微生物水泥相关酶的研究进展

微生物诱导碳酸钙沉积(microbial induced calcium carbonate precipitation,MICP)是微生物通过新陈代谢在其周围微环境中形成碳酸钙沉积的一种自然现象,根据其原理目前研发出了"微生物水泥".因其具有绿色环保、经济高效的特点,已成为生物、土木、环境等领域的研究热点.文中就与微...     

The role of Abeta peptides in Alzheimer's disease

The Abeta peptide has been identified as central to the onset and development of Alzheimer's disease (AD) and several hypotheses about toxicity involving Abeta peptides have been proposed including mechanisms of oxidative stress and disruption of calcium homeostasis. The biology, structure and physical properties of Abeta peptides are discussed, as well as existing therapeutics and future strategies for the treatment of AD.     

Calcium: just a chemical switch?

The calcium-signature hypothesis has evolved as a concept to explain specificity in signaling pathways that utilise calcium as a second messenger. In plant biology, this hypothesis was purely conceptual and based only upon correlative observations until recently. In the past few years, however, empirical data have emerged from experiments that were specifically designed to tackle the question of how specificity is encoded by calcium. In light of the attractive calcium-signature hypothesis, other potential explanations for signalling specificity have been overshadowed and ignored: it has been assumed that the calcium-signature dogma will explain all plant calcium signaling. However, there is a good deal of evidence supporting a counter-hypothesis in which calcium does not itself encode specificity but is merely an essential 'switch' in signaling. At the very least, both hypotheses are likely to be true in different situations, and it may well be that the calcium-signature hypothesis describes the exception rather than the rule.     

The mitochondrial permeability transition pore: an evolving concept critical for cell life and death

In this review, we summarize current knowledge of perhaps one of the most intriguing phenomena in cell biology: the mitochondrial permeability transition pore (mPTP). This phenomenon, which was initially observed as a sudden loss of inner mitochondrial membrane impermeability caused by excessive calcium, has been studied for almost 50 years, and still no definitive answer has been provided regarding its mechanisms. From its initial consideration as an in vitro artifact to the current notion that the mPTP is a phenomenon with physiological and pathological implications, a long road has been travelled. We here summarize the role of mitochondria in cytosolic calcium control and the evolving concepts regarding the mitochondrial permeability transition (mPT) and the mPTP. We show how the evolving mPTP models and mechanisms, which involve many proposed mitochondrial protein components, have arisen from methodological advances and more complex biological models. We describe how scientific progress and methodological advances have allowed milestone discoveries on mPTP regulation and composition and its recognition as a valid target for drug development and a critical component of mitochondrial biology.     

Genetic Analysis of Voltage-Dependent Calcium Channels

Molecular cloning of calcium channel subunit genes has identified an unexpectedly large number of genes and splicing variants, and a central problem of calcium channel biology is to now understand the functional significance of this genetic complexity. While electrophyisological, pharmacological, and molecular cloning techniques are providing one level of understanding, a complete understanding will require many additional kinds of studies, including genetic studies done in intact animals. In this regard, an intriguing variety of episodic diseases have recently been identified that result from defects in calcium channel genes. A study of these diseases illustrates the kind of insights into calcium channel function that can be expected from this method of inquiry.     

The evolution of calcium biochemistry

The role of calcium in evolution is best understood from a perspective based on its intrinsic value as a divalent cation able to bind and precipitate inorganic and organic anions rapidly. This binding can be useful or inhibitory. Now treatment of binding or precipitation has two different interests in biological cells. The first is thermodynamic, that is the stress is on systems biology and the second is structure, that is molecular biology. In evolution both have equal weight being connected through exchange. This paper outlines first the systems biology of the evolution of calcium functions from prokaryotes to animals with brains. The calcium ion was the only good available candidate in the environment for the functions it performs. The second section of the paper describes the evolution of the proteins which allow the messenger function. We have discussed elsewhere the structure/function relationships of the proteins. Overall the evolving and increasing involvement of calcium as possibly the major control messenger of events outside cells to action inside them is an inevitable feature of the nature of ecological, that is environmental/organism, evolution.     

Maintenance of normal serum calcium level in the hyperprolactinaemic rat.

The effect of experimentally induced chronic hyperprolactinaemia in male rats on the serum levels of calcium has been examined. Chronic elevation of circulating prolactin levels had no significant effect on the serum calcium levels and normal blood calcium homeostasis was still maintained.     

The cellular and molecular basis of store-operated calcium entry

The impact of calcium signalling on so many areas of cell biology reflects the crucial role of calcium signals in the control of diverse cellular functions. Despite the precision with which spatial and temporal details of calcium signals have been resolved, a fundamental aspect of the generation of calcium signals -- the activation of 'store-operated channels' (SOCs) -- remains a molecular and mechanistic mystery. Here we review new insights into the exchange of signals between the endoplasmic reticulum (ER) and plasma membrane that result in activation of calcium entry channels mediating crucial long-term calcium signals.     

