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

A single dose (1.7 mg/kg, s.c.) of diisopropylphosphorofluoridate (DFP) causes organophosphorus ester-induced delayed neurotoxicity (OPIDN) in susceptible species. We studied the effects of DFP administration on the mRNA expression of glyceraldehyde-3-phosphate dehydrogenase (GAPDH), an important glycolytic protein at different time points (1, 2, 5, 10 and 20 days) post-treatment. Total RNA was extracted from cerebrum, cerebellum, brainstem, midbrain, and spinal cord of the control and DFP-treated hens, and northern blots were prepared using standard protocols and hybridized with GAPDH, as well as beta-actin and 28S RNA cDNA (control) probes. There was a distinct spatial/temporal mRNA expression pattern for the different tissues studied. Non-susceptible tissue, cerebrum showed a dramatic increase in GAPDH mRNA at day 1, post-treatment and levels remained high at all time points, suggestive of protective mechanisms from the beginning. In contrast, highly susceptible tissues like brainstem, spinal cord and midbrain showed either no elevation or slight down-regulation at day 1, suggesting trauma and cell injury/cell death. Overall, there was moderate level of induction during the subsequent time points in these tissues, indicative of pathways of either recovery or degeneration. Cerebellum being the less susceptible tissue showed moderate increase initially, followed by higher induction, suggestive of rapid recovery. Our current data on GAPDH provides an important link in this complex network of molecular changes involving pathways identified by our group and others, such as nitric oxide (NO), CaM kinase-II (CaMK-II), protein kinase-A (PKA), c-fos, and phosphorylated-CREB (p-CREB) in DFP-induced OPIDN.
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PMID:Differential alteration of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA in the central nervous system of hens treated with diisopropylphosphorofluoridate (DFP). 1179 68

Inhibitory synapses on Purkinje cells show synaptic plasticity such as rebound potentiation (RP), which seems to contribute to refined information processing in the cerebellar cortex. Recent progress in the study on regulation mechanism of RP is reported. RP is induced by depolarization of a Purkinje cell and expressed as the increased postsynaptic responsiveness to GABA. RP might work as a homeostatic mechanism to maintain activity of a Purkinje cell sensing the strength of heterosynaptic excitatory inputs. However, there is a homosynaptic mechanism to regulate RP. RP is suppressed by the GABAergic transmission occurring during depolarization. Elaborate molecular regulation mechanism of RP induction, including GABA(B) receptors, Ca(2+), cyclic adenosine 3',5'-monophosphate (cAMP), kinases such as Ca(2+)- and calmodulin-dependent kinase II and protein kinase A, and protein phosphatases such as PP1 and PP2B, has been clarified. Application of systems biological analyses combined with electrophysiological experiments has revealed a critical role of phosphodiesterase 1 in determination of the Ca(2+) signal to induce RP.
Cerebellum 2012 Jun
PMID:Regulation of inhibitory synaptic plasticity in a Purkinje neuron. 2209 Mar 65