两种酪氨酸受体激酶对鼠嗅球神经元Kv1.3通道调节的比较

Receptors & channels Pub Date : 2004-01-01
B Colley, K Tucker, D A Fadool
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引用次数: 0

摘要

研究了Sprague Dawley大鼠和sv129 B6小鼠嗅球神经元(OBN)培养中受体酪氨酸激酶(RTK)、胰岛素(IRK)和神经营养因子B (TrkB)的激活情况。在对两种啮齿动物模型的二尖瓣细胞急性应用生长因子胰岛素或脑源性神经营养因子(BDNF)后,观察到电流抑制归因于延迟整流器Kv1.3 (Shaker家族的电压门控钾(Kv)通道)的调制。通过对通道中假定的酪氨酸磷酸化识别基元的定点诱变,我们发现用这些生长因子刺激Kv1.3会导致多种磷酸化,尽管是通过不同的RTK特异性残基组合。
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Comparison of modulation of Kv1.3 channel by two receptor tyrosine kinases in olfactory bulb neurons of rodents.

Activation of the receptor tyrosine kinase (RTK), insulin (IRK) or neurotrophin B (TrkB), was characterized and compared in olfactory bulb neuron (OBN) cultures from Sprague Dawley rats and sv129 B6 mice. Current suppression attributed to modulation of the delayed rectifier, Kv1.3, a voltage-gated potassium (Kv) channel of the Shaker family, was observed following acute application of the growth factors, insulin or brain-derived neurotrophic factor (BDNF), to mitral cells of either rodent model. Using site-directed mutagenesis of putative tyrosine phosphorylation recognition motifs in the channel, we find that stimulation of Kv1.3 with these growth factors causes multiple phosphorylation, albeit via different residue combinations that are RTK specific.

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