Relevant bibliographies by topics / Biological Mechanism of Action

Academic literature on the topic 'Biological Mechanism of Action'

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Published: 9 March 2023

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Journal articles on the topic "Biological Mechanism of Action"

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Krinsky, N. I. "Mechanism of Action of Biological Antioxidants." Experimental Biology and Medicine 200, no. 2 (June 1, 1992): 248–54. http://dx.doi.org/10.3181/00379727-200-43429.

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Davidse, L. C. "Benzimidazole Fungicides: Mechanism of Action and Biological Impact." Annual Review of Phytopathology 24, no. 1 (September 1986): 43–65. http://dx.doi.org/10.1146/annurev.py.24.090186.000355.

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ATANOV, Nikolai A., and Margarita A. SIDORENKO. "THE MECHANISM OF ACTION OF BIOCIDE." Urban construction and architecture 3, no. 4S (December 15, 2013): 11–14. http://dx.doi.org/10.17673/vestnik.2013.s4.3.

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Dealt with the question of the mechanism of action of biocides to regulate the intensity of the biological processes in the circulating water systems: classifi cation of biocides, resistance of biocenose to the action of a biocide, dosing modes of inhibition.
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TERADA, Hiroshi, and Yasuo SHINOHARA. "Mechanism of Energy Transduction in Biological Systems and Action Mechanism of Inhibitors." Journal of Pesticide Science 11, no. 4 (1986): 641–51. http://dx.doi.org/10.1584/jpestics.11.641.

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Gautam, Vertika, and Anand Gaurav. "NOS Inhibitors: Structure, Biological Activity and Mechanism of Action." Current Enzyme Inhibition 12, no. 1 (March 3, 2016): 16–29. http://dx.doi.org/10.2174/1573408012666151126185837.

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Kumari, Ranju, Seema Bansal, Garima Gupta, Shvetambri Arora, Ajit Kumar, Sanjay Goel, Prabhjot Singh, Prija Ponnan, Nivedita Priya, and Tapesh K. Tyagi. "Calreticulin transacylase: Genesis, mechanism of action and biological applications." Biochimie 92, no. 9 (September 2010): 1173–79. http://dx.doi.org/10.1016/j.biochi.2010.01.016.

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Orlemans, E. O. M., W. Verboom, M. W. Scheltinga, D. N. Reinhoudt, P. Lelieveld, H. H. Fiebig, B. R. Winterhalter, J. A. Double, and M. C. Bibby. "Synthesis, mechanism of action, and biological evaluation of mitosenes." Journal of Medicinal Chemistry 32, no. 7 (July 1989): 1612–20. http://dx.doi.org/10.1021/jm00127a035.

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Sehgal, S. N. "Sirolimus: its discovery, biological properties, and mechanism of action." Transplantation Proceedings 35, no. 3 (May 2003): S7—S14. http://dx.doi.org/10.1016/s0041-1345(03)00211-2.

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Christakos, Sylvia, and Yan Liu. "Biological actions and mechanism of action of calbindin in the process of apoptosis." Journal of Steroid Biochemistry and Molecular Biology 89-90 (May 2004): 401–4. http://dx.doi.org/10.1016/j.jsbmb.2004.03.007.

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Marjanović, Ana Marija, Ivan Pavičić, and Ivančica Trošić. "Biological indicators in response to radiofrequency/microwave exposure." Archives of Industrial Hygiene and Toxicology 63, no. 3 (September 25, 2012): 407–16. http://dx.doi.org/10.2478/10004-1254-63-2012-2215.

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Over the years, due to rapid technological progress, radiation from man-made sources exceeded that of natural origin. There is a general concern regarding a growing number of appliances that use radiofrequency/ microwave (RF/MW) radiation with particular emphasis on mobile communication systems. Since nonthermal biological effects and mechanisms of RF/MW radiation are still uncertain, laboratory studies on animal models, tissues, cells, and cell free system are of extraordinary importance in bioelectromagnetic research. We believe that such investigations play a supporting role in public risk assessment. Cellular systems with the potential for a clear response to RF/MW exposures should be used in those studies. It is known that organism is a complex electrochemical system where processes of oxidation and reduction regularly occur. One of the plausible mechanisms is connected with generation of reactive oxygen species (ROS). Depending on concentration, ROS can have both benefi cial and deleterious effects. Positive effects are connected with cell signalling, defence against infectious agents, and proliferative cell ability. On the other hand, excessive production, which overloads antioxidant defence mechanism, leads to cellular damage with serious potential for disease development. ROS concentration increase within the cell caused by RF/MW radiation seems to be a biologically relevant hypothesis to give clear insight into the RF/MW action at non-thermal level of radiation. In order to better understand the exact mechanism of action and its consequences, further research is needed in the fi eld. We would like to present current knowledge on possible biological mechanisms of RF/MW actions.
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Dissertations / Theses on the topic "Biological Mechanism of Action"

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Deans, Bryan. "Studies on the mechanism of action on antitumour imidazotetrazinones." Thesis, Aston University, 1994. http://publications.aston.ac.uk/11048/.

