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Akira Nagatani 《Journal of plant research》1997,110(1):123-130
Phytochromes are chromoproteins which mediate several light responses in plants. Phytochrome proteins are encoded by a gene
family which is currently being characterized in several plant species. Analysis of type-specific mutants of two well-characterized
members of the family, PhyA and PhyB, indicates that these proteins have distinct functions. Much remains to be learned about
the mechanisms by which the phytochromes carry out their distinct and diverse functions. It is hoped that information concerning
the localization of phytochromes, at the whole plant and subcellular levels, will aid in elucidating the mechanism of phytochrome
function. This review, which summarizes information about phytochrome distribution, has an emphasis on recent reports in which
the molecular species of phytochrome are differentiated. However, classical data are also included and reinterpreted using
knowledge of the phytochrome family. 相似文献
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A simple phosphorescence method is proposed for quercetin detection based on Al3+-amplified room-temperature phosphorescence (RTP) signals of 3-mercaptopropionic acid (MPA)-capped Mn-doped ZnS quantum dots (QDs). The sensor was established based on some properties as follows. Al3+ can interact with carboxyl groups on the surface of MPA-capped Mn-doped ZnS QDs via chelation, which will lead to the aggregation of QDs and amplification of RTP signals, After the addition of quercetin, it can form more stable complex with Al3+ in alkaline aqueous solution and dissociate Al3+ from the surface of Mn-doped ZnS QDs, which will result in significant recovery of RTP intensity of the MPA-capped Mn-doped ZnS–Al3+ system. Under the optimized conditions, the change of RTP intensity was proportional to the concentration of quercetin in the range from 0.1 to 6.0 mg L−1, with a high correlation coefficient of 0.996 and a detection limit of 0.047 mg L−1. The proposed method is potentially suitable for detection of quercetin in real samples without complicated pretreatment. 相似文献
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Abstract Resting cells of the fission yeast Schizosaccharomyces pombe , suspended in buffer with glucose, responded to the addition of asparagine by increasing trehalase activity. This response was preceded by a peak in cAMP concentration. The addition of the nitrogen source to resting cells, devoid of the catalytic subunit of cAMP-dependent protein kinase, produced the transient increase in cAMP but did not promote any change in trehalase activity. In the budding yeast Pachysolen iannophilus , the activation of trehalase by nitrogen source was also accompanied by a sharp peak in cAMP. These results suggest that in the two yeasts cAMP acts as a second messenger in the transduction of the nitrogen-source-induced signal causing the activation of trehalase. 相似文献
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M. Graciela Pucciarelli S. Ruschkowski T.J. Trust B.B. Finlay 《FEMS microbiology letters》1995,129(2-3):293-399
Abstract Helicobacter pylori is a bacterial pathogen of humans that infects the gastric mucosa. This infection has been associated with gastritis, peptic ulcers, and gastric carcinomas. Diverse in vitro studies have described efficient adherence of H. pylori to different types of epithelial cells. Because of its varied effects on host cells, we have analysed signal transduction events in H. pyfori -infected epithelial cells. Our results show that H. pylori induces an increase in inositol phosphates in all cultured epithelial cells used, including HeLa, Henle 407, Hep-2, and the human gastric adenocarcinoma cell line AGS. Bacterial growth medium supernatants induce a similar response in the host cell. The increase in inositol phosphates is not related to redistribution of cytoskeletal proteins such as actin or α-actinin nor tyrosine-phosphorylation of host cell proteins. The inositol phosphate increase is also observed in cells infected with low or non-adherent H. pylori mutants or mutants defective in the vacuolating toxin or urease holoenzyme. These results indicate that inositol phosphate release in H. pytori -infected cells is not dependent on bacterial adherence, and that a soluble bacterial factor, but not the vacuolating toxin or urease holoenzyme, mediates such an effect. 相似文献
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Second messengers are small rapidly diffusing molecules or ions that relay signals between receptors and effector proteins to produce a physiological effect. Lipid messengers constitute one of the four major classes of second messengers. The hydrolysis of two main classes of lipids, glycerophospholipids and sphingolipids, generate parallel profiles of lipid second messengers: phosphatidic acid (PA), diacylglycerol (DAG), and lysophosphatidic acid versus ceramide, ceramide-1-phosphate, sphingosine, and sphingosine-1-phosphate, respectively. In this review, we examine the mechanisms by which these lipid second messengers modulate aldosterone production at multiple levels. Aldosterone is a mineralocorticoid hormone responsible for maintaining fluid volume, electrolyte balance, and blood pressure homeostasis. Primary aldosteronism is a frequent endocrine cause of secondary hypertension. A thorough understanding of the signaling events regulating aldosterone biosynthesis may lead to the identification of novel therapeutic targets. The cumulative evidence in this literature emphasizes the critical roles of PA, DAG, and sphingolipid metabolites in aldosterone synthesis and secretion. However, it also highlights the gaps in our knowledge, such as the preference for phospholipase D-generated PA or DAG, as well as the need for further investigation to elucidate the precise mechanisms by which these lipid second messengers regulate optimal aldosterone production. 相似文献
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Ross A. Robinson Samuel C. Griffiths Lieke L. van de Haar Tomas Malinauskas Eljo Y. van Battum Pavol Zelina Rebekka A. Schwab Dimple Karia Lina Malinauskaite Sara Brignani Marleen H. van den Munkhof Özge Düdükcü Anna A. De Ruiter Dianne M.A. Van den Heuvel Benjamin Bishop Jonathan Elegheert A. Radu Aricescu R. Jeroen Pasterkamp Christian Siebold 《Cell》2021,184(8):2103-2120.e31
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A. Rogel Y. Bromberg O. Sperling E. Zoref-Shani 《Nucleosides, nucleotides & nucleic acids》2013,32(9-11):1283-1286
We have demonstrated before that exposure of neuronal cultures to poisoning by iodoacetic acid (IAA) followed by “reperfusion” (IAA-R insult), results in severe cytotoxicity, which could be markedly attenuated by prior activation of the adenosine A1 receptors. We also have demonstrated that adenosine activates a signal transduction pathway (STP), which involves activation of PKCε and opening of KATP channels. Here, we provide proof for the involvement also of phospholipase C (PLC) in the neuronal protective adenosine-activated STP. R-PIA, a specific A1 adenosine receptor agonist, was found to enhance neuronal PLC activity and protect against the IAA-R insult. The PLC inhibitor U73122, abrogated both R-PIA-induced effects. These results demonstrate that activation of PLC is a vital step in the neuronal protective adenosine-induced STP. 相似文献