The glucagon-insulin antagonism in the regulation of cytosolic protein binding to the 3' end of phosphoenolpyruvate carboxykinase mRNA in cultured rat hepatocytes. Possible involvement in the stabilization of the mRNA.
The glucagon-insulin antagonism in the regulation of cytosolic protein binding to the 3' end of phosphoenolpyruvate carboxykinase mRNA in cultured rat hepatocytes. Possible involvement in the stabilization of the mRNA.
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胰高血糖素-胰岛素拮抗作用调节培养的大鼠肝细胞中胞质蛋白与磷酸烯醇丙酮酸羧激酶 mRNA 3 端的结合。
DOI：
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
A. Nath
中科院分区：
文献类型：
--
作者：
B. Christ;A. Nath
由于认为与mRNA 3'端结合的蛋白质参与mRNA稳定性的控制，因此在不存在和存在胰岛素的情况下，胰高血糖素诱导的磷酸烯醇化酶-羧激酶-mRNA（PCK）水平变化的时间过程与24小时培养的大鼠肝细胞胞质蛋白与PCK mRNA 3'端结合变化的时间过程相关。通过北方印迹分析监测PCK-mRNA水平，并通过电泳迁移率变化分析分析蛋白结合。在2 - 4小时培养的大鼠肝细胞中，通过1 nM胰高血糖素处理并更换培养基，细胞溶质蛋白与PCK-mRNA 3'末端的结合和PCK-mRNA水平分别在2小时和2-4小时增加至瞬时最大值。与胰高血糖素同时加入的100 nM胰岛素使胰高血糖素诱导的蛋白结合最大值降低80%，PCK mRNA增加约30%。在没有激素治疗的对照组中，1 h时蛋白结合率也增加;胰岛素可阻止这种增加。在胰高血糖素后1小时加入100 nM胰岛素，可在1小时内将与PCK mRNA 3'端结合的蛋白质逆转至接近初始水平，并使胰高血糖素诱导的PCK-mRNA水平升高受损30%。转录抑制剂虫草素，1小时后加入胰高血糖素，没有阻止胰高血糖素增强蛋白结合的进一步增加，也没有逆转胰岛素。然而，它确实阻止了PCK mRNA的进一步显著增加。激素调节的蛋白质结合可定位于PCK-mRNA 3'末端的256个碱基。PCK-mRNA 3'端的近端466个碱基以及组蛋白-H1（0）-mRNA 3'端的1050个碱基和芳基硫酸酯酶-A-mRNA 3'端的1200个碱基也结合胞质蛋白，但这种蛋白结合不因胰高血糖素或胰岛素处理而改变。PCK、芳基硫酸酯酶A和H1（0）mRNA的3'端表现出与来自不同大鼠组织如心脏、肝脏和肺以及Fao大鼠肝癌细胞的胞质蛋白的强结合。来自脾的胞质蛋白显示弱结合，来自HeLa和U937肿瘤细胞的蛋白不结合。蛋白质结合与PCK mRNA的3'末端和来自肝脏的胞质提取物最显著。（400字处截断摘要）
Since protein binding to the 3' end of mRNA is believed to be involved in the control of mRNA stability, the time course of alterations in glucagon-induced phosphoenolpyruvate-carboxykinase-mRNA (PCK) levels, in the absence and presence of insulin, was correlated with the time course of changes in the binding of cytosolic protein from 24-h cultured rat hepatocytes to the 3' end of PCK mRNA. PCK-mRNA levels were monitored by Northern blot analysis and protein binding was analyzed by an electrophoretic mobility-shift assay. In 24-h cultured rat hepatocytes, binding of cytosolic protein to the PCK-mRNA 3' end and PCK-mRNA levels were increased to a transient maximum at 2 h and 2-4 h, respectively, by a 1-nM glucagon treatment, added with a change of medium. 100 nM insulin, added simultaneously with glucagon, reduced the glucagon-induced maximum of protein binding by 80% and the increase of PCK mRNA by about 30%. In controls without hormonal treatment protein binding at 1 h was also increased; this increase was prevented by insulin. 100 nM insulin, added 1 h after glucagon, reversed protein binding to the 3' end of PCK mRNA to nearly initial levels within 1 h and impaired the glucagon-induced increase in PCK-mRNA levels by 30%. The transcriptional inhibitor cordycepin, added 1 h after glucagon, did not prevent the further increase in glucagon-enhanced protein binding nor its reversal by insulin. It did, however, prevent a further significant increase in PCK mRNA. Hormonally regulated protein binding could be localized to the 256 distal bases of the PCK-mRNA 3' end. The proximal 466 bases of the PCK-mRNA 3' end as well as the 1050 bases of the histone-H1(0)-mRNA 3' end and the 1200 bases of the arylsulfatase-A-mRNA 3' end also bound cytosolic protein(s), but this protein binding was not altered by treatment with glucagon or insulin. The 3' end of PCK, arylsulfatase A and H1(0) mRNA exhibited strong binding of cytosolic protein(s) from diverse rat tissues such as heart, liver and lung as well as Fao rat hepatoma cells. Cytosolic protein(s) from spleen showed weak binding and proteins from HeLa and U937 tumor cells did not bind. Protein binding was most prominent with the 3' end of PCK mRNA and cytosolic extracts from liver.(ABSTRACT TRUNCATED AT 400 WORDS)
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DOI：
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发表时间：
1991
期刊：
The Journal of biological chemistry
影响因子：
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DOI：
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The Journal of biological chemistry
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13.8
作者：
Marzluff,WF;Pandey,NB
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影响因子：
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作者：
S. Jacob;M. Terns;J. A. Hengst-Zhang;R. S. Vulapalli
通讯作者：
S. Jacob;M. Terns;J. A. Hengst-Zhang;R. S. Vulapalli
环 AMP 可稳定磷酸烯醇丙酮酸羧激酶 (GTP) 的 mRNA，防止降解。
DOI：
--
发表时间：
1988
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Hod,Y;Hanson,RW
通讯作者：
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