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Involvement of protein kinase C in nerve growth factor‐ and K‐252a‐stimulated calcium uptake into PC12 cells
Author(s) -
Dickens Geneva,
Lavarreda Miriam,
Zheng WenHua,
Guroff Gordon
Publication year - 1997
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19970201)47:3<271::aid-jnr5>3.0.co;2-f
Subject(s) - staurosporine , calphostin , protein kinase c , nerve growth factor , calcium , calphostin c , stimulation , t type calcium channel , microbiology and biotechnology , protein kinase a , chemistry , voltage dependent calcium channel , calcium channel , biology , kinase , endocrinology , biochemistry , receptor , organic chemistry
Both nerve growth factor (NGF) and K‐252a stimulate the uptake of calcium into PC12 cells. Stimulation by either is prevented by pretreatment of the cells with the tumor promoter phorbol 12‐myristate 13‐acetate (PMA), suggesting an involvement of protein kinase C in the stimulation. The effect of PMA is specific in that the calcium uptake stimulated by either the L‐type channel agonist BAY K 8644 or by ATP is not altered in PMA‐pretreated cells. An involvement of kinase C is also suggested by the inhibition of NGF‐ or K‐252a‐stimulated calcium uptake by the kinase C inhibitors staurosporine and calphostin C. Inhibition by the isoform‐specific agents GO 6976 and thymeleatoxin implicates one of the classic calcium‐sensitive isoforms of kinase C. The close similarity in the profiles of inhibition of NGF‐stimulated and K‐252a‐stimulated calcium uptake by the various effectors suggests that NGF and K‐252a act on calcium uptake through some of the same signaling elements. J. Neurosci. Res. 47:271–276, 1997. © 1997 Wiley‐Liss, Inc.

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