|
|
|
|
|
| ID:
22444.0,
MPI für medizinische Forschung / Abteilung Zellphysiologie |
| Kir2.1 inward rectifier K+ channels are regulated independently by protein kinases and ATP hydrolysis |
| Translation of Title: | Kir2.1 inward rectifier K<SUP>+</SUP> channels are regulated independently by protein kinases and ATP hydrolysis | | Authors: | Fakler, Bernd; Brändle, Uwe; Glowatzki, E.; Zenner, H. P.; Ruppersberg, J. Peter | | Language: | English | | Date of Publication (YYYY-MM-DD): | 1994-12 | | Title of Journal: | Neuron | | Journal Abbrev.: | Neuron | | Volume: | 13 | | Issue / Number: | 6 | | Start Page: | 1413 | | End Page: | 1420 | | Review Status: | Peer-review | | Audience: | Experts Only | | Intended Educational Use: | No | | Abstract / Description: | Second messenger regulation of IRK1 (Kir2.1) inward rectifier K+ channels was investigated in giant inside-out patches from Xenopus oocytes. Kir2.1-mediated currents that run down completely within minutes upon excision of the patches could be partly restored by application of Mg-ATP together with > 10 microM free Mg2+ to the cytoplasmic side of the patch. As restoration could not be induced by the ATP analogs AMP-PNP or ATP gamma S, this suggests an ATPase-like mechanism. In addition to ATP, the catalytic subunit of cAMP-dependent protein kinase (PKA) induced an increase in current amplitude, which could, however, only be observed if channels were previously or subsequently stimulated by Mg-ATP and free Mg2+. This indicates that functional activity of Kir2.1 channels requires both phosphorylation by PKA and ATP hydrolysis. Moreover, currents could be down-regulated by N-heptyl-5-chloro-1-naphthalenesulfonamide, a specific stimulator of protein kinase C (PKC), suggesting that PKA and PKC mediate inverse effects on Kir2.1 channels. Regulation of Kir2.1 channels described here may be an important mechanism for regulation of excitability. | | External Publication Status: | published | | Document Type: | Article |
| Communicated by: | Wulf Kaiser | | Affiliations: | MPI für medizinische Forschung/Abteilung Zellphysiologie/
| | Identifiers: | URI:http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=... [Abstract] | |
|
|
|
The scope and number of records on eDoc is subject
to the collection policies defined by each institute
- see "info" button in the collection browse view.
|
|
Advanced