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This thesis attempts to identify the cellular targets important to the cytotoxicity of imidazotetrazinones, to elucidate the pathways by which this damage leads to cell death, and to identify mechanisms by which tumour cells may circumvent this action. The levels of the DNA repair enzymes O6-alkylguanine-DNA-alkyltransferase (O6-AGAT) and 3-methyladenine-DNA-glycosylase (3MAG) have been examined in a range of murine and human cell lines with differential sensitivity to temozolomide. All the cell lines were proficient in 3MAG despite there being 40-fold difference in sensitivity to temozolomide. This suggests that while 3-methyladenine is a major product of temozolomide alkylation of DNA it is unlikely to be a cytotoxic lesion. In contrast, there was a 20-fold variation in O6-AGAT levels and the concentration of this repair enzyme correlated with variations in cytotoxicity. Furthermore, depletion of this enzyme in a resistant, O6-AGAT proficient cell line (Raji), by pre-treatment with the free base O6-methylguanine resulted in 54% sensitisation to the effects of temozolomide. These observations have been extended to 3 glioma cell lines; results that support the view that the cytotoxicity of temozolomide is related to alkylation at the O6-position of guanine and that resistance to this drug is determined by efficient repair of this lesion. It is clear, however, the other factors may influence tumour response since temozolomide showed little differential activity towards 3 established solid murine tumours in vivo, despite different tumour O6-AGAT levels.
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Mungthin, Mathirut. "Studies on the mechanism of action and mechanism of resistance to quinoline-containing antimalarial drugs in Plasmodium falciparum." Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.263874.

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Sanders, Paul Michael. "Mechanism of action of a tumour derived lipid mobilising factor." Thesis, Aston University, 2003. http://publications.aston.ac.uk/11005/.

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Cancer cachexia comprises unintentional and debilitating weight loss associated with certain tumour types. Fat loss in cachexia is mediated by a 43kDa Lipid Mobilising Factor (LMF) sharing homology with endogenous Zinc-a2-Glycoprotein (ZAG). LMF and ZAG induced significant lipolysis in isolated epidydimal adipose tissue. This is attenuated by co-incubation with 10mM of antagonist SR59230A and partially attenuated by 25mM PD098059 (indicating b3-AR and MAPK involvement respectively). LMF/ZAG induced in vitro lipid depletion in differentiated 3T3-L1 adipocytes that seen to comprise a significant increase in lipolysis (p<0.01), with only a modest decrease in lipid synthesis (p=0.09). ZAG significantly increased in vitro protein synthesis (p<0.01) in C2C12 myotubes (without an effect on protein degradation). This increase was activated at transcription and attenuated by co-incubation with 10mM SR59230A. Proteolytic digestion of ZAG and LMF followed by sephadex G50 chromatography yielded active fragments of 6-15kDa, indication the entire molecule was not required for bioactivity. Cachexigenic MAC16 cells demonstrated significant in vitro ZAG expression over non-cachexigenic MAC13 (p<0.001). WAT and BAT excised from MAC16 mice of varying weight loss demonstrated increased ZAG expression compared to controls. Dosing of NMRI mice with s/c ZAG failed to reproduce this up-regulation, thus another cachectic factor is responsible. 0.58nM LMF conferred significant protection against hydrogen peroxide, paraquat and bleomycin-induced oxidative stress in the non-cachexigenic MAC13 cell line. This protection was attenuated by 10mM SR59230A indicating a b3-AR mediated effect. In addition, 0.58nM LMF significantly up regulated UCP2 expression (p<0.001), (a mitochondrial protein implicated in the detoxification of ROS) implying this to be the mechanism by which survival was achieved. In vitro, LMF caused significant up-regulation of UCP1 in BAT and UCP2 and 3 in C2C12 myotubes. This increase in uncoupling protein expression further potentiates the negative energy balance and wasting observed in cachexia.
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Matkar, Smita S. "Mechanism of action of potential anticancer drugs." Scholarly Commons, 2008. https://scholarlycommons.pacific.edu/uop_etds/2368.

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Traditionally, inoperable or metastatic cancers have been treated by causing massive DNA damage in order to induce self-destruction (apoptosis) of the rapidly multiplying cancer cells. Initially, this strategy works for many cancers, in particular those which express normal p53 tumor suppressor protein. However, most cancers eventually aquire mutations in either p53 or other signaling molecules and fail to initiate apoptosis in response to severe DNA damage. During this study three types of compounds were investigated for their DNA damaging and anticancer effects: a pair of novel metal containing compounds, a pair of natural products, and a known synthetic drug which had been used many years ago for completely different indication. It was shown that all stop the growth of cancer cells and that the latter two classes do not require functional p53 because they work equally well in cells with normal (wildtype), mutant or no p53. The two nickel complexes investigated in this dissertation, differ in their ability to cause DNA damage and cell death. The oxidized form of the nickel complex, [Ni(CR-2H)] 2+ causes DNA damage and cell death at a much lower concentration than its reduced counterpart [Ni(CR)] 2+ . The phenanthridine alkaloids, Sanguinarine and Chelerythine cause high levels of DNA strand breaks and extremely rapid apoptosis which is not due to DNA damage because the quick onset precludes extensive signaling. The effects of the phenanthridines were linked to production of large amounts of reactive oxygen species (ROS), in particular hydrogen peroxide (H 2 O 2 ). The importance of ROS for the action of anticancer drugs as well as antibiotics is increasingly being recognized. In addition we also investigated the thioxanthone Lucanthone or Miracil D (which was used for the treatment of parasitic worms more than 50 years ago). It causes DNA strand breaks and apoptosis. Apoptosis occurs on a timescale consistent with signaling. However, p53 does not seem to be involved and alternative mechanisms are being investigated. This work provides new directions for designing novel anticancer drugs that are not subject to the limitations of DNA damaging agents.
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Duan, Xuchen. "Physiological and biological mechanisms of bisphosphonate action." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:36b0439d-2f89-4c1e-8bb3-941b4e6ee847.

