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1.
Nadia Kallala Wissal M’sehli Karima Jelali Marwa Batnini Mounawer Badri Issam Nouairi Haythem Mhadhbi 《Plant Species Biology》2019,34(3):95-109
Iron (Fe) deficiency is one of the major environmental stresses affecting plant production in the world. The selection of tolerant genotypes is considered an effective remediation strategy for this stress. The present study was carried out in order to investigate the biodiversity within Medicago truncatula plants in response to Fe deficiency, to identify tolerant genotypes and to assess the main tolerance mechanisms. To do this, a screening test was performed on 20 M. truncatula genotypes cultivated in minimal medium. Biometric and physiological markers were analyzed, including plant biomass, chlorophyll and root architecture. Results showed a biodiversity among the 20 genotypes. Interestingly, Fe deficiency tolerance was highest in TN8.20 and A17 genotypes. However, the lowest tolerance behavior was observed in TN1.11 and TN6.18. In order to investigate the main tolerance mechanisms, an experiment was conducted in the hydroponic system on already selected genotypes. Assessment of Fe deficiency tolerance was performed mainly on plant growth parameters, Fe (III)-chelate-reductase activity, rhizosphere acidification and antioxidant system defense. The relative better tolerance of A17 and TN8.20 to Fe deficiency was positively correlated with their capacity to maintain higher Fe-acquisition efficiency in roots via rhizosphere acidification and the stimulation of Fe (III)-chelate-reductase activity. Moreover, tolerant genotypes showed the lowest decreases in chlorophyll content and photosynthetic activity (CO2 assimilation) compared to the sensitive ones. The efficiency of antioxidant capacity of the tolerant genotypes was revealed in stimulation of catalase (CAT) and peroxidase (POX) activities as well as accumulation of polyphenols, leading to the maintenance of cell integrity under Fe deficiency. 相似文献
2.
Sara L. Payne Sonsoles Rodriguez-Aristegui Julia Bardos Céline Cano Bernard T. Golding Ian R. Hardcastle Marcus Peacock Nahida Parveen Roger J. Griffin 《Bioorganic & medicinal chemistry letters》2010,20(12):3649-3653
Replacement of the core heterocycle of a defined series of chromen-4-one DNA-PK inhibitors by the isomeric chromen-2-one (coumarin) and isochromen-1-one (isocoumarin) scaffolds was investigated. Structure–activity relationships for DNA-PK inhibition were broadly consistent, albeit with a reduction of potency compared with the parent chromenone. 相似文献
3.
Erik J.B. Landin Christopher Williams Sara A. Ryan Alice Bochel Nahida Akter Christina Redfield Richard B. Sessions Neesha Dedi Richard J. Taylor Matthew P. Crump 《The Journal of biological chemistry》2021,297(6)
The α1-acid glycoprotein (AGP) is an abundant blood plasma protein with important immunomodulatory functions coupled to endogenous and exogenous ligand-binding properties. Its affinity for many drug-like structures, however, means AGP can have a significant effect on the pharmokinetics and pharmacodynamics of numerous small molecule therapeutics. Staurosporine, and its hydroxylated forms UCN-01 and UCN-02, are kinase inhibitors that have been investigated at length as antitumour compounds. Despite their potency, these compounds display poor pharmokinetics due to binding to both AGP variants, AGP1 and AGP2. The recent renewed interest in UCN-01 as a cytostatic protective agent prompted us to solve the structure of the AGP2–UCN-01 complex by X-ray crystallography, revealing for the first time the precise binding mode of UCN-01. The solution NMR suggests AGP2 undergoes a significant conformational change upon ligand binding, but also that it uses a common set of sidechains with which it captures key groups of UCN-01 and other small molecule ligands. We anticipate that this structure and the supporting NMR data will facilitate rational redesign of small molecules that could evade AGP and therefore improve tissue distribution. 相似文献
4.
In this article we report Eu3+ luminescence in novel K3Ca2(SO4)3Cl phosphors prepared by wet chemical methods. The Eu3+ emission was observed at 594 nm and 615 nm, keeping the excitation wavelength constant at 396 nm nearer to light‐emitting diode excitation, Furthermore, phosphors were characterized by X‐ray diffraction for the confirmation of crystallinity. The variation of the photoluminescence intensity with impurity concentration has also been discussed. Thus, prominent emission in the red region makes prepared phosphors more applicable for white light‐emitting diodes. Copyright © 2013 John Wiley & Sons, Ltd. 相似文献
5.
Nahida Haddam Sekkal Samira Xavier Dumont Abdesselem Taleb Vincent Haufroid Dominique Lison 《Biomarkers》2013,18(5):292-298
Serum Clara cell protein (CC16) and surfactant-associated protein D (SP-D) were measured in 161 workers exposed to sulphur dioxide (SO2) in a non-ferrous smelter. Seventy workers from a blanket manufacture served as referents. Exposure to SO2 and tobacco smoking were associated with a decrease of CC16 and an increase of SP-D in serum. Tobacco smoking and exposure SO2 interacted synergistically to decrease serum CC16 but not to increase serum SP-D. While further illustrating the potential of serum CC16 and SP-D, our study confirms that SO2 can cause airways damage at exposure levels below current occupational exposure limits. 相似文献
6.
