Targeting SUR1/Abcc8-type neuroendocrine KATP channels in pancreatic islet cells.
Targeting SUR1/Abcc8-type neuroendocrine KATP channels in pancreatic islet cells.
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DOI：
10.1371/journal.pone.0091525
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Bryan J
中科院分区：
文献类型：
--
作者：
Nakamura Y;Bryan J
ATP敏感性K+通道（KATP）在胰岛α、β和δ细胞中起调节作用。有针对性的通道删除将有助于胰岛内调节网络的分析和解剖。为此，产生Abcc8/Sur1 flox小鼠，并通过与胰高血糖素-（GCG）-cre小鼠杂交以选择性靶向α-细胞KATP通道来测试。使用激动剂抗性来定量缺乏通道的α细胞的百分比。41%的Sur1loxP/loxP; GCG-cre+和1064%的Sur1loxP/−; GCG-cre + α-细胞缺乏KATP通道，而在ROSA-EYFP/GCG-cre交配中，1065%的α-细胞表达增强型黄色荧光蛋白（EYFP）。结果与随机两次重组事件机制以及删除两个floxed等位基因的要求一致。
ATP-sensitive K+ (KATP) channels play a regulatory role in hormone-secreting pancreatic islet α-, β- and δ-cells. Targeted channel deletion would assist analysis and dissection of the intraislet regulatory network. Toward this end Abcc8/Sur1 flox mice were generated and tested by crossing with glucagon-(GCG)-cre mice to target α-cell KATP channels selectively. Agonist resistance was used to quantify the percent of α-cells lacking channels. 41% of Sur1loxP/loxP;GCG-cre+ and ∼64% of Sur1loxP/−;GCG-cre+ α-cells lacked KATP channels, while ∼65% of α-cells expressed enhanced yellow fluorescent protein (EYFP) in ROSA-EYFP/GCG-cre matings. The results are consistent with a stochastic two-recombination event mechanism and a requirement that both floxed alleles are deleted.
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