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Bisphosphonates (BPs) are stable analogues of pyrophosphate widely used for the treatment of bone diseases characterised by increased bone resorption. Studies over the years have shown that the pharmacological potencies of BPs are dependent both on their binding affinities for bone mineral and on their inhibitory actions on osteoclasts. In addition, potential effects on other cell types present locally in the environment of skeletal tissues have been reported. The present study systematically evaluated the relative mineral-binding affinities of individual BPs of clinically relevance in mixtures of these compounds and the changes with elution pH by using column chromatography with ceramic hydroxyapatite and fluoroapatite combined with mass spectrometric identification and quantitation of the individual BPs. The results indicate that pH has a profound effect on the ionisation of the phosphonate and R2 functional groups, with BPs having greater affinities at lower pH as shown by increased retention times. Moreover, two other approaches, namely using Langmuir adsorption isotherms and competition assays based on fluorescent BP, have been developed to assess the mineral-binding capacities and dissociation constants of BPs. These results suggest that there are substantial differences among BPs in their binding to hydroxyapatite. From the cellular aspect of my study, I present evidence for the anti-apoptotic effects of BPs in osteocytes and osteoblasts. However, the study of prosurvival signalling pathways involved in these cells needs to be optimised. The work described in this thesis provides novel insights into the physiological and biological mechanisms of BP action. My project has provided a better knowledge of the physicochemical properties of BPs, which are highly relevant to their differential distributions within bone, their biological potencies, and their durations of action. Additionally, the cell culture studies may provide new information on the cellular effects of BPs on osteocytes and osteoblasts.
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Moreno, González M. del Carmen. "Characterization and mechanism of action of the biological control agent Pantoea agglomerans EPS125." Doctoral thesis, Universitat de Girona, 2006. http://hdl.handle.net/10803/7796.

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La soca EPS125 ha mostrat ser un efectiu agent de control biològic de diferents patògens fúngics de postcollita en diferents fruits. Degut a la seva elevada eficàcia, es va plantejar desenvolupar aquesta soca comercialment i per aquest motiu en el present treball es plantejà complementar la informació necessària pel seu registre.
D'acord amb els resultats obtinguts mitjançant proves fenotípiques i genotípiques, la soca EPS125 queda inclosa dins l'espècie Pantoea agglomerans (Enterobacter agglomerans-Erwinia herbicola). En relació a la utilització de fonts de carboni, en el perfil i contingut d'àcids grassos cel·lulars i en el polimorfisme en la longitud dels fragments de macrorestricció genòmica (MRFLP), la soca EPS125 mostrà trets característics que la diferencien d'altres soques. Els dos marcadors moleculars (125.2 i 125.3) específics per la soca EPS125 dissenyats en el present treball mostraren ser semiespecífics per la seva detecció mitjançant la tècnica PCR i Real Time PCR. Quedant pendent l'anàlisi d'especificitat de l'ús combinat dels dos marcadors moleculars en una reacció PCR multiplex. P. agglomerans EPS125 ha mostrat ser molt efectiva en el control de Penicillium expansum en poma amb una dosi efectiva mitjana de 2.7x105 a 7x105 ufc/ml, i una ratio de 25-101 cèl·lules de la soca EPS125 per inactivar una espora del patogen segons el model de saturació hiperbòlica. Segons les aproximacions fenotípiques i estudis genotípics realitzats, sembla que els mecanismes de biocontrol utilitzats per la soca EPS125 contra P. expansum en poma estan directament relacionats amb la capacitat de formació de biofilm per aquesta soca.
Strain EPS125 has shown effectiveness against a wide range of fungal pathogens in a large variety of fruit. However, to develop this strain as commercial biopesticide an extensive characterization is essential. For this reason, the objective of this PhD thesis was to complete the necessary information for its future registration.
According to morphological and biochemical tests, strain EPS125 pertain to Pantoea agglomerans (Enterobacter agglomerans-Erwinia herbicola) species. This strain showed typical traits different from other bacteria in relation to the ability to use several carbon sources, the fatty acid profiles and the macrorestriction fragment length polymorphism (MRFLP) pattern. The two DNA molecular markers of P. agglomerans EPS125 (125.2 and 125.3) obtained in the present work were semispecific in the detection of strain EPS125 by means of PCR and Real Time PCR. However, the combined use of the two primer sets in a multiplex PCR reaction would be specific. P. agglomerans EPS125 was highly effective against P. expansum in apple fruit having a median effective dose from 2.7x105 to 7x105 cfu/ml and a ratio of 101 and 25 EPS125 cells to inactivate one pathogen spore according to the hyperbolic saturation model.
Biocontrol mechanisms used by P. agglomerans EPS125 against P. expansum in apple fruit may be related with the ability of biofilm formation by this strain as show phenotypic approaches and genotypic studies.
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Tatarski, Miloš. "Molecular mechanism of dBigH1 action." Doctoral thesis, Universitat de Barcelona, 2018. http://hdl.handle.net/10803/663021.