Banu NA Daly RS Buda A Moorghen M Baker J Pignatelli M 《Cell communication & adhesion》2011,18(1-2):1-8
Cyclooxygenase (COX)-2 is a key molecular target of colon cancer prevention. However, the mechanisms by which COX-2 inhibitors confer protective effects against tumour development are not completely understood. The aim of this study was to elucidate the effects of NS-398 in the 1,2-dimethylhydrazine (DMH) mouse model with respect to alteration in the expression of COX-2 and E-cadherin-catenin complex. Alterations in cell proliferation, apoptosis, and vascular density were investigated. NS-398 showed reduced COX-2 immunoreactivity in adenomas with a decrease in vascular density in non-dysplastic mucosa. Adenomas revealed increased E-cadherin and beta-catenin reactivity. NS-398 reduced the percentages of tumour cells with nuclear localisation of beta-catenin and cyclin D1. Bromodeoxyuridine (BrdUrd) index in adenomas was significantly higher in untreated animals. NS-398 resulted in significant increase in apoptosis in adenomas. Our results suggest a protective role of NS-398 on tumour development associated with reduced COX-2 expression, reduced vascular density and perturbation of beta-catenin signalling pathway. 相似文献
7.
Ben Salah I Jelali N Slatni T Gruber M Albacete A Martínez Andújar C Martinez V Pérez-Alfocea F Abdelly C 《Acta biologica Hungarica》2012,63(1):97-112
In order to explore the relationship between leaf hormonal status and source-sink relations in the response of symbiotic nitrogen fixation (SNF) to salt stress, three major phytohormones (cytokinins, abscisic acid and the ethylene precursor 1-aminocyclopropane-1-carboxylic acid), sucrose phosphate synthase activity in source leaves and sucrolytic activities in sink organs were analysed in two lines of Medicago ciliaris (salt-tolerant TNC 1.8 and salt-sensitive TNC 11.9). SNF (measured as nitrogenase activity and amount of N-fixed) was more affected by salt treatment in the TNC 11.9 than in TNC 1.8, and this could be explained by a decrease in nodule sucrolytic activities. SNF capacity was reflected in leaf biomass production and in the sink activity under salinity, as suggested by the higher salt-induced decrease in the young leaf sucrolytic activities in the sensitive line TNC 11.9, while they were not affected in the tolerant line TNC 1.8. As a consequence of maintaining sink activities in the actively growing organs, the key enzymatic activity for synthesis of sucrose (sucrose phosphate synthase) was also less affected in the mature leaves of the more tolerant genotype. Ours results showed also that the major hormone factor associated with the relative tolerance of TNC 1.8 was the stimulation of abscisic acid concentration in young leaves under salt treatment. This stimulation may control photosynthetic organ growth and also may contribute to a certain degree in the maintenance of coordinated sink-source relationships. Therefore, ABA may be an important component which conserves sucrose synthesis in source leaves. 相似文献
8.
Maya C. Poffenberger Nadine Straka Nahida El Warry Dianne Fang Iryna Shanina Marc S. Horwitz 《PloS one》2009,4(7)
Background
Chronic myocarditis is often initiated by viral infection, the most common of which is coxsackievirus infection. The precise mechanism by which viral infection leads to chronic autoimmune pathology is poorly understood, however it is clear that the early immune response plays a critical role. Previous results have shown that the inflammatory cytokine interleukin (IL)-6 is integral to the development of experimental-induced autoimmune myocarditis. However, the function of IL-6 during viral-mediated autoimmunity has yet to be elucidated.Methods and Results
To address the requirement of IL-6 during disease induction, IL-6 deficient mice were infected with coxsackievirus B3 (CB3). Following infection, mice lacking IL-6 developed increased chronic autoimmune disease pathology compared to wild type controls without a corresponding change in the level of viral replication in the heart. This increase in disease severity was accompanied by elevated levels of TNF-α, MCP-1, IL-10, activated T cells and cardiac infiltrating macrophage/monocytes. Injection of recombinant IL-6 early following infection in the IL-6 deficient mice was sufficient to lower the serum cytokines TNF-α and IL-10 as well as the serum chemokines MCP-1, MIP-1β, RANTES and MIG with a corresponding decrease in the chronic disease pathology strongly suggests an important regulatory role for IL-6 during the early response.Conclusions
While IL-6 plays a pathogenic role in experimental-induced autoimmune disease, its function following viral-induced autoimmunity is not reprised. By regulating the early immune response and thereby controlling the severity of chronic disease, IL-6 directs the outcome of chronic autoimmune myocarditis. 相似文献9.
10.
