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John McCallum Noel Porter Bruce Searle Martin Shaw Bodhi Bettjeman Michael McManus 《Plant and Soil》2005,269(1-2):151-158
Although glasshouse studies have conclusively demonstrated that S nutrition can affect onion (Allium cepaL.) pungency this has been rarely observed in field-based studies due to difficulties in controlling S nutrition and lack
of efficient methods for measurement of flavour bioactives. We have developed a rapid automated method for determination of
onion lachrymatory factor ((Z, E)-thiopropanal-S-oxide; LF) based on juice extraction into dichloromethane and gas chromatography (GC) analysis with flame photometric detection.
We evaluated this in a field trial of a mild (cv. ‘Encore’) and a pungent (cv. ‘Kojak’) onion cultivar grown on a low S soil
with and without S addition, under high or low N treatments. No treatments significantly affected bulb fresh weight but S
fertilisation significantly increased bulb total S, sulfate, pungency, LF and flavour precursor levels in both varieties.
Analysis of bulb flavour precursors by HPLC confirmed that juice LF levels paralleled levels of the flavour precursor S-1-propenyl cysteine sulfoxide. The pungent cultivar also exhibited significant N main effects on bulb LF, total S and sulfate.
We also assayed the key S-assimilatory enzyme, APS reductase (APR) in leaves before and during bulbing. Specific activities
in the range of 1 to 11 nmol mg−1·min−1 were observed in youngest leaves, but only the milder cultivar exhibited significant stage × N × S effects. These findings
suggest that sulfur metabolism of mild and pungent onions respond differently to N fertility, and that GC of LF is practical
for field-based studies of onion flavour. 相似文献
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Smac mimetics activate the E3 ligase activity of cIAP1 protein by promoting RING domain dimerization
Feltham R Bettjeman B Budhidarmo R Mace PD Shirley S Condon SM Chunduru SK McKinlay MA Vaux DL Silke J Day CL 《The Journal of biological chemistry》2011,286(19):17015-17028
The inhibitor of apoptosis (IAP) proteins are important ubiquitin E3 ligases that regulate cell survival and oncogenesis. The cIAP1 and cIAP2 paralogs bear three N-terminal baculoviral IAP repeat (BIR) domains and a C-terminal E3 ligase RING domain. IAP antagonist compounds, also known as Smac mimetics, bind the BIR domains of IAPs and trigger rapid RING-dependent autoubiquitylation, but the mechanism is unknown. We show that RING dimerization is essential for the E3 ligase activity of cIAP1 and cIAP2 because monomeric RING mutants could not interact with the ubiquitin-charged E2 enzyme and were resistant to Smac mimetic-induced autoubiquitylation. Unexpectedly, the BIR domains inhibited cIAP1 RING dimerization, and cIAP1 existed predominantly as an inactive monomer. However, addition of either mono- or bivalent Smac mimetics relieved this inhibition, thereby allowing dimer formation and promoting E3 ligase activation. In contrast, the cIAP2 dimer was more stable, had higher intrinsic E3 ligase activity, and was not highly activated by Smac mimetics. These results explain how Smac mimetics promote rapid destruction of cIAP1 and suggest mechanisms for activating cIAP1 in other pathways. 相似文献
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The mammalian pyruvate dehydrogenase complex (PDC) is a mitochondrial multienzyme complex that connects glycolysis to the tricarboxylic acid cycle by catalyzing pyruvate oxidation to produce acetyl-CoA, NADH, and CO2. This reaction is required to aerobically utilize glucose, a preferred metabolic fuel, and is composed of three core enzymes: pyruvate dehydrogenase (E1), dihydrolipoyl transacetylase (E2), and dihydrolipoyl dehydrogenase (E3). The pyruvate-dehydrogenase-specific kinase (PDK) and pyruvate-dehydrogenase-specific phosphatase (PDP) are considered the main control mechanism of mammalian PDC activity. However, PDK and PDP activity are allosterically regulated by several effectors fully overlapping PDC substrates and products. This collection of positive and negative feedback mechanisms confounds simple predictions of relative PDC flux, especially when all effectors are dynamically modulated during metabolic states that exist in physiologically realistic conditions, such as exercise. Here, we provide, to our knowledge, the first globally fitted, pH-dependent kinetic model of the PDC accounting for the PDC core reaction because it is regulated by PDK, PDP, metal binding equilibria, and numerous allosteric effectors. The model was used to compute PDH regulatory complex flux as a function of previously determined metabolic conditions used to simulate exercise and demonstrates increased flux with exercise. Our model reveals that PDC flux in physiological conditions is primarily inhibited by product inhibition (~60%), mostly NADH inhibition (~30–50%), rather than phosphorylation cycle inhibition (~40%), but the degree to which depends on the metabolic state and PDC tissue source. 相似文献
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