Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.11.17 (CaMKII)
 4,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Injection of small volumes of N-methyl-D-aspartate (NMDA) or Sin-1 molsidomine (a nitric oxide releasing agent) onto the dendrites of granule cells in the hippocampal dentate gyrus leads to changes in the level of expression of a number of genes. There is a fall in prodynorphin mRNA levels with a corresponding increase in proenkephalin mRNA levels. Similar changes in opioid gene expression occur following the induction of long-term potentiation (LTP). We report here that at short time periods (1-6 h) after injections of NMDA or sin-1 molsidomine, there is an increase in the levels of the mRNA encoding the alpha subunit of Ca2+/calmodulin-dependent protein kinase II (CaMKII alpha), consistent with a report of elevated CaMKII alpha mRNA in postsynaptic neurons in the CA1 region of the hippocampus following LTP induction [54]. However, we also report that 24 h after injection of NMDA or sin-1, there is a dramatic decrease in CaMKII alpha mRNA levels in the vicinity of the injection. This effect is specific for CaMKII alpha mRNA, in that many other mRNA species are not affected, and occurs in the dendritic population of CaMKII alpha mRNA as well as in the pool of mRNA in the granule cell bodies. The effect is blocked by an inhibitor of cGMP-dependent protein kinase. The biphasic regulation of CaMKII alpha mRNA may be of considerable functional importance for the long-term response of granule cells to local stimulation of NMDA receptors or NO release.
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PMID:N-methyl-D-aspartate and nitric oxide regulate the expression of calcium/calmodulin-dependent kinase II in the hippocampal dentate gyrus. 747 22

The regulation of prodynorphin (proDYN) mRNA levels by cAMP and protein kinase C (PKC) pathways was studied in cultured rat spinal cord cells. Spinal cord cells were cultured from 14 day (E 14) embryos of Sprague-Dawley rats. After 7 days in vitro, the spinal cord cells were incubated with either forskolin (5 microM) or phorbol-13-myristate acetate (PMA; 2.5 microM) for 1, 3, 6, 9, 12, or 24 h and the total RNA was isolated for Northern blot analyses. The proDYN mRNA level began to increase 1 h, then reached and remained at a peak 3-6 h after stimulation by forskolin or PMA. proDYN mRNA levels in forskolin treated cells decreased slightly from their peak after 9 h of treatment, whereas the level of proDYN mRNA returned to the basal level in PMA-treated cells. Pretreatment of cells with cycloheximide (a protein synthesis inhibitor; 10 microM) did not affect the forskolin- or PMA-induced increase in proDYN mRNA, but pretreatment with nimodipine (a L-type Ca2+ channel blocker; 2 microM), omega-conotoxin (a N-type Ca2+ channel blocker; 1 microM), or KN-62 (a Ca2+/calmodulin-dependent protein kinase II inhibitor; 5 microM) inhibited induction of proDYN mRNA both by forskolin and PMA. Additionally, dexamethasone did not affect the expression of proDYN mRNA level induced by forskolin. Our results suggest that proDYN mRNA levels in spinal cord cells is regulated by both cAMP and PKC pathways. Calcium influx through both L- and N-type calcium channels and Ca2+/calmodulin-dependent protein kinase II appear to be involved in the increase of proDYN mRNA levels induced by either forskolin or PMA. Furthermore, ongoing protein synthesis is not required for forskolin- or PMA-induced responses.
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PMID:The regulation of prodynorphin gene expression in cultured spinal cord cells: involvement of second messengers. 917 64