Phytonanofabrication: Methodology and Factors Affecting Biosynthesis of Nanoparticles

The greener way of producing silver nanoparticles is the easiest, cheapest and most efficient way of producing large-scale nanoparticles that have no adverse effect on the environment. The nanosynthesis using various methodologies and the biological synthesis of silver nanoparticles have been discussed in detail. Plant extracts have been known to be competent for the extracellular biosynthesis of silver nanoparticles suggested by the various publications. Further, effects of various sources and methods on nanoparticle synthesis have been examined. Additionally, the impact of conditions such as dark, light, heating, boiling, sonication, autoclave on the size and shape of colloidal nanoparticles has been analyzed. Moreover, effects of specific parameters such as leaf extract concentration, AgNO3, reaction temperature, pH, light and stirring time for nanoparticle synthesis are discussed, and the impact of silver nanoparticles on plant physiology has examined

Effects of Pesticides, Temperature, Light, and Chemical Constituents of Soil on Nitrogen Fixation

Nitrogen is a vital component of atmosphere and plays important roles in the biochemistry of all life forms on the earth. Various mechanisms of biological nitrogen fixation and recycling in the environment have been evolved in all known ecosystems. For example, symbiotic nitrogen fixation is the major N2-fixing mechanism in the agroecosystems. Symbiotic nitrogen fixation is dependent on the biotic factors, such as host plant genotypes and the microbial strains. However, the interaction of these biotic factors is influenced by abiotic factors, such as climate and environmental conditions. The effects of various environmental variables, such as pesticides, temperature, and light as well as acidity, alkalinity, salinity, phosphorus, and water content status of the soils on the nitrogen fixation have been discussed briefly in this chapter

Synthesis, Characterization of Dichlorofluorescein Silver Nanoparticles (DCF-SNPs) and Their Effect on Seed Germination of <em>Vigna radiata</em>

The main objective of this study was to investigate whether dichlorofluorescein (DCF) is adequate for the formulation of stable dichlorofluorescein-induced silver nanoparticles under the boiling method to analyze their effects on the seed germination of Mung seeds (Vigna radiata). Preliminary dichlorofluoresceine nanoparticles (DCF-SNPs) synthesis evidence by noticing the solution color transformed from a light green color to a dark brown color. The 2.5 ml of dichlorofluoresceine (DCF) solution was found sufficient for the formulation of dichlorofluoresceine induced silver nanoparticles at boiling conditions. Purified dichlorofluoresceine nanoparticles (DCF-SNPs) measure an average diameter of 293 nm where the majority of nanoparticles were around 159 nm in size with the surface load of-9.35 mV zeta potential value. The impact of dichlorofluorescein silver nanoparticles (DCF-SNPs) on the germination percentage of V. radiata has shown that, the 25% concentration of DCF-SNPs is excellent for the growth of Mung seeds (V. radiata). Overall, the dichlorofluorescein silver nanoparticles may be constructive for improving the percentage of seed germination at 25% of its concentration and may also be useful for fluorescent measurement using the confocal microscopy technique. Hence, dichlorofluorescein silver nanoparticles (DCF-SNPs) are proposed as an efficient detection system for nanoparticles in agrochemicals for plants

Conserved and Distinct Modes of CREB/ATF Transcription Factor Regulation by PP2A/B56γ and Genotoxic Stress

Activating transcription factor 1 (ATF1) and the closely related proteins CREB (cyclic AMP resonse element binding protein) and CREM (cyclic AMP response element modulator) constitute a subfamily of bZIP transcription factors that play critical roles in the regulation of cellular growth, metabolism, and survival. Previous studies demonstrated that CREB is phosphorylated on a cluster of conserved Ser residues, including Ser-111 and Ser-121, in response to DNA damage through the coordinated actions of the ataxia-telangiectasia-mutated (ATM) protein kinase and casein kinases 1 and 2 (CK1/2). Here, we show that DNA damage-induced phosphorylation by ATM is a general feature of CREB and ATF1. ATF1 harbors a conserved ATM/CK cluster that is constitutively and stoichiometrically phosphorylated by CK1 and CK2 in asynchronously growing cells. Exposure to DNA damage further induced ATF1 phosphorylation on Ser-51 by ATM in a manner that required prior phosphorylation of the upstream CK residues. Hyperphosphorylated ATF1 showed a 4-fold reduced affinity for CREB-binding protein. We further show that PP2A, in conjunction with its targeting subunit B56γ, antagonized ATM and CK1/2-dependent phosphorylation of CREB and ATF1 in cellulo. Finally, we show that CK sites in CREB are phosphorylated during cellular growth and that phosphorylation of these residues reduces the threshold of DNA damage required for ATM-dependent phosphorylation of the inhibitory Ser-121 residue. These studies define overlapping and distinct modes of CREB and ATF1 regulation by phosphorylation that may ensure concerted changes in gene expression mediated by these factors

