Affiliation: Istituto di Ricerche Farmacologiche Mario Negri
- Differential pH sensitivity of Kir4.1 and Kir4.2 potassium channels and their modulation by heteropolymerisation with Kir5.1M Pessia
Department of Vascular Medicine and Pharmacology, Istituto di Ricerche Farmacologiche Mario Negri, Consorzio Mario Negri Sud, 66030 Santa Maria Imbaro Chieti, Italy
J Physiol 532:359-67. 2001..g. pancreas) and that these novel channels are likely to be regulated by changes in intracellular pH. In addition, the extreme pH sensitivity of Kir4.2 has implications for the role of this subunit as a homotetrameric channel...
- Mutations in the KCNA1 gene associated with episodic ataxia type-1 syndrome impair heteromeric voltage-gated K(+) channel functionM C D'Adamo
Istituto di Ricerche Farmacologiche Mario Negri, Consorzio Mario Negri Sud, Department of Pharmacology and Molecular Pathology, Chieti, Italy
FASEB J 13:1335-45. 1999..2 and Kv1.1 subunits coassemble to form a novel channel with distinct gating properties that are altered profoundly by EA-1 mutations, thus uncovering novel physiopathogenetic mechanisms of episodic ataxia type-1 myokymia syndrome...
- pH dependence of the inwardly rectifying potassium channel, Kir5.1, and localization in renal tubular epitheliaS J Tucker
University Laboratory of Physiology, Parks Road, Oxford OX1 3PT, United Kingdom
J Biol Chem 275:16404-7. 2000..1 subunit. These findings suggest that Kir5.1/Kir4.1 heteromeric channels are likely to exist in vivo and implicate an important and novel functional role for the Kir5.1 subunit...
- Cloning and expression of a family of inward rectifier potassium channelsC T Bond
Vollum Institute, Oregon Health Sciences University, Portland 97201
Receptors Channels 2:183-91. 1994..The results demonstrate the existence of a large and widely expressed family of inward rectifier potassium channel subunits with distinct tissue distributions and functional properties...
- Episodic ataxia results from voltage-dependent potassium channels with altered functionsJ P Adelman
Vollum Institute, Oregon Health Sciences University, Portland 97201, USA
Neuron 15:1449-54. 1995..The results suggest a cellular mechanism underlying EA in which the affected nerve cells cannot efficiently repolarize following an action potential because of altered delayed rectifier function...