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Titolo:
Genistein inhibits slow component delayed-rectifier K currents via a tyrosine kinase-independent pathway
Autore:
Washizuka, T; Horie, M; Obayashi, K; Sasayama, S;
Indirizzi:
KyotoKyoto, Grad Sch Med, Div Cardiac Electrophysiol, Dept Cardiovasc Med,Kyoto Univ Kyoto Japan 60601 ardiac Electrophysiol, Dept Cardiovasc Med,
Titolo Testata:
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
fascicolo: 12, volume: 30, anno: 1998,
pagine: 2577 - 2590
SICI:
0022-2828(199812)30:12<2577:GISCDK>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
III ANTIARRHYTHMIC AGENTS; VENTRICULAR MYOCYTES; POTASSIUM CHANNEL; RECEPTOR; CALCIUM; PROLONGATION; MODULATION; MECHANISM; VANADATE; CELLS;
Keywords:
cardiac myocytes; genistein; daidzein; delayed-rectifier K current;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Horie, M KyotoKyoto, Grad Sch Med, Div Cardiac Electrophysiol, Dept Cardiovasc Med, Kyoto Univ Kyoto Japan 60601 ectrophysiol, Dept Cardiovasc Med,
Citazione:
T. Washizuka et al., "Genistein inhibits slow component delayed-rectifier K currents via a tyrosine kinase-independent pathway", J MOL CEL C, 30(12), 1998, pp. 2577-2590

Abstract

In single guinea pig ventricular cells, genistein, a potent inhibitor of protein tyrosine kinase (PTK), was found to suppress the delayed-rectifier It (I-K) current. The present study was carried out to examine the underlying mechanism. Ventricular myocytes were voltage-clamped in the conventional whole-cell mode (36 degrees C). The amplitudes of tail and steady-state (2-s pulse) currents were measured as I-K. Genistein (10-100 mu M) reversibly inhibited both basal and intrapipette cAMP (1 mM)-enhanced I-K currents in a concentration-dependent manner with a half-maximum inhibitory concentration (IC50) at similar to 30 mu M. In contrast, lavendustin A (10 mu M; n = 5) and tyrphostin 51 (100 mu M; n = 5) had no effect on the currents. The inhibitory action of genistein was also seen after I-K currents were activated by forsIrolin (500 nM) plus intrapipette orthovanadate (500 mu M). The intrapipette cAMP-enhanced I-K was also reduced to a lesser degree by daidzein, an inactive analogue of genistein. Envelope tail and short pulse protocols revealed that genistein inhibits the slow component of I-K (I-Ks). Thus,the inhibitory action of genistein is not mediated via an inhibition of PTK but may be due to the block of I-Ks channels. (C) 1998 Academic Press.

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Documento generato il 14/07/20 alle ore 18:43:17