Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.13 (protein kinase C)
 49,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin B(1) (thiamine) is an essential nutrient for humans. Vitamin B(1) deficiency causes beriberi, which disturbs the central nervous and circulatory systems. In countries in which rice (Oryza sativa) is a major food, thiamine deficiency is prevalent because polishing of rice removes most of the thiamine in the grain. We demonstrate here that thiamine, in addition to its nutritional value, induces systemic acquired resistance (SAR) in plants. Thiamine-treated rice, Arabidopsis (Arabidopsis thaliana), and vegetable crop plants showed resistance to fungal, bacterial, and viral infections. Thiamine treatment induces the transient expression of pathogenesis-related (PR) genes in rice and other plants. In addition, thiamine treatment potentiates stronger and more rapid PR gene expression and the up-regulation of protein kinase C activity. The effects of thiamine on disease resistance and defense-related gene expression mobilize systemically throughout the plant and last for more than 15 d after treatment. Treatment of Arabidopsis ecotype Columbia-0 plants with thiamine resulted in the activation of PR-1 but not PDF1.2. Furthermore, thiamine prevented bacterial infection in Arabidopsis mutants insensitive to jasmonic acid or ethylene but not in mutants impaired in the SAR transduction pathway. These results clearly demonstrate that thiamine induces SAR in plants through the salicylic acid and Ca(2+)-related signaling pathways. The findings provide a novel paradigm for developing alternative strategies for the control of plant diseases.
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PMID:Vitamin B1 functions as an activator of plant disease resistance. 1598 Feb 1

Accumulation of triosephosphates arising from high cytosolic glucose concentrations in hyperglycemia is one likely or potential trigger for biochemical dysfunction leading to the development of diabetic complications. This may be prevented by disposal of excess triosephosphates via the reductive pentosephosphate pathway. This pathway is impaired in experimental and clinical diabetes by mild thiamine deficiency. The expression and activity of the thiamine-dependent enzyme, transketolase--the pacemaking enzyme of the reductive pentosephosphate pathway, is consequently decreased. Correction of thiamine deficiency in experimental diabetes by high dose therapy with thiamine and the thiamine monophosphate prodrug, Benfotiamine, restores disposal of triosephosphates by the reductive pentosephosphate pathway in hyperglycemia. This prevented multiple mechanisms of biochemical dysfunction: activation of protein kinase C, activation of the hexosamine pathway, increased glycation and oxidative stress. Consequently, the development of incipient diabetic nephropathy, neuropathy and retinopathy were prevented. Both thiamine and Benfotiamine produced other remarkable effects in experimental diabetes: marked reversals of increased diuresis and glucosuria without change in glycemic status. High dose thiamine also corrected dyslipidemia in experimental diabetes--normalizing cholesterol and triglycerides. Dysfunction of beta-cells and impaired glucose tolerance in thiamine deficiency and suggestion of a link of impaired glucose tolerance with dietary thiamine indicates that thiamine therapy may have a future role in prevention of type 2 diabetes. More immediately, given the emerging multiple benefits of thiamine repletion, even mild thiamine deficiency in diabetes should be avoided and thiamine supplementation to high dose should be considered as adjunct nutritional therapy to prevent dyslipidemia and the development of vascular complications in clinical diabetes.
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PMID:The potential role of thiamine (vitamin B1) in diabetic complications. 1822 Jun 5

Effects of yokukansan, a traditional Japanese medicine, on thiamine deficiency (TD)-induced decrease of glutamate uptake were examined in cultured rat cortical astrocytes. Yokukansan (100-500 microg/ml) ameliorated the TD-induced decrease in glutamate uptake by astrocytes, implying that yokukansan may contain active herbs and compounds possessing this effect. Among the seven constituent herbs of yokukansan, significant effects were found for glycyrrhiza. Furthermore, glycyrrhizin and its metabolite 18 beta-glycyrrhetinic acid (10(-7)-10(-4)M), among the eight components of glycyrrhiza, ameliorated the TD-induced decrease of glutamate uptake in astrocytes in a concentration-dependent manner. These substances inhibited protein kinase C (PKC) activity under the in vitro conditions. These lines of evidence suggest that glycyrrhizin, a main component of glycyrrhiza, and its metabolite 18 beta-glycyrrhetinic acid are likely responsible for amelioration of dysfunction of glutamate transport in astrocytes. The inhibition of the PKC activity might be related to the pharmacological efficacy of these substances.
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PMID:Glycyrrhizin and its metabolite 18 beta-glycyrrhetinic acid in glycyrrhiza, a constituent herb of yokukansan, ameliorate thiamine deficiency-induced dysfunction of glutamate transport in cultured rat cortical astrocytes. 1981 47