Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.16 (calcineurin)
 17,112 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We proposed that acute ammonia toxicity is mediated by activation of NMDA receptors. To confirm this hypothesis we have tested whether different NMDA receptor antagonists, acting on different sites of NMDA receptors, prevent death of mice induced by injection of 14 mmol/Kg of ammonium acetate, a dose that induces death of 95% of mice. MK-801, phencyclidine and ketamine, which block the ion channel of NMDA receptors, prevent death of at least 75% of mice. CPP, AP-5, CGS 19755, and CGP 40116, competitive antagonists acting on the binding site for NMDA, also prevent death of at least 75% of mice. Butanol, ethanol and methanol which block NMDA receptors, also prevent death of mice. There is an excellent correlation between the EC50 for preventing ammonia-induced death and the IC50 for inhibiting NMDA-induced currents. Acute ammonia toxicity is not prevented by antagonists of kainate/AMPA receptors, of muscarinic or nicotinic acetylcholine receptors or of GABA receptors. Inhibitors of nitric oxide synthase afford partial protection against ammonia toxicity while inhibitors of calcineurin, of glutamine synthetase or antioxidants did not prevent ammonia-induced death of mice. These results strongly support the idea that acute ammonia toxicity is mediated by activation of NMDA receptors.
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PMID:NMDA receptor antagonists prevent acute ammonia toxicity in mice. 892 86

cis,trans-Abscisic acid (ABA) plays an important role in plant growth and development, regulation of seed maturation, germination, and adaptation to environmental stresses. Knowledge of ABA mechanisms of action and the interactions of components required for ABA signal transduction is far from complete. Using transient gene expression in rice protoplasts, we observed additive and inhibitory effects between maize VP1 (Viviparous-1, a transcriptional activator) and a dominant-negative mutant protein phosphatase, ABI1-1 (ABA-insensitive-1-1), from Arabidopsis. Lanthanide ions were shown to be specific agonists of ABA-inducible gene expression and to interact synergistically with ABA and overexpressed VP1. Both VP1 and lanthanum activities could be antagonized by coexpression of ABI1-1, which demonstrates the specific ABA dependence of these effectors on ABA-regulated gene expression. We obtained pharmacological evidence that phospholipase D (PLD) functions in ABA-inducible gene expression in rice. Antagonism of ABA, VP1, and lanthanum synergy by 1-butanol, a specific inhibitor of PLD, was similar to the inhibition by coexpression of ABI1-1. These results demonstrate that ABA, VP1, lanthanum, PLD, and ABI1 are all involved in ABA-regulated gene expression and are consistent with an integrated model whereby La(3+) acts upstream of PLD.
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PMID:Functional interactions of lanthanum and phospholipase D with the abscisic acid signaling effectors VP1 and ABI1-1 in rice protoplasts. 1113 77

Abscisic acid (ABA) regulates seed maturation, germination, and adaptation of vegetative tissues to environmental stresses. The mechanisms of ABA action and the specificity conferred by signaling components in overlapping pathways are not completely understood. The ABI5 gene (ABA insensitive 5) of Arabidopsis encodes a basic leucine zipper factor required for ABA response in the seed and vegetative tissues. Using transient gene expression in rice protoplasts, we provide evidence for the functional interactions of ABI5 with ABA signaling effectors VP1 (viviparous 1) and ABI1 (ABA insensitive 1). Co-transformation experiments with ABI5 cDNA constructs resulted in specific transactivation of the ABA-inducible wheat Em, Arabidopsis AtEm6, bean beta-Phaseolin, and barley HVA1 and HVA22 promoters. Furthermore, ABI5 interacted synergistically with ABA and co-expressed VP1, indicating that ABI5 is involved in ABA-regulated transcription mediated by VP1. ABI5-mediated transactivation was inhibited by overexpression of abi1-1, the dominant-negative allele of the protein phosphatase ABI1, and by 1-butanol, a competitive inhibitor of phospholipase D involved in ABA signaling. Lanthanum, a trivalent ion that acts as an agonist of ABA signaling, potentiated ABI5 transactivation. These results demonstrate that ABI5 is a key target of a conserved ABA signaling pathway in plants.
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PMID:ABI5 interacts with abscisic acid signaling effectors in rice protoplasts. 1170 78

The creosote bush (Larrea tridentata) is a xerophytic evergreen C3 shrub thriving in vast arid areas of North America. As the first step toward understanding the molecular mechanisms controlling the drought tolerance of this desert plant, we have isolated a dozen genes encoding transcription factors, including LtWRKY21 that encodes a protein of 314 amino acid residues. Transient expression studies with the GFP-LtWRKY21 fusion construct indicate that the LtWRKY21 protein is localized in the nucleus and is able to activate the promoter of an abscisic acid (ABA)-inducible gene, HVA22, in a dosage-dependent manner. The transactivating activity of LtWRKY21 relies on the C-terminal sequence containing the WRKY domain and a N-terminal motif that is essential for the repression activity of some regulators in ethylene signaling. LtWRKY21 interacts synergistically with ABA and transcriptional activators VP1 and ABI5 to control the expression of the HVA22 promoter. Co-expression of VP1, ABI5, and LtWRKY21 leads to a much higher expression of the HVA22 promoter than does the ABA treatment alone. In contrast, the Lt-WRKY21-mediated transactivation is inhibited by two known negative regulators of ABA signaling: 1-butanol, an inhibitor of phospholipase D, and abi1-1, a dominant negative mutant protein phosphatase. Interestingly, abi1-1 does not block the synergistic effect of LtWRKY21, VP1, and ABI5 co-expression, indicating that LtWRKY21, VP1, and ABI5 may form a complex that functions downstream of ABI1 to control ABA-regulated expression of genes.
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PMID:A WRKY gene from creosote bush encodes an activator of the abscisic acid signaling pathway. 1550 32

Stomata open in response to blue light under a background of red light. The plant hormone abscisic acid (ABA) inhibits blue light-dependent stomatal opening, an effect essential for promoting stomatal closure in the daytime to prevent water loss. However, the mechanisms and molecular targets of this inhibition in the blue light signaling pathway remain unknown. Here, we report that phosphatidic acid (PA), a phospholipid second messenger produced by ABA in guard cells, inhibits protein phosphatase 1 (PP1), a positive regulator of blue light signaling, and PA plays a role in stimulating stomatal closure in Vicia faba. Biochemical analysis revealed that PA directly inhibited the phosphatase activity of the catalytic subunit of V. faba PP1 (PP1c) in vitro. PA inhibited blue light-dependent stomatal opening but did not affect red light- or fusicoccin-induced stomatal opening. PA also inhibited blue light-dependent H(+) pumping and phosphorylation of the plasma membrane H(+)-ATPase. However, PA did not inhibit the autophosphorylation of phototropins, blue light receptors for stomatal opening. Furthermore, 1-butanol, a selective inhibitor of phospholipase D, which produces PA via hydrolysis of phospholipids, diminished the ABA-induced inhibition of blue light-dependent stomatal opening and H(+) pumping. We also show that hydrogen peroxide and nitric oxide, which are intermediates in ABA signaling, inhibited the blue light responses of stomata and that 1-butanol diminished these inhibitions. From these results, we conclude that PA inhibits blue light signaling in guard cells by PP1c inhibition, accelerating stomatal closure, and that PP1 is a cross talk point between blue light and ABA signaling pathways in guard cells.
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PMID:Phosphatidic acid inhibits blue light-induced stomatal opening via inhibition of protein phosphatase 1 [corrected]. 2049 35