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INTRODUCTION: For decades it was known that many species contain embryo specific linker histone H1 variants that replace the somatic H1 during early embryogenesis. This is especially important because the early embryo shows typically zero to very little activity of transcription, and the first cleavages of the embryo depend exclusively on maternally deposited factors that are important for transcription and chromatin assembly. The first species shown to contain an embryo specific histone H1 was the sea urchin. Other species like the mouse, Xenopus or the zebrafish followed. Even in humans there are embryo specific H1 variants. Drosophila seemed to be an exception to this, until in 2013 the first linker histone H1 variant was discovered that was called dBigH1. Like other embryo H1 variants, dBigH1 is expressed in the early embryo and disappears when cellularization starts and it gets replaced by the somatic H1. Likewise, to its counterparts in other species, dBigH1 is responsible for the inhibition of transcription during the early stage of fly development. OBJECTIVES: In this thesis, we addressed the questions about the mechanism of inhibition of dBigH1 as well as the factors that are responsible for its deposition into chromatin. RESULTS: To answer the first question, we used an in vitro system for chromatin reconstitution based on an extract from early Drosophila embryos (DREX) that contains dBigH1 and all other factors needed for proper chromatin assembly. We then used the reconstituted chromatin in transcription experiments using HeLa nuclear extract that contains all factors needed for transcription. We saw that transcription for chromatin reconstituted in DREX could be reduced when the extract was previously depleted from dBigH1 using specific antibodies against it. By adding back recombinant dBigH1 to the depleted extract we were able to restore the initial lever of transcription. This showed us that dBigH1 was the repressive factor, as it was already confirmed in vivo. We then used a truncated construct of dBigH1 where we depleted the N-terminal domain of the protein. This was of particular interest as the N-terminal region of dBigH1 is the one that differs most form the somatic H1. It is much longer and more importantly very enriched with acidic residues, something that is very unique amongst all embryo specific H1 variants. We saw that when using the truncated construct, transcription was inhibited to a much lesser extent than with the full length dBigH1, proposing that the N-terminal domain is indeed responsible for the inhibition of transcription. To answer the second question about the factors needed for dBigH1 deposition, we used Drosophila testis to study dBigH1 in vivo. dBigH1 shows a very similar expression pattern in testis as the chromatin remodeler ACF1. This is why we decided to investigate a possible interaction between those two proteins. Additionally, we knew that ACF1 uses NAP1 as a histone chaperone for H1 in some species, so we also asked if NAP1 could play a role in dBigH1 deposition as well. Indeed, we saw that when using flies deficient for ACF1 we see much less dBigH1 in the testis tip where the germal stem cells (GSC) reside, suggesting that ACF1 plays an important role in dBigH1 deposition. In accordance, we see more dBigH1 in the GSCs when using flies overexpressing ACF1. At the same time, we can see that when depleting NAP1 from DREX, we see more dBigH1.
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Muraro, Lucia. "Studies of Botulinum Neurotoxins Mechanism of Action." Doctoral thesis, Università degli studi di Padova, 2009. http://hdl.handle.net/11577/3425607.

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Botulinum neurotoxins (7 serotypes of BoNTs, named from A to G) and tetanus neurotoxin (TeNT) are the most powerful clostridial toxins (CNTs). They are responsible for botulism and tetanus respectively. TeNT and BoNTs bind to peripheral nerve terminals and inhibit neurotransmitter release from presynaptic neuronal cells by proteolytic cleavage of proteins involved in the fusion of synaptic vesicles with the cell membrane. BoNTs act at the level of Peripheral Nervous System (PNS) causing flaccid paralysis whereas TeNT acts at the level of Central Nervous System (CNS) causing spastic paralysis. In particular BoNT A cleaves and disables SNAP25 (synaptosome-associated protein 25), impairing the release of acetylcholine at neuromuscular junction. Structurally, CNTs are composed of two polypeptide chains linked by a single disulphide bond: the 50 kDa Light Chain (LC), which acts in the cytosol as a metalloprotease; and the 100 kDa Heavy chain, which includes a translocation domain (HN) and a receptor binding domain (HC). The three functional domains are structurally distinct and arranged in a linear fashion, such that there is no contact between the LC and HC domain. HC is further composed of two distinct subdomains HCN and HCC. These neurotoxins act at femtomolar concentration and the high affinity binding is due to multiple binding sites, either for membrane ganglioside and neuronal specific membrane proteins. BoNT/A binds to SV2 (synaptic vesicle 2) and to the ganglioside GT1b. It was thought that these two binding sites were located one in HCN subdomain and the other in the HCC subdomain. HCN share some sequence homology with lectins so it was a good candidate to bind ganglioside. Recently by crystallographic analysis it has been shown that both the protein receptor and ganglioside sites of BoNT/B are in the HCC domain. Due to the high homology between all CNTs it is likely that also the SV2 and GT1b sites are in the BoNT A HCC domain. If this is the case the role of N-terminal subdomain of BoNT A is still unknown. The aim of this project is to investigate the role of HCN in the binding of BoNT A to the plasma membrane. It is important to notice that the sequence of this toxin portion is conserved among all CNTs. The sequence of BoNT/A coding for the HCN domain (aa from 855 to 1093) has been cloned as His-Tag fusion protein, and fused to the Enhanced Green Fluorescent Protein (EGFP) and to the monomeric cherry red fluorescent protein (mCherry). By fluorescent microscopy observations we have shown that both the fluorescent chimera were able to bind to the plasma membrane of epithelial and neuronal cells. The fluorescent HCN domain remains at the plasma membrane during incubation times that allow the internalization of whole binding domain, HC. The fluorescent staining is not homogenous on the plasma membrane but is enriched in bright spots. For TeNT binding a role of lipid raft have been establish but for BoNTs the question seems to be still open. Ours data show that the sphingomyelin binding toxin lysenin, colocalized with HCN staining and treatment with sphingomyelinase diminished the HCN binding on epithelial cells. Moreover, in dot blot analysis HCN was able to directly interact with anionic lipid in particular phosphatidylinositol 5 phosphate (PI(5)P). A role for negative charged lipid in the binding of BoNTs and TeNT to lipid bilayer, it was already suggested; our hypothesis is that the N-terminal portion of the binding domain is able to bind anionic lipid in the environment of lipid raft. We suggest that these additional interactions with the membrane surface may play the role of positioning the toxin on the membrane surface ready for membrane insertion.
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Ashraf, Sadia. "Study of mechanism of action of Scorpion neurotoxins." Doctoral thesis, Università degli studi di Padova, 2013. http://hdl.handle.net/11577/3423586.

