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Literature DB >> 8794088

Regulation of potassium channels by protein kinases.

Abstract

Studies of the role of protein phosphorylation in the modulation of neuronal excitability are beginning to identify specific sites on ion channels that are substrates for serine/threonine kinases and that contribute to short-term and long-term regulation of current amplitude and kinetics. In addition, it is becoming apparent that phosphorylation of tyrosine residues may produce acute changes in the characteristics of ion channels. These recent findings are best illustrated by examining the Shaker superfamily of potassium channels.

Entities: Chemical

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Year: 1996 PMID： 8794088 DOI： 10.1016/s0959-4388(96)80114-0

Source DB: PubMed Journal: Curr Opin Neurobiol ISSN： 0959-4388 Impact factor: 6.627

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Cited

59 in total

1. Coregulation of voltage-dependent kinetics of Na(+) and K(+) currents in electric organ.

Authors: M L McAnelly; H H Zakon
Journal: J Neurosci Date: 2000-05-01 Impact factor: 6.167

2. Membrane-delimited coupling between sigma receptors and K+ channels in rat neurohypophysial terminals requires neither G-protein nor ATP.

Authors: P J Lupardus; R A Wilke; E Aydar; C P Palmer; Y Chen; A E Ruoho; M B Jackson
Journal: J Physiol Date: 2000-08-01 Impact factor: 5.182

Review 3. The other half of Hebb: K+ channels and the regulation of neuronal excitability in the hippocampus.

Authors: Laura A Schrader; Anne E Anderson; Andrew W Varga; Michael Levy; J David Sweatt
Journal: Mol Neurobiol Date: 2002-02 Impact factor: 5.590

4. TrkB activation by brain-derived neurotrophic factor inhibits the G protein-gated inward rectifier Kir3 by tyrosine phosphorylation of the channel.

Authors: S L Rogalski; S M Appleyard; A Pattillo; G W Terman; C Chavkin
Journal: J Biol Chem Date: 2000-08-18 Impact factor: 5.157

5. Frequency-dependent inactivation of mammalian A-type K+ channel KV1.4 regulated by Ca2+/calmodulin-dependent protein kinase.

Authors: J Roeper; C Lorra; O Pongs
Journal: J Neurosci Date: 1997-05-15 Impact factor: 6.167

10. Quantitative single-cell-reverse transcription-PCR demonstrates that A-current magnitude varies as a linear function of shal gene expression in identified stomatogastric neurons.

Authors: D J Baro; R M Levini; M T Kim; A R Willms; C C Lanning; H E Rodriguez; R M Harris-Warrick
Journal: J Neurosci Date: 1997-09-01 Impact factor: 6.167

Regulation of potassium channels by protein kinases.

1. Coregulation of voltage-dependent kinetics of Na(+) and K(+) currents in electric organ.

2. Membrane-delimited coupling between sigma receptors and K+ channels in rat neurohypophysial terminals requires neither G-protein nor ATP.

Review 3. The other half of Hebb: K+ channels and the regulation of neuronal excitability in the hippocampus.

4. TrkB activation by brain-derived neurotrophic factor inhibits the G protein-gated inward rectifier Kir3 by tyrosine phosphorylation of the channel.

5. Frequency-dependent inactivation of mammalian A-type K+ channel KV1.4 regulated by Ca2+/calmodulin-dependent protein kinase.

6. Two heteromeric Kv1 potassium channels differentially regulate action potential firing.

Review 7. Sigma receptors: biology and therapeutic potential.

8. Regulation of the ATP-sensitive potassium channel subunit, Kir6.2, by a Ca2+-dependent protein kinase C.

9. Multifaceted modulation of K+ channels by protein-tyrosine phosphatase ε tunes neuronal excitability.

10. Quantitative single-cell-reverse transcription-PCR demonstrates that A-current magnitude varies as a linear function of shal gene expression in identified stomatogastric neurons.