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Titolo:
Tyrosine kinases modulate K+ channel gating in mouse Schwann cells
Autore:
Peretz, A; Sobko, A; Attali, B;
Indirizzi:
Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel Weizmann Inst Sci Rehovot Israel IL-76100 biol, IL-76100 Rehovot, Israel
Titolo Testata:
JOURNAL OF PHYSIOLOGY-LONDON
fascicolo: 2, volume: 519, anno: 1999,
pagine: 373 - 384
SICI:
0022-3751(19990901)519:2<373:TKMKCG>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
CA2+/CALMODULIN-DEPENDENT PROTEIN-KINASE; KV1.3 POTASSIUM CHANNEL; ELECTROSTATIC INTERACTIONS; ACETYLCHOLINE-RECEPTOR; DEPENDENT SUPPRESSION; PHOSPHORYLATION; INACTIVATION; ACTIVATION; CURRENTS; SEGMENTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Attali, B Weizmann Inst Sci, Dept Neurobiol, IL-76100 Rehovot, Israel Weizmann Inst Sci Rehovot Israel IL-76100 6100 Rehovot, Israel
Citazione:
A. Peretz et al., "Tyrosine kinases modulate K+ channel gating in mouse Schwann cells", J PHYSL LON, 519(2), 1999, pp. 373-384

Abstract

1. The whole-cell configuration of the patch-clamp technique and immunoprecipitation experiments were used to investigate the effects of tyrosine kinases on voltage-dependent K+ channel gating in cultured mouse Schwann cells.2. Genistein, a broad-spectrum tyrosine kinase inhibitor, markedly reducedthe amplitude of a slowly inactivating delayed-rectifier current (I-K) and, to a lesser extent, that of a transient K+ current (I-A). Similar resultswere obtained on I-K with another tyrosine kinase inhibitor, herbimycin A. Daidzein, the inactive analogue of genistein, was without effect.3. Unlike herbimycin A, genistein produced additional effects on I-A by profoundly affecting its gating properties. These changes consisted of sloweractivation kinetics with an increased time to peak, a positive shift in the voltage dependence of activation (by +30 mV), a decrease in the steepnessof activation gating (9 mV per e-fold change) and an acceleration of channel deactivation.4. The steepness of the steady-state inactivation was increased by genistein treatment, while the recovery from inactivation was not significantly altered.5. The action of genistein on voltage-dependent K+ (Kv) currents was accompanied by a decrease in tyrosine phosphorylation of Kv1.4 as well as Kv1.5 and Kv2.1 encoding transient and slowly inactivating delayed-rectifier K+ channel alpha subunits, respectively.6. In conclusion, the present study shows that tyrosine kinases markedly affect the amplitude of voltage-dependent K+ currents in Schwann cells and finely tune the gating properties of the transient K+ current component I-A. These modulations may be functionally relevant in the control of K+ channel activity during Schwann cell development and peripheral myelinogenesis.

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Documento generato il 06/12/20 alle ore 00:01:03