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Aspergillus
Published in Yoshikatsu Murooka, Tadayuki Imanaka, Recombinant Microbes for Industrial and Agricultural Applications, 2020
The secretion process in molds has not been investigated in any detail, although many of the gross features associated with protein secretion in the yeast S. cerevisiae [83-86] may well pertain in the molds. An illustration of some of the features expected is given in Figure 2 and serves only to illustrate some important facets of protein secretion and modification that require investigation in molds. The Golgi is represented as a morphological entity in Figure 2, although the Golgi is better regarded as the focus for protein sorting (i.e., recognition of the various sorting signals that determine the ultimate destination of proteins occurs in the Golgi) [87]. Under many conditions S. cerevisiae, unlike some other yeast species, lacks a Golgi stack recognizable by electron microscopy, although the Golgi can still be defined as a functional entity [86-88]. In molds, protein secretion occurs at hyphal tips in developing mycelia [89] and is mediated through the fusion of membranous vesicles with the hyphal tip membrane [90], although it is also possible that some protein secretion occurs away from the hyphal tips. Important events are protein targeting and entry of the polypeptide into the endoplasmic reticulum, processing and folding of the protein, sorting and targeting of proteins destined for export to the hyphal tip and, occasionally, glycosylation of the protein.
Nucleoprotein-Based Nanodevices in Drug Design and Delivery
Published in Tuan Vo-Dinh, Nanotechnology in Biology and Medicine, 2017
Elizabeth Singer, Katarzyna Lamparska-Kupsik, Jarrod Clark, Kristofer Munson, Leo Kretzner, Steven S. Smith
In general, gene expression patterns are randomized during tumorigenesis by genetic damage and natural selection during tumor progression. Hallmarks of this process are the establishment of patterns of ectopic gene expression and ectopic gene silencing that adapt them for their role as invasive tumors. This has led to the development of drugs directed at the disruption of stable patterns of gene expression, in the hope that selective delivery to tumor cells will inhibit growth or induce cell death [43]. Among the drugs that have been discovered are a variety of histone deacetylase inhibitors and DNA (cytosine-5) methyltransferase inhibitors [44] that tend to act synergistically [45,46] to disrupt these gene silencing systems. These drugs can also be effective alone. In principle, DNA methyltransferases can be inhibited by either the direct interaction of the inhibitor with the enzyme active site or its protein targeting signals, or by selectively interfering with methyltransferase synthesis. The DNA Y-junction can be used to target DNA methyltransferase traps (noncompetitive inhibitors of the enzyme) or DNAzymes targeting the messenger RNA for the methyltransferase itself to the nucleus.
Aptamers as Tools for Targeted Drug Delivery
Published in Rakesh N. Veedu, Aptamers, 2017
An anti-gp 120 aptamer–siRNA chimera was developed against cells expressing HIV-1 gp 120 [100]. Both the aptamer and the siRNA (anti-tat/rev siRNA) had anti-HIV activity, and the authors report that this dual functioning chimera allowed selective delivery into the target cells and inhibited HIV replication and spread [100]. A targeted approach using aptamer for combinatorial delivery of antiviral and host dicer substrate siRNA (DsiRNA) was tested for treatment in HIV infection [102]. In this facile strategy, 3′ 7-carbon linker (7C3) bound to a 16-nucleotide 2′ OMe/2′ Fl GC rich bridge was used to aid the binding of various siRNAs with the targeting aptamer. An HIV-1 gp120 aptamer targeted the DsiRNAs, and the in vivo antiviral activity was studied in a humanized mouse model. The results report the delivery of siRNA and long-term suppression of HIV-1 viral load [102]. An RNA aptamer–siRNA chimera was developed as a combination approach for the treatment of HIV infection [58]. The HIV-1 envelope protein-targeting aptamer was attached to the siRNA targeting the viral RNA through a linker. The antiviral effect was tested in the humanized Rag2-/-gc-/- (RAG-hu) mouse model, which mimics the HIV-1 replication and CD4+ T-cell depletion in humans. This nontoxic therapeutic approach reports efficient viral suppression by the dual anti-HIV activity offered by the aptamer and the siRNA [58].