Melanie A. Higgins Garrett E. Whitworth Nahida El Warry Mialy Randriantsoa Eric Samain Robert D. Burke David J. Vocadlo Alisdair B. Boraston 《The Journal of biological chemistry》2009,284(38):26161-26173
The presence of a fucose utilization operon in the Streptococcus pneumoniae genome and its established importance in virulence indicates a reliance of this bacterium on the harvesting of host fucose-containing glycans. The identities of these glycans, however, and how they are harvested is presently unknown. The biochemical and high resolution x-ray crystallographic analysis of two family 98 glycoside hydrolases (GH98s) from distinctive forms of the fucose utilization operon that originate from different S. pneumoniae strains reveal that one enzyme, the predominant type among pneumococcal isolates, has a unique endo-β-galactosidase activity on the LewisY antigen. Altered active site topography in the other species of GH98 enzyme tune its endo-β-galactosidase activity to the blood group A and B antigens. Despite their different specificities, these enzymes, and by extension all family 98 glycoside hydrolases, use an inverting catalytic mechanism. Many bacterial and viral pathogens exploit host carbohydrate antigens for adherence as a precursor to colonization or infection. However, this is the first evidence of bacterial endoglycosidase enzymes that are known to play a role in virulence and are specific for distinct host carbohydrate antigens. The strain-specific distribution of two distinct types of GH98 enzymes further suggests that S. pneumoniae strains may specialize to exploit host-specific antigens that vary from host to host, a factor that may feature in whether a strain is capable of colonizing a host or establishing an invasive infection.Streptococcus pneumoniae asymptomatically colonizes the nasopharynx of 10–40% of people, but given the appropriate opportunity, it can become an extremely aggressive pathogen (1–3). This bacterium causes millions of deaths annually (1), is acquiring antibiotic resistance (4), and shows a disturbing and lethal synergy with the Influenza virus (5). The ability of S. pneumoniae to cause invasive disease is increasingly being linked with the capacity of this bacterium to attack and process the glycans present in host tissues (see Ref. 6 for a review). Indeed, large scale screening of pneumococcal virulence factors has revealed a large complement of genes devoted to complex carbohydrate metabolism that contribute to pneumococcal virulence (7–9). Recent elegant studies have focused on showing how a group of three exo-glycosidases sequentially trim complex human N-glycans (10, 11). These enzymes, however, only make up a fraction of the 39 glycosidases predicted to be in the pneumococcal genome (TIGR4 strain); at least 18 of these 39 are required for full virulence of the bacterium (7). Despite the growing appreciation for the role of carbohydrate metabolism in pneumococcal virulence and the possibility of targeting such metabolic pathways with small molecule therapeutic compounds, the bulk of the carbohydrate-active proteins of S. pneumoniae remain unexamined. As such, we presently have a relatively superficial but growing appreciation for the array of host glycans that S. pneumoniae can degrade.Several S. pneumoniae genes whose protein products are dedicated to the harvesting and processing of the sugar fucose are beginning to emerge as an important set of pneumococcal virulence factors (12). Comparative genomic studies of several S. pneumoniae genomes has suggested genetic variability at this locus; however, some components of the operon were observed to be present in all of the studied isolates (13). Through our recent identification and characterization of a novel solute-binding protein present in an alternate pneumococcal fucose utilization operon, we have made the observation that there are two different fucose utilization operons distributed among pneumococcal strains (14). Although the organization and composition of the two operons is different, both pathways are predicted to be initiated by the action of a family 98 glycoside hydrolase that is probably secreted (for a discussion of the sequence classification system of glycoside hydrolases, see Ref. 15). This GH98 is the same as that identified as a virulence factor in the TIGR4 strain (7). Remarkably, the GH98 enzymes from the two different pathways display different modular architectures, and their shared catalytic modules only have modest amino acid sequence identity. Given the placement of these enzymes in a fucose utilization operon, we hypothesized that they have activity on fucose-containing glycans; however, their divergent sequences and different modular arrangements led us to postulate that they would have different glycan substrate specificities.Here we describe the specificity and catalytic mechanism for these two different types of S. pneumoniae GH98 enzymes, one from the TIGR4 strain (Sp4GH98) and the other from the SP3-BS71 strain (Sp3GH98). Both enzymes act as endo-β-1,4-galactosidases on the galactosyl-β-1,4-N-acetylglucosamine linkage found in type 2 carbohydrate blood group antigens, although Sp4GH98 displays specificity for the LewisY antigen, whereas Sp3GH98 is highly selective for the same linkage in the blood group A/B-antigens. The biochemical analysis of these enzymes in combination with the determination of their structures in complex with products and substrates provides molecular level insight to their catalytic mechanism and how they discriminate between their respective substrates. We discuss these results in the context of the recent association of the pneumococcal fucose utilization operon with the virulence of S. pneumoniae (7, 12) and the possible strain-specific dependence of pneumococcal virulence on the carbohydrate antigens presented by different hosts. 相似文献