ArticleThe Journal of physiology1999
Tyrosine kinases modulate K+ channel gating in mouse Schwann cells.
Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 41 citations in OpenAlex.
- Non-conducting functions of ion channels: The case of integrin-ion channel complexes.Channels (Austin, Tex.) · 2022Review
- Genistein Inhibits AβCellular and molecular neurobiology · 2019Article
- Article
- Oxidation of KCNB1 K(+) channels in central nervous system and beyond.World journal of biological chemistry · 2014Review
- Common themes in PrP signaling: the Src remains the same.Frontiers in cell and developmental biology · 2014Article
- Multifaceted modulation of K+ channels by protein-tyrosine phosphatase ε tunes neuronal excitability.The Journal of biological chemistry · 2012Article
- Inhibition of Kv4.3 by genistein via a tyrosine phosphorylation-independent mechanism.American journal of physiology. Cell physiology · 2011Article
- The activity of spontaneous action potentials in developing hair cells is regulated by Ca(2+)-dependence of a transient K+ current.PloS one · 2011Article
- Genistein inhibits voltage-gated sodium currents in SCG neurons through protein tyrosine kinase-dependent and kinase-independent mechanisms.Pflugers Archiv : European journal of physiology · 2008Article
- Tyrosine phosphatases epsilon and alpha perform specific and overlapping functions in regulation of voltage-gated potassium channels in Schwann cells.Molecular biology of the cell · 2006Article
- Effect of genistein on voltage-gated potassium channels in guinea pig proximal colon smooth muscle cells.World journal of gastroenterology · 2006Article
- Downregulation of platelet-derived growth factor-alpha receptor-mediated tyrosine kinase activity as a cellular mechanism for K+-channel regulation during oligodendrocyte development in situ.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Genistein inhibits the activity of kv1.3 potassium channels in human T lymphocytes.The Journal of membrane biology · 2005Article
- Modulation of homomeric and heteromeric KCNQ1 channels by external acidification.The Journal of physiology · 2002Article
- Gene-targeted deletion of neurofibromin enhances the expression of a transient outward K+ current in Schwann cells: a protein kinase A-mediated mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
- Hypomyelination and increased activity of voltage-gated K(+) channels in mice lacking protein tyrosine phosphatase epsilon.The EMBO journal · 2000Article
- Modulation of Kv1.5 currents by Src tyrosine phosphorylation: potential role in the differentiation of astrocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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 reduced the amplitude of a slowly inactivating delayed-rectifier current (IK) and, to a lesser extent, that of a transient K+ current (IA). Similar results were obtained on IK 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 IA by profoundly affecting its gating properties. These changes consisted of slower activation kinetics with an increased time to peak, a positive shift in the voltage dependence of activation (by +30 mV), a decrease in the steepness of 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 IA. These modulations may be functionally relevant in the control of K+ channel activity during Schwann cell development and peripheral myelinogenesis.
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