Specific regulation of IRS-2 expression by glucose in rat primary pancreatic islet β-cells
Specific regulation of IRS-2 expression by glucose in rat primary pancreatic islet β-cells
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DOI：
10.1074/jbc.m600356200
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发表时间：
2006-06-09
影响因子：
4.8
通讯作者：
Rhodes, Christopher J.
中科院分区：
文献类型：
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作者：
Lingohr, Melissa K.;Briaud, Isabelle;Rhodes, Christopher J.
胰岛素受体底物2 （IRS-2）在胰腺β细胞中起关键作用。升高的IRS-2表达促进β细胞生长和存活，而降低的IRS-2水平导致细胞凋亡。研究发现，IRS-2在大鼠胰岛β细胞中的转换速度很快，mRNA和蛋白的半衰期分别接近90 min和2 h。然而，这被特异性葡萄糖调节的IRS-2在转录水平介导的表达所抵消。葡萄糖（>= 6 mM）以剂量依赖的方式增加irs - 2mrna和蛋白质水平，在>= 12mM葡萄糖时，irs - 2mrna最高增加4倍，IRS-2蛋白水平增加5-6倍
Insulin receptor substrate 2 (IRS-2) plays a critical role in pancreatic beta-cells. Increased IRS-2 expression promotes beta-cell growth and survival, whereas decreased IRS-2 levels lead to apoptosis. It was found that IRS-2 turnover in rat islet beta-cells was rapid, with mRNA and protein half-lives of similar to 90 min and similar to 2 h, respectively. However, this was countered by specific glucose-regulated IRS-2 expression mediated at the transcriptional level. Glucose (>= 6 mM) increased IRS-2 mRNA and protein levels in a dose-dependent manner, reaching a maximum 4-fold increase in IRS-2mRNAand a 5-6-fold increase in IRS-2 protein levels at >= 12mM glucose (p