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Summary Scorpions are important representative of arthropods. They have been well adapted to the extremes of environmental conditions. Scorpions also play a vital role in ecological systems by maintaining balance between different populations in an ecosystem. Apart from their positive role scorpions are responsible for more than 1.2 million stings per year with almost 3000 deaths worldwide per year and thus posing serious threat to public health. Two families of scorpions i.e. Buthida and Hemiscorpiidae are dangerous for humans. Scorpion sting can result in mild effects of redness and pain to very severe and lethal effects which can result failure of multiple organs eventually leading to death. Scorpion venom is composed of many different components such as low molecular weight peptides, nucleotides, lipids and certain enzymes. The diverse detrimental effects of scorpion sting result due to presence of many different types of toxins (neurotoxin, cardiotoxin, nephrotoxin, hemolytic toxin) and different enzymes (phosphodiesterases, phospholipases and hyaluronidases) in their venom. Since scorpions have a long evolutionary history during this long time period scorpions have developed a series of venom peptides that display a diverse range of biological functions. The most widely studied components of scorpion venom are the ion channel-modulating toxins which have been studied and described in detail in literature. Antarease a new class of unique scorpion metalloproteases capable of cleaving SNARE proteins has been described only recently with no previous evidence on presence of such enzymes in scorpions. Up till now SNARE proteins have only been shown to be targets of clostridial neurotoxins. To investigate such a class of metalloproteases we have analyzed the action of different scorpion venoms both on recombinant SNARE proteins as well as in neuronal cell models. Conclusion: This study shows for the first time the presence of antarease like proteins in scorpion species: Buthus eupeus and Orthochirus scrobiculosus. Both of the scorpion species contain active components i.e. metalloproteases that are able to cleave SNARE proteins in a mechanism similar to antarease.
RIASSUNTO Gli Scorpioni sono importanti rappresentanti del phylum Artropodi. Essi si sono ben adattati a condizioni ambientali estreme e giocano un ruolo fondamentale in diversi ecosistemi. Allo stesso tempo gli scorpioni sono responsabili di più di 1.2 milioni di punture per anno con quasi 3000 morti in tutto il mondo. Sono due le famiglie di scorpioni pericolose per l’uomo: Buthida e Hemiscorpiidae. Le punture di scorpione possono causare da effetti lievi come rossore, e dolore a effetti gravi che causano danni a diversi organi ed eventualmente la morte del soggetto colpito. Il veleno di scorpione è costituito da diversi componenti come peptidi a basso peso molecolare, lipidi ed enzimi. Gli effetti patologici della puntura di scorpione sono causati dalla presenza di diverse tossine (neurotossina, cardiotossina, nefrotossina, tossina emolitica) e diversi enzimi (fosfodiesterasi, fosfolipasi, ialuronidasi) nel veleno. Dato che gli scorpioni hanno una lunga storia evolutiva, durante questo lungo periodo hanno sviluppato un serie di peptidi e proteine che possiedono diverse funzioni biologiche. Grazie alla loro abbondanza e quindi alla facilità d’isolamento, i componenti del veleno più studiati sono le tossine che esplicano la loro azione sui canali ionici i quali sono stati molto studiati e descritti in dettaglio in letteratura. Recentemente è stata descritta una nuova classe di metalloproteasi di scorpione capace di proteolizzare le proteine SNARE che è stata denominata Antarease. Fino ad ora le proteine SNARE che hanno un ruolo chiave nel processo di neuroesocitosi, sono state descritte essere il bersaglio molecolare solo di neurotossine batteriche quali le tossine del tetano e del botulismo. Per studiare questa nuova classe di metalloproteasi, abbiamo analizzato l’azione di diversi veleni di scorpioni sia su proteine SNARE ricombinanti sia su modelli di neuroni primari in coltura. Questo studio ha dimostrato la presenza di metalloproteasi simili all’Antarease in specie di scorpioni Buthus eupeus e Orthochirus scrobiculosus e che questi enzimi sono in grado di proteolizzare in maniera specifica le proteine SNARE.
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LIPARI, Elisa. "DEVELOPMENT AND QUALIFICATION OF BIOANALYTICAL METHODS FOR DEAMIDATED IFNβ-1a AND INVESTIGATION ABOUT THE MECHANISM OF ACTION." Doctoral thesis, Università degli Studi di Palermo, 2021. http://hdl.handle.net/10447/497430.

