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c‐Jun functions as a calcium‐regulated transcriptional activator in the absence of JNK/SAPK1 activation
Author(s) -
Cruzalegui Francisco H.,
Hardingham Giles E.,
Bading Hilmar
Publication year - 1999
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/18.5.1335
Subject(s) - library science , biology , computer science
Calcium is the principal second messenger in the control of gene expression by electrical activity in neurons. Recruitment of the coactivator CREB‐binding protein, CBP, by the prototypical calcium‐responsive transcription factor, CREB and stimulation of CBP activity by nuclear calcium signals is one mechanism through which calcium influx into excitable cells activates gene expression. Here we show that another CBP‐interacting transcription factor, c‐Jun, can mediate transcriptional activation upon activation of L‐type voltage‐gated calcium channels. Calcium‐activated transcription mediated by c‐Jun functions in the absence of stimulation of the c‐Jun N‐terminal protein kinase (JNK/SAPK1) signalling pathway and does not require c‐Jun amino acid residues Ser63 and Ser73, the two major phosphorylation sites that regulate c‐Jun activity in response to stress signals. Similar to CREB‐mediated transcription, activation of c‐Jun‐mediated transcription by calcium signals requires calcium/ calmodulin‐dependent protein kinases and is dependent on CBP function. These results identify c‐Jun as a calcium‐regulated transcriptional activator and suggest that control of coactivator function (i.e. recruitment of CBP and stimulation of CBP activity) is a general mechanism for gene regulation by calcium signals.