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961.
962.
Chlorophylls are the most abundant classes of natural pigments and their biosynthesis is therefore a major metabolic activity in the ecosphere. Two pathways exist for chlorophyll biosynthesis, one taking place in darkness and the other requiring continuous light as a precondition. The key process for Chl synthesis is the reduction of protochlorophyllide (Pchlide). This enzymatic reaction is catalysed by two different enzymes — DPOR (dark-operative Pchlide oxidoreductase) or the structurally distinct LPOR (light-dependent Pchlide oxidoreductase). DPOR which consists of three subunits encoded by three plastid genes in eukaryotes was subject of our study. A short overview of our present knowledge of chlorophyll biosynthesis in Chlamydomonas reinhardtii in comparison with other plants is presented. Presented at the International Symposium Biology and Taxonomy of Green Algae V, Smolenice, June 26–29, 2007, Slovakia.  相似文献   
963.
Net CO2 flux measurements conducted during the summer and winter of 1994–96 were scaled in space and time to provide estimates of net CO2 exchange during the 1995–96 (9 May 1995–8 May 1996) annual cycle for the Kuparuk River Basin, a 9200 km2 watershed located in NE Alaska. Net CO2 flux was measured using dynamic chambers and eddy covariance in moist‐acidic, nonacidic, wet‐sedge, and shrub tundra, which comprise 95% of the terrestrial landscape of the Kuparuk Basin. CO2 flux data were used as input to multivariate models that calculated instantaneous and daily rates of gross primary production (GPP) and whole‐ecosystem respiration (R) as a function of meteorology and ecosystem development. Net CO2 flux was scaled up to the Kuparuk Basin using a geographical information system (GIS) consisting of a vegetation map, digital terrain map, dynamic temperature and radiation fields, and the models of GPP and R. Basin‐wide estimates of net CO2 exchange for the summer growing season (9 May?5 September 1995) indicate that nonacidic tundra was a net sink of ?31.7 ± 21.3 GgC (1 Gg = 109 g), while shrub tundra lost 32.5 ± 6.3 GgC to the atmosphere (negative values denote net ecosystem CO2 uptake). Acidic and wet sedge tundra were in balance, and when integrated for the entire Kuparuk River Basin (including aquatic surfaces), whole basin summer net CO2 exchange was estimated to be in balance (?0.9 ± 50.3 GgC). Autumn to winter (6 September 1995–8 May 1996) estimates of net CO2 flux indicate that acidic, nonacidic, and shrub tundra landforms were all large sources of CO2 to the atmosphere (75.5 ± 8.3, 96.4 ± 11.4, and 43.3 ± 4.7 GgC for acidic, nonacidic, and shrub tundra, respectively). CO2 loss from wet sedge surfaces was not substantially different from zero, but the large losses from the other terrestrial landforms resulted in a whole basin net CO2 loss of 217.2 ± 24.1 GgC during the 1995–96 cold season. When integrated for the 1995–96 annual cycle, acidic (66.4 + 25.25 GgC), nonacidic (64.7 ± 29.2 GgC), and shrub tundra (75.8 ± 8.4 GgC) were substantial net sources of CO2 to the atmosphere, while wet sedge tundra was in balance (0.4 + 0.8 GgC). The Kuparuk River Basin as a whole was estimated to be a net CO2 source of 218.1 ± 60.6 GgC over the 1995–96 annual cycle. Compared to direct measurements of regional net CO2 flux obtained from aircraft‐based eddy covariance, the scaling procedure provided realistic estimates of CO2 exchange during the summer growing season. Although winter estimates could not be assessed directly using aircraft measurements of net CO2 exchange, the estimates reported here are comparable to measured values reported in the literature. Thus, we have high confidence in the summer estimates of net CO2 exchange and reasonable confidence in the winter net CO2 flux estimates for terrestrial landforms of the Kuparuk river basin. Although there is larger uncertainty in the aquatic estimates, the small surface area of aquatic surfaces in the Kuparuk river basin (≈ 5%) presumably reduces the potential for this uncertainty to result in large errors in basin‐wide CO2 flux estimates.  相似文献   
964.
The phytoplankton and ice algal assemblages in the SiberianLaptev Sea during the autumnal freeze-up period of 1995 aredescribed. The spatial distribution of algal taxa (diatoms,dinoflagellates, chrysophytes, chlorophytes) in the newly formedice and waters at the surface and at 5 m depth differed considerablybetween regions. This was also true for algal biomass measuredby in situ fluorescence, chlorophyll (Chl) a and taxon-specificcarbon content. Highest in situ fluorescence and Chl a concentrations(ranging from 0.1 to 3.2 µg l–1) occurred in surfacewaters with maxima in Buor Khaya Bay east of Lena Delta. Thealgal standing stock on the shelf consisted mainly of diatoms,dinoflagellates, chrysophytes and chlorophytes with a totalabundance (excluding unidentified flagellates <10 µm)in surface waters of 351–33 660 cells l–1. Highestalgal abundance occurred close to the Lena Delta. Phytoplanktonbiomass (phytoplankton carbon; PPC) ranged from 0.1 to 5.3 µgC l–1 in surface waters and from 0.3 to 2.1 µg Cl–1 at 5 m depth, and followed the distribution patternof abundances. However, the distribution of Chl a differed considerablyfrom the distribution pattern shown by PPC. The algal assemblagein the sea ice, which could not be quantified due to high sedimentload, was dominated by diatom species, accompanied by dinoflagellates.Thus, already during the early stage of autumnal freeze-up,incorporation processes, selective enrichment and subsequentgrowth lead to differences between surface water and sea icealgal assemblages.  相似文献   
965.