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Interferon beta-1a (IFNβ-1a) is a recombinant IFNβ with the tradename Rebif involved in several biological activities. Recently, it has been reported that artificial deamidation of IFNb-1a increases its biological response. Given the therapeutical potential, an investigation on the deamidated variant has been carried out via different approaches to discover the mechanism underlying this biological effect. The antiviral and immunomodulatory activity of deamidated cytokine was assessed using two precise and accurate cell-based assays. As expected, deamidated IFNβ-1a showed an increase in the biological response and its canonical pathway and receptor binding affinity were thorough analysed. Deamidated interferon beta increases STAT1 phosphorylation and ISGs expression compared to its native form. A full in-depth analysis in receptor binding highlighted a change in receptor affinity in deamidated IFNβ-1a. In particular, deamidation destabilizes the interaction with IFNAR2 through a change in the H-bonds network, increasing the affinity to IFNAR1 and consequently to the whole receptor complex. The higher receptor binding and the consequent strong signaling and gene expression, explains the greater biological activity of the deamidated IFNβ-1a compared to the native fcorm. These results open new perspective on the therapeutic potential of this molecule which could have significant beneficial effects on patients with MS and beyond
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Books on the topic "Biological Mechanism of Action"

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1941-, Coxon J. M., ed. Mechanisms of biological importance. Greenwich, Conn: JAI Press, 1992.

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International, Symposium on Biological Reactive Intermediates (3rd 1985 University of Maryland College Park). Biological reactive intermediates III: Mechanisms of action in animal models and human disease. New York: Plenum Press, 1986.

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Sarma, Aluru S. Secondary metabolites from marine sponges. Berlin: Ullstein Mosby, 1993.

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Holland, Cheng R., and Hammar Lena, eds. Conformational proteomics of macromolecular architecture: Approaching the structure of large molecular assemblies and their mechanisms of action. Singapore: World Scientific Pub., 2004.

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1937-, Kanno Morio, and Hattori Yuichi, eds. Current aspects of cellular and subcellular mechanism of drug actions. Sapporo, Japan: Hokkaido University School of Medicine, 2000.

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Sensorimotor control and learning: An introduction to the behavioral neuroscience of action. Basingstoke, Hampshire: Palgrave Macmillan, 2012.

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S, Meskin Mark, ed. Phytochemicals: Mechanisms of action/ edited by Mark S. Meskin ... [et al.]. Boca Raton: CRC Press, 2004.

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S, Meskin Mark, and Foodnetbase, eds. Phytochemicals: Mechanisms of action / edited by Mark S. Meskin ... [et al.]. Boca Raton, Fla: CRC Press, 2004.

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1944-, Yaksh T. L., ed. Anesthesia: Biologic foundations. Philadelphia: Lippincott-Raven, 1998.

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1925-, Kuby Stephen Allen, ed. Mechanism of enzyme action. Boca Raton: CRC Press, 1991.

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Book chapters on the topic "Biological Mechanism of Action"

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Merrill, J., H. L. Kim, and S. Safe. "Helenalin: Mechanism of Toxic Action." In Biological Reactive Intermediates III, 891–96. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5134-4_84.

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Smagghe, G., and D. Degheele. "Ecdysone Agonists: Mechanism and Biological Activity." In Insecticides with Novel Modes of Action, 25–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-662-03565-8_2.

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Kovacic, Peter, James R. Ames, Mikolaj Jawdosiuk, and Michael D. Ryan. "Electron Transfer Mechanism for Cocaine Action." In Redox Chemistry and Interfacial Behavior of Biological Molecules, 323–31. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-9534-2_23.

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Chaudhary, Karan, and Dhanraj T. Masram. "Biological Activities of Nanoparticles and Mechanism of Action." In Model Organisms to Study Biological Activities and Toxicity of Nanoparticles, 19–34. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1702-0_2.

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Godfraind, T. "Cellular and Subcellular Approaches to the Mechanism of Action of Calcium Antagonists." In Calcium in Biological Systems, 411–21. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2377-8_45.

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Zimmerman, Thomas P., Gerald Wolberg, Carolyn R. Stopford, Karen L. Prus, and Marie A. Iannone. "Studies Concerning the Mechanism of Action of 3-Deazaadenosine in Leukocytes." In Biological Methylation and Drug Design, 417–26. Totowa, NJ: Humana Press, 1986. http://dx.doi.org/10.1007/978-1-4612-5012-8_35.