In Vivo Analysis of Voltage-Dependent Calcium Channels

The molecular cloning of calcium channel subunits has identified an unexpectedly large number of genes and splicing variants, many of whichhave complex expression patterns: a central problem of calcium channel biology is to understand the functional significance of this genetic complexity. The genetic analysis of voltage-dependent calcium channels (VDCCs) provides an approach to defining channel function that is complimentary to pharmacological, electrophysiological, and other molecular methods. By discovering or creating alleles of VDCC genes, one can gain an understanding of the VDCC function at the whole animal level. Of particular interest are mutations in the alpha1 genes that encode the pore forming subunits, as they define the specific channel subtypes. In fact, a variety of calcium channelopathies and targeted mutations have been described for these genes in the last 6 years. The mutant alleles described below illustrate how phenotype analysis of these alleles has uncovered very specific functional roles that can be localized to specific synapses or cells.     

Capacitative calcium entry: sensing the calcium stores

A long-standing mystery in the cell biology of calcium channel regulation is the nature of the signal linking intracellular calcium stores to plasma membrane capacitative calcium entry channels. An RNAi-based screen of selected Drosophila genes has revealed that a calcium-binding protein, stromal interaction molecule (STIM), plays an essential role in the activation of these channels and may be the long sought sensor of calcium store content.     

Writing and speaking: communication for biologists

A workshop for university biology teachers examined the teaching to undergraduates of writing and speaking. There was agreement that the communication of results and ideas was an integral part of scientific method. Proposals for the teaching of different aspects of communication during the undergraduate course are given and an Appendix lists some material which has been used with, and found suitable for biology students.     

Role of proton gradients and vacuola H(+)-ATPases in the refilling of intracellular calcium stores in exocrine cells

Numerous hormones and neurotransmitters activate cells by increasing cytosolic calcium concentration ([Ca(2+)](i)), a key regulatory factor for many cellular processes. A pivotal feature of these Ca(2+) signals is the release of Ca(2+) from intracellular stores, which is followed by activation of extracellular calcium influx, allowing refilling of the stores by SERCA pumps associated with the endoplasmic reticulum. Although the mechanisms of calcium release and calcium influx have been extensively studied, the biology of the Ca(2+) stores is poorly understood. The presence of heterogeneous calcium pools in cells has been previously reported [1] [2] [3]. Although recent technical improvements have confirmed this heterogeneity [4], knowledge about the mechanisms underlying Ca(2+) transport within the stores is very scarce and rather speculative. A recent study in polarized exocrine cells [5] has revealed the existence of Ca(2+) tunneling from basolateral stores to luminal pools, where Ca(2+) is initially released upon cell activation. Here, we present evidence that, during stimulation, Ca(2+) transported into basolateral stores by SERCA pumps is conveyed toward the luminal pools driven by proton gradients generated by vacuolar H(+)-ATPases. This finding unveils a new aspect of the machinery of Ca(2+) stores.     

钙在植物花发育过程中的作用

对于园林观赏植物,开花是一个非常重要的发育阶段,它直接影响花卉的品质。近年来,植物花发育的分子生物学研究进展迅速,并取得了一些突破性成果。钙作为第二信使在植物信号转导中起着非常重要的作用,大量研究显示,钙有可能参与开花控制。本文总结了钙信号与植物花发育这一领域的最新研究进展,包括以下几个方面的内容：钙在植物成花诱导(包括光周期诱导和低温诱导)中的作用;花芽分化时期钙在植物叶芽和花芽中的动态分布及组织培养条件下不同钙浓度对花芽分化的影响;钙与花衰老的关系。     

钙在植物花发育过程中的作用

对于园林观赏植物,开花是一个非常重要的发育阶段,它直接影响花卉的品质。近年 来,植物花发育的分子生物学研究进展迅速,并取得了一些突破性成果。钙作为第二信使在植物信号转导中起着非常重要的作用,大量研究显示,钙有可能参与开花控制。本文总结了钙信号与植物花发育这一领域的最新研究进展,包括以下几个方面的内容：钙在植物成花诱 导（包括光周期诱导和低温诱导）中的作用;花芽分化时期钙在植物叶芽和花芽中的动态分布及组织培养条件下不同钙浓度对花芽分化的影响;钙与花衰老的关系。      

A reexamination of the chelex competitive calcium binding assay

The chelex competitive calcium binding assay has been examined as a tool for the analysis of the kinetic parameters of calcium binding substances. Scatchard analysis of calcium binding demonstrates that chelex binds calcium with apparent negative cooperativity or with more than one class of calcium binding sites, and therefore, cannot be used to provide accurate estimations of the dissociation constant or total number of binding sites on an unknown ligand. Results presented in this study indicate that the chelex assay can be effectively used for the qualitative detection of calcium binding substances in tissue extracts or biological fluids.     

