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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] | |
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