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Saranya, Sivakumar, Adikesavan Selvi, Ranganathan Babujanarthanam, Aruliah Rajasekar, and Jagannathan Madhavan. "Insecticidal Activity of Nanoparticles and Mechanism of Action." In Model Organisms to Study Biological Activities and Toxicity of Nanoparticles, 243–66. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-1702-0_12.

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Nagel, G. A., A. Ammon, H. H. Bartsch, K. Krönke, and K. Pfizenmaier. "Biological Response Modifiers: Mechanisms of Action." In Cancer Therapy, 139–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74683-3_15.

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Arteca, Richard N. "Chemistry, Biological Effects, and Mechanism of Action of Plant Growth Substances." In Plant Growth Substances, 45–103. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4757-2451-6_3.

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Moss, Alan C. "Mechanism of Action and Pharmacokinetics of Biologics." In Treatment of Inflammatory Bowel Disease with Biologics, 1–11. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-60276-9_1.

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Conference papers on the topic "Biological Mechanism of Action"

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Korablev, R. A., E. N. Busarin, and A. E. Busarina. "Mechanism of action of infrared light on biological objects." In Лесные экосистемы как глобальный ресурс биосферы: вызовы, угрозы, решения в контексте изменения климата. Воронеж: Воронежский государственный лесотехнический университет им. Г.Ф. Морозова, 2022. http://dx.doi.org/10.58168/iff2022_47-51.

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Garee, J., R. Meyer, and S. Oesterreich. "Sumoylation of Corepressor SAFB1 – Mechanism of Action and Biological Relevance in Breast Cancer." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-4142.

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Oesterreich, S., S. Jiang, E. Verdin, A. Lee, and S. Malik. "Estrogen Receptor-Mediated Repression of Target Genes: Mechanism of Action, and Biological Significance." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-4136.

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Rivera-Ortiz, Phillip, and Domitilla Del Vecchio. "Integral action with time scale separation: A mechanism for modularity in biological systems." In 2014 IEEE 53rd Annual Conference on Decision and Control (CDC). IEEE, 2014. http://dx.doi.org/10.1109/cdc.2014.7039358.

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Karwa, Amolkumar, Raghavan Rajagopalan, Amruta R. Poreddy, Carolyn Sympson, Gary E. Cantrell, and Richard B. Dorshow. "In vitro biological effects of novel type I photosensitizers and their mechanism of action." In BiOS, edited by David H. Kessel. SPIE, 2010. http://dx.doi.org/10.1117/12.844971.

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Klebanov, Gennady I., and Evgeny A. Poltanov. "Photochemical mechanisms of biological action of low-intensity laser irradiation." In SPIE Proceedings, edited by Valery V. Tuchin. SPIE, 2004. http://dx.doi.org/10.1117/12.578306.

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"Larvicidal Activity of Mistletoe Lectin on Lepidopteran Pests: Mechanisms of Action." In International Conference on Civil, Biological and Environmental Engineering. International Institute of Chemical, Biological & Environmental Engineering, 2014. http://dx.doi.org/10.15242/iicbe.c514525.

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Garee, JP, R. Meyer, and S. Oesterreich. "Sumoylation of corepressor scaffold attachment factor b1-mechanism of action and biological relevance in breast cancer." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-3046.

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Shim, Youn Young, Timothy Tse, and Martin Reaney. "Biological Activities of Flaxseed Peptides (Linusorbs)." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/zrcc3198.

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Flaxseed (Linum usitatissimum >L.) is gaining popularity in the food industry as a superfood due to its health-promoting properties. The flax plant synthesizes an array of biologically active cyclic peptides or linusorbs (LOs, a.k.a. cyclolinopeptides) from three or more ribosome-derived precursors. [1–9-NαC]-linusorb B3 and [1–9-NαC]-linusorb B2, suppress immunity, induce apoptosis in human epithelial cancer cell line (Calu-3) cells, and inhibit T-cell proliferation, but the mechanism of LOs action is unknown. Using gene expression analysis in nematode cultures and human cancer cell lines we have observed that LOs exert their activity, in part, through induction of apoptosis. Specific LOs’ properties include: 1) distribute throughout the body after flaxseed consumption; 2) induce heat shock protein (HSP) 70A production as an indicator of stress and addressed the issue in Caenorhabditis elegans (exposure of nematode cultures to [1–9-NαC]-linusorb B3 induced a 30% increase in production of the HSP 70A protein); 3) induce apoptosis in Calu-3 cells; and 4) modulate regulatory genes in microarray analysis. These diverse activities indicate that LOs might induce apoptosis in cancer cells or act as versatile platforms to deliver a variety of biologically active molecules for cancer therapy.
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Chen, X., S. J. Bonvini, E. D. Dubuis, T. Ariyasu, S. Ushio, M. A. Birrell, and M. G. Belvisi. "Cromoglycate Inhibits Oxidative Stress Triggered Airway Sensory Nerves Through Its Actions on the Ion Channel TRPV2: A New Insight into Biological Mechanism of Action." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a6115.

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Reports on the topic "Biological Mechanism of Action"

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Werren, John H., Einat Zchori-Fein, and Moshe Coll. Parthenogenesis-Inducing Microorganisms in Parasitic Hymenoptera: Their Mode of Action and Utilization for Improvement of Biological Control Agents. United States Department of Agriculture, June 1996. http://dx.doi.org/10.32747/1996.7573080.bard.

