Metabolism of inositol 1,4,5-trisphosphate in guinea-pig hepatocytes.
Metabolism of inositol 1,4,5-trisphosphate in guinea-pig hepatocytes.
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豚鼠肝细胞中肌醇 1,4,5-三磷酸的代谢。
DOI：
10.1042/bj2420797
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
PutneyJr,JW
中科院分区：
文献类型：
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作者：
Tennes,KA;McKinney,JS;PutneyJr,JW
在透化豚鼠肝细胞中研究了肌醇 1,4,5-三磷酸的代谢。 [3H]肌醇1,4,5-三磷酸向极性更强的3H标记化合物的转化发生得很快，并且早在5秒内就被检测到。该材料由 h.p.l.c 共洗脱。与肌醇 1,3,4,5 四[32P]磷酸酯一起，推测是肌醇四磷酸酯。从 h.p.l.c 中共洗脱的 3H 标记材料显着增加。肌醇1,3,4-三磷酸仅在一定的滞后期后发生。将透化的肝细胞与肌醇 1,3,4,5-四[32P]磷酸一起孵育，导致形成 32P 标记物质，并与肌醇 1,3,4-三磷酸共洗脱；没有产生肌醇1,4,5-三[32P]磷酸，表明5-磷酸单酯酶的作用。肌醇1,3,4,5-四[32P]磷酸酯的水解半衰期约为。 2,3-二磷酸甘油酸将1分钟增加至3分钟。类似地，由四磷酸酯暂时设计为肌醇1,3,4-三[32P]磷酸酯的材料的生产速率被10mM-2,3-二磷酸甘油酸降低。在不存在 ATP 的情况下，[3H]肌醇 1,4,5-三磷酸不会转化为 [3H]肌醇四磷酸或 [3H]肌醇 1,3,4-三磷酸，这表明 1,3,4 异构体不是由肌醇 1,4,5-三磷酸异构化产生的。这项研究的结果表明，分离的肝细胞中肌醇三磷酸的1,3,4异构体的起源是肌醇1,3,4,5-四磷酸，并且肌醇1,4,5-三磷酸快速转化为这种四磷酸。 2,3-二磷酸甘油酸（红细胞膜 5-磷酸单酯酶的抑制剂）抑制四磷酸分解的能力表明，从肌醇 1,4,5-三磷酸中除去 5-磷酸的酶也可能起到将四磷酸转化为肌醇 1,3,4-三磷酸的作用。目前尚不清楚肌醇1,4,5-三磷酸激酶的作用是否是使肌醇1,4,5-三磷酸失活，或者四磷酸产物是否可能在细胞中具有信使功能。
Metabolism of inositol 1,4,5-trisphosphate was investigated in permeabilized guinea-pig hepatocytes. The conversion of [3H]inositol 1,4,5-trisphosphate to a more polar 3H-labelled compound occurred rapidly and was detected as early as 5 s. This material co-eluted from h.p.l.c. with inositol 1,3,4,5 tetrakis[32P]phosphate and is presumably an inositol tetrakisphosphate. A significant increase in the 3H-labelled material co-eluting from h.p.l.c. with inositol 1,3,4-trisphosphate occurred only after a definite lag period. Incubation of permeabilized hepatocytes with inositol 1,3,4,5-tetrakis[32P]phosphate resulted in the formation of 32P-labelled material that co-eluted with inositol 1,3,4-trisphosphate; no inositol 1,4,5-tris[32P]phosphate was produced, suggesting the action of a 5-phosphomonoesterase. The half-time of hydrolysis of inositol 1,3,4,5-tetrakis[32P]phosphate of approx. 1 min was increased to 3 min by 2,3-bisphosphoglyceric acid. Similarly, the rate of production of material tentatively designed as inositol 1,3,4-tris[32P]phosphate from the tetrakisphosphate was reduced by 10 mM-2,3-bisphosphoglyceric acid. In the absence of ATP there was no conversion of [3H]inositol 1,4,5-trisphosphate to [3H]inositol tetrakisphosphate or to [3H]inositol 1,3,4-trisphosphate, which suggests that the 1,3,4 isomer does not result from isomerization of inositol 1,4,5-trisphosphate. The results of this study suggest that the origin of the 1,3,4 isomer of inositol trisphosphate in isolated hepatocytes is inositol 1,3,4,5-tetrakisphosphate and that inositol 1,4,5-trisphosphate is rapidly converted to this tetrakisphosphate. The ability of 2,3-bisphosphoglyceric acid, an inhibitor of 5-phosphomonoesterase of red blood cell membrane, to inhibit the breakdown of the tetrakisphosphate suggests that the enzyme which removes the 5-phosphate from inositol 1,4,5-trisphosphate may also act to convert the tetrakisphosphate to inositol 1,3,4-trisphosphate. It is not known if the role of inositol 1,4,5-trisphosphate kinase is to inactivate inositol 1,4,5-trisphosphate or whether the tetrakisphosphate product may have a messenger function in the cell.