Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.1 (protein kinase)
 81,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plant mitogen-activated protein kinases represented by tobacco WIPK (wounding-induced protein kinase) and its orthologs in other species are unique in their regulation at transcriptional level in response to stress and pathogen infection. We previously demonstrated that transcriptional activation of WIPK is essential for induced WIPK activity, and activation of salicylic acid-induced protein kinase (SIPK) by the constitutively active NtMEK2(DD) is sufficient to induce WIPK gene expression. Here, we report that the effect of SIPK on WIPK gene expression is mediated by reactive oxygen species (ROS). Using a combination of pharmacological and gain-of-function transgenic approaches, we studied the relationship among SIPK activation, WIPK gene activation in response to fungal cryptogein, light-dependent ROS generation in chloroplasts, and ROS generated via NADPH oxidase. In the conditional gain-of-function GVG-NtMEK2(DD) transgenic tobacco, induction of WIPK expression is dependent on the ROS generation in chloroplasts. Consistently, methyl viologen, an inducer of ROS generation in chloroplasts, highly activated WIPK expression. In addition to chloroplast-originated ROS, H(2)O(2) generated from the cell-surface NADPH oxidase could also activate WIPK gene expression, and inhibition of cryptogein-induced ROS generation also abolished WIPK gene activation. Our data demonstrate that WIPK gene activation is mediated by ROS, which provides a mechanism by which ROS influence cellular signalling processes in plant stress/defence response.
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PMID:Reactive oxygen species in signalling the transcriptional activation of WIPK expression in tobacco. 2439 54

A subgroup of anticonvulsant and neuroleptic drugs acts through the potentiation of GABA pathways. The regulatory role of GABA in neuronal circuit formation is related to its depolarizing action that supports activity-dependent synaptogenesis. We hypothesized that elevated levels of GABA in the immature brain modify synaptogenesis in excitatory synapses and consequently affect mice behavior. In support of this theory, we showed previously that neonatal exposure to a GABA-transaminase inhibitor (Vigabatrin, GVG) modifies the expression of presynaptic proteins and suppresses excitatory synaptic potentials. To further characterize this phenomenon, we examined the effect of GVG applied during postnatal days 4-14, during the switch in GABA function from a depolarizing to a hyperpolarizing substance, on the development of excitatory synapses and mice sociability. Early exposure to GVG induced differential effects on synaptic proteins in the hippocampus and the cerebral cortex, including the downregulation of GluR1/GluR2 and NR2A/NR2B ratios in the hippocampus cytoplasm, a minute effect on the regulatory proteins CAMKII and PKA in the cerebral cortex, and increases in pGluR1, CAMKII, PKA and Reelin levels. Early GVG exposure was also associated with region specific regulation of monoamines, reduction in hippocampal DA, and enhancement of cortical NE levels. Age-dependent modified sociability and lack of preference for social interactions were observed in mice treated with GVG. Overall, early life exposure to GVG is expected to alter cortico-hippocampal axis connectivity and balance due to the different effects GVG has on key synaptic proteins in the associated brain regions, thus potentially causing behavioral impairment.
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PMID:Long-lasting glutamatergic modulation induced by neonatal GABA enhancement in mice. 2446 20