ArticleBritish journal of pharmacology2006
Insensitivity of cardiac delayed-rectifier I(Kr) to tyrosine phosphorylation inhibitors and stimulators.
Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Genistein and tyrphostin AG556 decrease ultra-rapidly activating delayed rectifier KBritish journal of pharmacology · 2017Article
- Inhibition of Kv4.3 by genistein via a tyrosine phosphorylation-independent mechanism.American journal of physiology. Cell physiology · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The rapidly activating delayed-rectifying K+ current (I(Kr)) in heart cells is an important determinant of repolarisation, and decreases in its density are implicated in acquired and inherited long QT syndromes. The objective of the present study on I(Kr) in guinea-pig ventricular myocytes was to evaluate whether the current is acutely regulated by tyrosine phosphorylation. 2. Myocytes configured for ruptured-patch or perforated-patch voltage-clamp were depolarised with 200-ms steps to 0 mV for measurement of I(Kr) tail amplitude on repolarisations to -40 mV. 3. I(Kr) in both ruptured-patch and perforated-patch myocytes was only moderately (14-20%) decreased by 100 microM concentrations of protein tyrosine kinase (PTK) inhibitors tyrphostin A23, tyrphostin A25, and genistein. However, similar-sized decreases were induced by PTK-inactive analogues tyrphostin A1 and daidzein, suggesting that they were unrelated to inhibition of PTK. 4. Ruptured-patch and perforated-patch myocytes were also treated with promoters of tyrosine phosphorylation, including phosphotyrosyl phosphatase (PTP) inhibitor orthovanadate, exogenous c-Src PTK, and four receptor PTK activators (insulin, insulin-like growth factor-1, epidermal growth factor, and basic fibroblast growth factor). None of these treatments had a significant effect on the amplitude of I(Kr). 5. We conclude that Kr channels in guinea-pig ventricular myocytes are unlikely to be regulated by PTK and PTP.
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