CALPAIN MAY PRODUCE A CA2+-INDEPENDENT FORM OF KINASE-C IN LONG-TERM POTENTIATION

被引：45

作者：

SUZUKI, T ^{[1
]}

OKUMURANOJI, K ^{[1
]}

OGURA, A ^{[1
]}

TANAKA, R ^{[1
]}

NAKAMURA, K ^{[1
]}

KUDO, Y ^{[1
]}

机构：

[1] MITSUBISHI KASEI INST LIFE SCI, MACHIDA, TOKYO 194, JAPAN

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 1992年 / 189卷 / 03期

关键词：

D O I：

10.1016/0006-291X(92)90247-I

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：

Both an enhancement of Ca2+-independent kinase activity in the supernatant fraction and enhanced breakdown of type β kinase C (PKC-β) were observed in the hippocampus after induction of tetanus-induced long-term potentiation (LTP) in the hippocampal CA1 region of rat. The enhanced activity was inhibited by the PKC-specific inhibitor, PKC19-36. Both phenomena were also observed simultaneously in the in vitro model system in which hippocampal homogenate was treated with CaCl2, and both enhancements were inhibited by the addition of calpain inhibitors, leupeptin and benzyloxycarbonyl-Leu-Met-H. The results suggest that Ca2+-independent kinase activity enhanced in the supernatant fraction during LTP derives from the catalytic fragment of PKC-β released by calpain. © 1992.

引用

页码：1515 / 1520

页数：6

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