Background

The design of anticancer metallodrugs is currently focused on platinum complexes which form on DNA major adducts that cannot readily be removed by DNA repair systems. Hence, antitumor azolato-bridged dinuclear PtII complexes, such as [{cis-Pt(NH3)2}2(μ‐OH)(μ-pyrazolate)]2+ (AMPZ), have been designed and synthesized. These complexes exhibit markedly higher toxic effects in tumor cell lines than mononuclear conventional cisplatin.

Methods

Biophysical and biochemical aspects of the alterations induced in short DNA duplexes uniquely and site-specifically modified by the major DNA adduct of AMPZ, namely 1,2-GG intrastrand cross-links, were examined. Attention was also paid to conformational distortions induced in DNA by the adducts of AMPZ and cisplatin, associated alterations in the thermodynamic stability of the duplexes, and recognition of these adducts by high-mobility-group (HMG) domain proteins.

Results

Chemical probing of DNA conformation, DNA bending studies and translesion synthesis by DNA polymerase across the platinum adduct revealed that the distortion induced in DNA by the major adduct of AMPZ was significantly less pronounced than that induced by similar cross-links from cisplatin. Concomitantly, the cross-link from AMPZ reduced the thermodynamic stability of the modified duplex considerably less. In addition, HMGB1 protein recognizes major DNA adducts of AMPZ markedly less than those of cisplatin.

General significance

The experimental evidence demonstrates why the major DNA adducts of the new anticancer azolato-bridged dinuclear PtII complexes are poor substrates for DNA repair observed in a previously published report. The relative resistance to DNA repair explains why these platinum complexes show major pharmacological advantages over cisplatin in tumor cells.  相似文献   
966.
967.
968.
969.
Bone morphogenetic proteins (BMPs), a subset of the transforming growth factor (TGF)-beta superfamily, regulate a diverse array of cellular functions during development and in the adult. BMP-9 (also known as growth and differentiation factor (GDF)-2) potently induces osteogenesis and chondrogenesis, has been implicated in the differentiation of cholinergic neurons, and may help regulate glucose metabolism. We have determined the structure of BMP-9 to 2.3 A and examined the differences between our model and existing crystal structures of other BMPs, both in isolation and in complex with their receptors. TGF-beta ligands are translated as precursors, with pro-regions that generally dissociate after cleavage from the ligand, but in some cases (including GDF-8 and TGF-beta1, -2, and -3), the pro-region remains associated after secretion from the cell and inhibits binding of the ligand to its receptor. Although the proregion of BMP-9 remains tightly associated after secretion, we find, in several cell-based assays, that the activities of BMP-9 and BMP-9.pro-region complex were equivalent. Activin receptor-like kinase 1 (ALK-1), an orphan receptor in the TGF-beta family, was also identified as a potential receptor for BMP-9 based on surface plasmon resonance studies (BIAcore) and the ability of soluble ALK-1 to block the activity of BMP-9.pro-region complex in cell-based assays.  相似文献   
970.
Given the modulatory role of neuropeptide Y (NPY) in the immune system, we investigated the effect of NPY on the production of NO and IL-1β in microglia. Upon LPS stimulation, NPY treatment inhibited NO production as well as the expression of inducible nitric-oxide synthase (iNOS). Pharmacological studies with a selective Y(1) receptor agonist and selective antagonists for Y(1), Y(2), and Y(5) receptors demonstrated that inhibition of NO production and iNOS expression was mediated exclusively through Y(1) receptor activation. Microglial cells stimulated with LPS and ATP responded with a massive release of IL-1β, as measured by ELISA. NPY inhibited this effect, suggesting that it can strongly impair the release of IL-1β. Furthermore, we observed that IL-1β stimulation induced NO production and that the use of a selective IL-1 receptor antagonist prevented NO production upon LPS stimulation. Moreover, NPY acting through Y(1) receptor inhibited LPS-stimulated release of IL-1β, inhibiting NO synthesis. IL-1β activation of NF-κB was inhibited by NPY treatment, as observed by confocal microscopy and Western blotting analysis of nuclear translocation of NF-κB p65 subunit, leading to the decrease of NO synthesis. Our results showed that upon LPS challenge, microglial cells release IL-1β, promoting the production of NO through a NF-κB-dependent pathway. Also, NPY was able to strongly inhibit NO synthesis through Y(1) receptor activation, which prevents IL-1β release and thus inhibits nuclear translocation of NF-κB. The role of NPY in key inflammatory events may contribute to unravel novel gateways to modulate inflammation associated with brain pathology.  相似文献   
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