Mitochondria in health and disease: perspectives on a new mitochondrial biology

The integrity of mitochondrial function is fundamental to cell life. It follows that disturbances of mitochondrial function will lead to disruption of cell function, expressed as disease or even death. In this review, I consider recent developments in our knowledge of basic aspects of mitochondrial biology as an essential step in developing our understanding of the contributions of mitochondria to disease. The identification of novel mechanisms that govern mitochondrial biogenesis and replication, and the delicately poised signalling pathways that coordinate the mitochondrial and nuclear genomes are discussed. As fluorescence imaging has made the study of mitochondrial function within cells accessible, the application of that technology to the exploration of mitochondrial bioenergetics is reviewed. Mitochondrial calcium uptake plays a major role in influencing cell signalling and in the regulation of mitochondrial function, while excessive mitochondrial calcium accumulation has been extensively implicated in disease. Mitochondria are major producers of free radical species, possibly also of nitric oxide, and are also major targets of oxidative damage. Mechanisms of mitochondrial radical generation, targets of oxidative injury and the potential role of uncoupling proteins as regulators of radical generation are discussed. The role of mitochondria in apoptotic and necrotic cell death is seminal and is briefly reviewed. This background leads to a discussion of ways in which these processes combine to cause illness in the neurodegenerative diseases and in cardiac reperfusion injury. The demands of mitochondria and their complex integration into cell biology extends far beyond the provision of ATP, prompting a radical change in our perception of mitochondria and placing these organelles centre stage in many aspects of cell biology and medicine.     

Priming of calcium mobilization in human neutrophils by granulocyte-macrophage colony-stimulating factor: Evidence for an involvement of phospholipase D-derived phosphatidic acid

Human neutrophils pre-incubated with granulocyte-macrophage-colony-stimulating factor (GM-CSF) exhibit an enhanced mobilization of calcium in response to secondary stimuli such as chemotactic factors. The mechanisms underlying this priming effect of GM-CSF were examined. It was first demonstrated that the additional calcium mobilized by chemotactic factors in GM-CSF-treated cells was derived from intracellular stores and was associated neither with an increased permeability to calcium nor with production of inositol 1,4,5-trisphosphate. These results indicated that GM-CSF called upon a novel mechanism in order to enhance the mobilization of calcium in human neutrophils. The growth factor has recently been shown to prime phospholipase D leading to an enhanced activation by chemotactic factors and an augmented production of phosphatidic acid. Furthermore the ability of exogenous phosphatidic acid to mobilize calcium in cell types other than neutrophils has been previously demonstrated. Therefore, we examined the potential involvement of phospholipase D in the priming of the calcium response by GM-CSF in human neutrophils. Inhibition of the production of the fMet-Leu-Phe-stimulated production of phosphatidic acid by ethanol or wortmannin had only marginal effects on the concurrent mobilization of calcium. However, the priming of the mobilization of calcium by GM-CSF was greatly decreased in cells treated with either ethanol or wortmannin. These results provide strong support for the hypothesis that the production of phosphatidic acid, which is enhanced in GM-CSF-treated cells, is linked to an increased mobilization of intracellular calcium. These results may have relevance to the mechanism of action of GM-CSF in mature haematopoeitic cells as well to the mitogenic activity of other growth factors.     

A method for estimation of drug affinity constants to the open conformational state of calcium channels.

The affinity of D600 to calcium channels in the open state has been examined in isolated smooth muscle cells of the rabbit ear artery. Calcium channel currents were measured in high external barium solution by means of the patch-clamp technique. The current inhibition in various D600 concentrations (3-100 microM) on application of trains of short test pulses (20-80 ms) has been studied in nonmodified calcium channels and in cells where the calcium channels were modified by the agonist dihydropyridine (+) 202,791 (100 nM). The kinetics of the peak current decay has been analyzed with a mathematical model which is based on the experimental finding that D600 interacts primarily with calcium channels in the open conformational state. The model approach allows the estimation of drug affinity constants of D600 to the calcium channel in the open conformation. An association rate constant to the open conformational state of D600 of 6.16 x 10(4) M-1 s-1 was estimated. The association rate of the drug was not significantly changed after the calcium channels have been modified with 100 nM (+) 202,791. A method for correction of rate constants for possible drug trapping is discussed.     

Calcium ions are involved in the delay of plant cell cycle progression by abiotic stresses

Higher plants respond to environmental stresses by a sequence of reactions which include the reduction of growth by affecting cell division. It has been shown that calcium ions plays a role as a second messenger in mediating various defence responses under environmental stresses. In this study, the role of calcium ions on cell cycle progression under abiotic stresses has been examined in tobacco BY-2 suspension culture cells. Using synchronized BY-2 cells expressing the endogenous calcium sensor aequorin as experimental system, we could show that oxidative and hypoosmotic stress both induce an increase of intracellular calcium and cause a delay of the cell cycle. The inhibitory effect of these abiotic stress stimuli on cell cycle progression could be mimicked by increasing the intracellular calcium concentration via application of an external electrical field. Likewise, depletion of calcium ions in the culture medium suppressed the effect of the stimuli tested. These results demonstrate that calcium signalling is involved in the regulation of cell cycle progression in response to abiotic stress.