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Nuccitelli, R., Pliquett, U., Chen, X., Ford, W., James Swanson, R., Beebe, S. J., et al. (2006). Nanosecond pulsed electric fields cause melanomas to self-destruct. Biochemical and Biophysical Research Communications, 343(2), 351–360.
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Zoltowski, B. D., & Gardner, K. H. (2011). Tripping the light fantastic: blue-light photoreceptors as examples of environmentally modulated protein-protein interactions. Biochemistry, 50(1), 4–16.
Abstract: Blue-light photoreceptors play a pivotal role in detecting the quality and quantity of light in the environment, controlling a wide range of biological responses. Several families of blue-light photoreceptors have been characterized in detail using biophysics and biochemistry, beginning with photon absorption, through intervening signal transduction, to regulation of biological activities. Here we review the light oxygen voltage, cryptochrome, and sensors of blue light using FAD families, three different groups of proteins that offer distinctly different modes of photochemical activation and signal transduction yet play similar roles in a vast array of biological responses. We cover mechanisms of light activation and propagation of conformational responses that modulate protein-protein interactions involved in biological signaling. Discovery and characterization of these processes in natural proteins are now allowing the design of photoregulatable engineered proteins, facilitating the generation of novel reagents for biochemical and cell biological research.
Keywords: Animals; Bacteria/chemistry/metabolism; Bacterial Proteins/chemistry/*metabolism; Biotechnology; Cryptochromes/chemistry/*metabolism; Flavoproteins/chemistry/*metabolism; Halorhodospira halophila/chemistry/metabolism; Humans; Light; Models, Molecular; Photochemical Processes; Photoreceptor Cells/chemistry/*metabolism; Photoreceptors, Microbial/chemistry/*metabolism; Protein Interaction Maps; Protein Structure, Tertiary; Signal Transduction
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Plotnikov, A., Zehorai, E., Procaccia, S., & Seger, R. (2011). The MAPK cascades: signaling components, nuclear roles and mechanisms of nuclear translocation. Biochim Biophys Acta, 1813(9), 1619–1633.
Abstract: The MAPK cascades are central signaling pathways that regulate a wide variety of stimulated cellular processes, including proliferation, differentiation, apoptosis and stress response. Therefore, dysregulation, or improper functioning of these cascades, is involved in the induction and progression of diseases such as cancer, diabetes, autoimmune diseases, and developmental abnormalities. Many of these physiological, and pathological functions are mediated by MAPK-dependent transcription of various regulatory genes. In order to induce transcription and the consequent functions, the signals transmitted via the cascades need to enter the nucleus, where they may modulate the activity of transcription factors and chromatin remodeling enzymes. In this review, we briefly cover the composition of the MAPK cascades, as well as their physiological and pathological functions. We describe, in more detail, many of the important nuclear activities of the MAPK cascades, and we elaborate on the mechanisms of ERK1/2 translocation into the nucleus, including the identification of their nuclear translocation sequence (NTS) binding to the shuttling protein importin7. Overall, the nuclear translocation of signaling components may emerge as an important regulatory layer in the induction of cellular processes, and therefore, may serve as targets for therapeutic intervention in signaling-related diseases such as cancer and diabetes. This article is part of a Special Issue entitled: Regulation of Signaling and Cellular Fate through Modulation of Nuclear Protein Import.
Keywords: Active Transport, Cell Nucleus/genetics/*physiology; Chromatin Assembly and Disassembly/physiology; Gene Expression Regulation; Genes, Immediate-Early; Humans; MAP Kinase Signaling System/genetics/*physiology; Models, Biological; Nuclear Localization Signals/physiology; Receptors, Cytoplasmic and Nuclear/physiology; Stress, Physiological; Transcription Factors/physiology
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Kroupova, J., Bartova, E., Fojt, L., Strasak, L., Kozubek, S., & Vetterl, V. (2007). Low-frequency magnetic field effect on cytoskeleton and chromatin. Bioelectrochemistry, 70(1), 96–100.
Abstract: The effect of magnetic fields on the living systems is studied in vivo or in vitro in very broad spectrum of organisms, cells and tissues. The mechanism of their acting is not known until now. We studied low-frequency magnetic field effect on cytoskeleton and on the structure of chromatin in human cells. We used cell line of small lung carcinoma (A549) and the effects of magnetic field on cytoskeleton and higher-order chromatin structure were analyzed 96 h of magnetic field exposure. Magnetic field generated by the cylindrical soil was homogenous and the cells were cultivated at 37 degrees C in humidified atmosphere containing 5% CO(2). Magnetic field induction was B(m)=2 mT and the net frequency f=50 Hz. In such affected and control cells the F-actin was estimated using FITC-conjugated Phalloidin and mitochondria were studied using MitoTracker (Molecular Probes). Images of cytoskeleton and genetic loci were acquired using confocal microscopy and analysis was performed by FISH 2.0 software. Slight morphological changes of F-actin filaments and mitochondria were observed in affected cells and nuclear condensation was found. These effects could be related to the process of cell death apoptosis probably induced by magnetic field. The studies aimed at centromeric heterochromatin (9cen) did not show statistically significant changes. Therefore, we suggest that magnetic field has no influence on higher order chromatin structure but certain changes could be observed on the level of cytoskeleton. However, these statements need a thorough verification. Our preliminary experiments will be extended and the effect of magnetic field on another structures of cytoskeleton and cell nuclei will be further studied.
Keywords: Cell Line, Tumor; Centromere; Chromatin/chemistry/genetics/*metabolism; Chromosomes, Human, Pair 8/genetics/metabolism; Cytoskeleton/*metabolism; *Electromagnetic Fields; Humans
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Beneduci, A., Chidichimo, G., Tripepi, S., Perrotta, E., & Cufone, F. (2007). Antiproliferative effect of millimeter radiation on human erythromyeloid leukemia cell line K562 in culture: ultrastructural- and metabolic-induced changes. Bioelectrochemistry, 70(2), 214–220.
Abstract: In the present study we compared the proliferation behavior, the ultrastructural morphology and the glycolitic metabolism of K562 cells irradiated by low-power wide-band millimeter waves, with those of sham-exposed K562 cells (control), maintained in the same culture conditions. The gigaHertz radiation treatments, performed between 53-78 10(9) Hz, induced a noticeable inhibition of the cell proliferation that could be related to relevant ultrastructural changes. Such effects brought the irradiated cell system to lose the homeostasis and to trigger defense/reparatory mechanisms in order to reestablish a new steady state. (13)C-Nuclear magnetic resonance data on the kinetic of glucose metabolism demonstrated that the irradiated cells enhanced the glycolitic aerobic pathway, indicating that such system need to produce an extra-bioenergy. Most of the ATP synthesized served probably to perform the above processes resulting in a significant decrease of the proliferation rate without significant cell death increment.
Keywords: Cell Proliferation/*drug effects; Cell Survival/*radiation effects; Dose-Response Relationship, Radiation; Glucose/*metabolism; Glycolysis/*radiation effects; Humans; K562 Cells; Metabolic Clearance Rate/radiation effects; *Microwaves; Radiation Dosage
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