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Wolbachia are intracellular bacteria known to cause reproductive and sex ratio disorders in many insects. In various parasitic Hymenoptera, Wolbachia induce thelytokous reproduction. The overall goal of this research was the improvement of biological control agents by reversion of their mode of reproduction. This was attempted from two directions: 1) studying the effect of naturally occurring Wolbachia on the thelytokous species Muscidifuraxuniraptor and 2) trying to transmit thelytoky-inducing Wolbachia to Nasoniavitripennis. In M. uniraptor, gamete duplication was found to be the mode of diploidy restoration and Wolbachia density had a strong effect on sex ratio but not on host fitness. Studies on the natural horizontal transmission of Wolbachia between Nasonia wasps and their Protocalliphora hosts using the Wolbachia Outer Surface Protein (WOSP) gene revealed that (a) two Nasonia species (N. giraulti and N. longicornis) possess closely related strains of B-group Wolbachia, but N. vitripennisapparently acquired B Wolbachia by horizontal transmission from an unknown source, (b) Nasonia and its Protocalliphora host have similar Wolbachia, and (c) the Protocalliphora Wolbachia WOSP gene is a recombinant between the one found in N. giraulti/longicornis and N. vitripennis. Results show parasitoid-host insect transmission of Wolbachia and recombination among Wolbachia strains. Results from gynandromorph studies suggest a novel mechanism of sex determination in Nasonia.
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Chalutz, Edo, Michael Wisniewski, Samir Droby, Yael Eilam, and Ilan Chet. Mode of Action of Yeast Biocontrol Agents of Postharvest Diseases of Fruits. United States Department of Agriculture, June 1996. http://dx.doi.org/10.32747/1996.7613025.bard.

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In a previous BARD-supported study, three of the investigators of this research were involved in a study on biological control of postharvest diseases of citrus and deciduous fruits. Several naturally occurring, non-antibiotic producing yeast antagonists were identified. Application of some of these antagonists resulted in very high levels of biocontrol under laboratory conditions but lower efficacy in semi-commercial tests. It was felt that the lack of knowledge on the mode of action of the biocontrol agents was limiting their efficient use. The current study was aimed at narrowing this gap in our knowledge. Two specific objectives were outlined: to study the mechanism by which calcium salts enhance biocontrol activity and to determine the role, if any, of the yeast extracellular materials and/or enzymes which degrade fungal cell walls during the interaction between the antagonists, the pathogen and the host. CaCl2 but not MgCl2, inhibited spore germination, and germ-tube elongation of Botrytis cinerea, Penicillium expansum and P. digitatum in culture. It also inhibited the pectinolytic activity of the pathogens. Biocontrol of apple decay by isolate 182 of Candida oleophila, an effective biocontrol agent, was enhanced by the addition of CaCl2 whereas there was no effect on the biocontrol activity of isolate 247 of this yeast. Similarly, CaCl2 enhanced efficacy of the US-7 isolate of Pichia guilliermondii in reducing infection of P. digitatum in citrus fruit. CaCl2 by itself also reduced the infection of peel wounds and stimulated ethylene production by grapefruit peel. This antagonist exhibited a very high ability to maintain cytosolic Ca2+ homeostasis when exposed to high CaCl2 concentrations. It is postulated, therefore, that enhanced biocontrol activity by calcium is the result of direct inhibition of the pathogen by calcium ions on spore germination and metabolism and indirectly due to the ability of the biocontrol agent to maintain normal metabolism in the presence of high levels of calcium. The extracellular materials produced by P. guilliermondii in culture and on the fruit inhibited, at low concentrations, the pathogen in culture and reduced percent infection of the fruit. The direct inhibition of the pathogen by these materials may thus be involved in the mode of action of the antagonist. This study contributed to our knowledge on the action of calcium salts and the yeast antagonist extracellular materials on biocontrol activity and will contribute to a more efficient use of this technology in the control of postharvest diseases of fruits.
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Roberts, Jr, and Charles T. A Novel Mechanism of Androgen Receptor Action. Fort Belvoir, VA: Defense Technical Information Center, January 2008. http://dx.doi.org/10.21236/ada489364.

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Roberts, Jr, and Charles T. A Novel Mechanism of Androgen Receptor Action. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada503252.

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Bates, Paula J. Mechanism of Action of Novel Antiproliferative Oligonucleotides. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada406133.

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Roberts, Jr, and Charles T. A Novel Mechanism of Androgen Receptor Action. Fort Belvoir, VA: Defense Technical Information Center, January 2007. http://dx.doi.org/10.21236/ada466168.

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Kamasani, Uma R., and George Prendergast. Mechanism of RhoB/FTI Action in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2004. http://dx.doi.org/10.21236/ada446332.

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Rane, Neena S., and George C. Prendergast. Mechanism of RhoB/FTI Action in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada412302.

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Rogers, Terry B. Mechanism of Action of the Presynaptic Neurotoxin, Tetanus Toxin. Fort Belvoir, VA: Defense Technical Information Center, July 1991. http://dx.doi.org/10.21236/ada246780.

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Rogers, Terry B. Mechanism of Action of the Presynaptic Neurotoxins Tetanus Toxin. Fort Belvoir, VA: Defense Technical Information Center, January 1992. http://dx.doi.org/10.21236/ada246495.

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