)

1. Mutations in Kir2.1 cause the developmental and episodic electrical phenotypes of Andersen's syndrome
2. Inward rectifier potassium channels
3. + conduction and selectivity
4. K1
5. Role of ER export signals in controlling surface potassium channel numbers
6. Genetic and molecular basis of cardiac arrhythmias: Impact on clinical management parts I and II
7. Simulation study of cellular electric properties in heart failure
8. K1) as revealed by the targeted deletion of the murine Kir2.1 and Kir2.2 genes
9. + currents during pre- and postnatal development
10. Human myoblast fusion requires expression of functional inward rectifier Kir2.1 channels
11. Bone development
12. Bone resorption by osteoclasts
13. Electrophysiological characterization of ion channels in osteoclasts isolated from human deciduous teeth
14. +-mediated vasodilation