Mutation analysis of the MDM4 gene in German breast cancer patients

<p>Abstract</p> <p>Background</p> <p>MDM4 is a negative regulator of p53 and cooperates with MDM2 in the cellular response to DNA damage. It is unknown, however, whether <it>MDM4 </it>gene alterations play some role in the inherited component of breast cancer susceptibility.</p> <p>Methods</p> <p>We sequenced the whole <it>MDM4 </it>coding region and flanking untranslated regions in genomic DNA samples obtained from 40 German patients with familial breast cancer. Selected variants were subsequently screened by RFLP-based assays in an extended set of breast cancer cases and controls.</p> <p>Results</p> <p>Our resequencing study uncovered two <it>MDM4 </it>coding variants in 4/40 patients. Three patients carried a silent substitution at codon 74 that was linked with another rare variant in the 5'UTR. No association of this allele with breast cancer was found in a subsequent screening of 133 patients with bilateral breast cancer and 136 controls. The fourth patient was heterozygous for the missense substitution D153G which is located in a less conserved region of the MDM4 protein but may affect a predicted phosphorylation site. The D153G substitution only partially segregated with breast cancer in the family and was not identified on additional 680 chromosomes screened.</p> <p>Conclusion</p> <p>This study did not reveal clearly pathogenic mutations although it uncovered two new unclassified variants at a low frequency. We conclude that there is no evidence for a major role of <it>MDM4 </it>coding variants in the inherited susceptibility towards breast cancer in German patients.</p

Inhibition of Melanogenesis by the Pyridinyl Imidazole Class of Compounds: Possible Involvement of the Wnt/β-Catenin Signaling Pathway

While investigating the role of p38 MAPK in regulating melanogenesis, we found that pyridinyl imidazole inhibitors class compounds as well as the analog compound SB202474, which does not inhibit p38 MAPK, suppressed both α-MSH-induced melanogenesis and spontaneous melanin synthesis. In this study, we demonstrated that the inhibitory activity of the pyridinyl imidazoles correlates with inhibition of the canonical Wnt/β-catenin pathway activity. Imidazole-treated cells showed a reduction in the level of Tcf/Lef target genes involved in the β-catenin signaling network, including ubiquitous genes such as Axin2, Lef1, and Wisp1 as well as cell lineage-restricted genes such as microphthalmia-associated transcription factor and dopachrome tautomerase. Although over-expression of the Wnt signaling pathway effector β-catenin slightly restored the melanogenic program, the lack of complete reversion suggested that the imidazoles interfered with β-catenin-dependent transcriptional activity rather than with β-catenin expression. Accordingly, we did not observe any significant change in β-catenin protein expression. The independence of p38 MAPK activity from the repression of Wnt/β-catenin signaling pathway was confirmed by small interfering RNA knockdown of p38 MAPK expression, which by contrast, stimulated β-catenin-driven gene expression. Our data demonstrate that the small molecule pyridinyl imidazoles possess two distinct and opposite mechanisms that modulate β-catenin dependent transcription: a p38 inhibition-dependent effect that stimulates the Wnt pathway by increasing β-catenin protein expression and an off-target mechanism that inhibits the pathway by repressing β-catenin protein functionality. The p38-independent effect seems to be dominant and, at least in B16-F0 cells, results in a strong block of the Wnt/β-catenin signaling pathway