CA2+ INFLUX GATED BY INOSITOL-3,4,5,6-TETRAKISPHOSPHATE IN NIH/3T3 FIBROBLASTS

被引:10
作者
HASHII, M
HIRATA, M
OZAKI, S
NOZAWA, Y
HIGASHIDA, H
机构
[1] KANAZAWA UNIV,SCH MED,DEPT BIOPHYS,KANAZAWA 920,ISHIKAWA,JAPAN
[2] NATL CTR NEUROL & PSYCHIAT,DEPT CORT FUNCT DISORDER,KODAIRA,TOKYO 187,JAPAN
[3] KYUSHU UNIV,FAC DENT,DEPT BIOCHEM,FUKUOKA 812,JAPAN
[4] EHIME UNIV,FAC ENGN,DEPT APPL CHEM,MATSUYAMA,EHIME 790,JAPAN
[5] GIFU UNIV,SCH MED,DEPT BIOCHEM,GIFU 500,JAPAN
关键词
D O I
10.1006/bbrc.1994.1592
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The functional role of three inositol tetrakisphosphate isomers on Ca2+ influx was examined by intracellular application in NIH/3T3 mouse fibroblasts. Infusion of inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P-4), inositol-l,3,4,6-tetrakisphosphate, and inositol-3,4,5,6-tetrakisphosphate (Ins(3,4,5,6)P-4) from the patch pipette into the cytoplasm produced a transient increase in cytoplasmic free Ca2+ concentration by fura-2 recording in extracellular Ca2+-dependent fashion. Stimulation of NIH/3T3 cells with bradykinin increased the levels of Ins(1,3,4,5)Pq and Ins(3,4,5,6)Pq. These results suggest that mouse fibroblast cells possess a Ca2+ influx pathway gated occuring inositol tetrakisphosphates in response to stimulation with bradykinin. (C) 1994 Academic Press, Inc.
引用
收藏
页码:1300 / 1306
页数:7
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