Interactions of zinc(II) complexes with 5′-GMP and their cytotoxic activity
Published in Journal of Coordination Chemistry, 2019
Tanja V. Soldatović, Enisa Selimović, Biljana Šmit, Darko Ašanin, Nevena S. Planojević, Snežana D. Marković, Ralph Puchta, Basam M. Alzoubi
Design of novel non-platinum DNA- and protein-targeting metal-based anticancer agents with potential in vitro toxicity have gained importance in recent years [1, 2]. The non-platinum antitumor complexes could be alternatives to platinum-based drugs due to their better characteristics and less negative side effects. Some transition metal ions are essential cellular components involved in several biochemical processes. They act mainly as Lewis acids, having unique characteristics such as redox activity, variable coordination modes, kinetics properties and reactivity towards biological relevant nucleophiles [1]. Due to their characteristics and roles in physiological processes, the compounds of essential transition metals could be more effective as drugs in treatment of cancers.
Substitution behavior of square-planar and square-pyramidal Cu(II) complexes with bio-relevant nucleophiles
Published in Journal of Coordination Chemistry, 2018
Enisa Selimović, Andrei V. Komolkin, Andrei V. Egorov, Tanja Soldatović
Over the past decades, transition metal complexes have attracted considerable attention in medicinal inorganic chemistry, especially as synthetic metallonucleases and metal-based anticancer drugs that are able to bind to DNA under physiological conditions [1–3]. The use of metal-based drugs presents the most important strategy in the development of new anticancer and antimicrobial agents [4–8]. Negative side effects during treatment (such as vomiting, resistance, nephrotoxicity, ototoxicity, neurotoxicity, cardiotoxicity, etc.) prompted researchers to design new classes of DNA and protein-targeting metal-based anticancer agents with potential in vitro selectivity and less toxicity [4].
An exploration on the toxicity mechanisms of phytotoxins and their potential utilities
Published in Critical Reviews in Environmental Science and Technology, 2022
Huiling Chen, Harpreet Singh, Neha Bhardwaj, Sanjeev K. Bhardwaj, Madhu Khatri, Ki-Hyun Kim, Wanxi Peng
Fungal pathogens are a constant danger to crop production, causing preharvest and postharvest diseases. Fungi have various life cycles containing a variety of mechanisms that affect their host plants. They are highly dissimilar in which plant families they infect. Plant–fungal relationships are not always destructive; they can be symbiotic and beneficial, as in the case of mycorrhizal roots. Mycotoxins are metabolites commonly produced by filamentous fungi, that harmfully affect plant growth. They can cause numerous symptoms in plants, such as leaf spots, wilting, chlorosis, and necrosis (Akpaninyang & Opara, 2017; Amusa, 2006; Evidente et al., 2019). Based on the phytotoxic activity of the fungi, mycotoxins can be categorized as host-selective toxins and non–host selective toxins. In the former, the toxins cause pathogenicity in only those plants that are usual hosts of the fungus. In the latter, the toxins are not always required for pathogenicity and are nonspecific to their hosts (Möbius & Hertweck, 2009; Varejão et al., 2013). Fungal toxins produce toxicity in plant cells (apoptosis) by different mechanisms (Figure 2), such as protein targeting, damaging the membrane structure, and disintegrating the cytoskeleton via siderophore generation (Möbius & Hertweck, 2009). Mycotoxins are produced by fungi of the genera Fusarium, Aspergillus, and Penicillium under particular conditions of temperature and moisture (Alshannaq & Yu, 2017; Gruber-Dorninger et al., 2017; Moretti et al., 2017). They contaminate food chains by entering through plant-based food or feed products, contaminated water, and direct fungal growth. The most dangerous mycotoxins are the aflatoxins and ochratoxins, whose consumption can cause chronic toxicity, genotoxicity, carcinogenicity, and mutagenicity in humans (Picardo et al., 2019; Shephard, 2016). Some examples of fungal phytotoxins are fusaric acid, solanapyrone, fumonisin, β-nitropropionic acid, tenuazonic acid, and cercosporin (Frisvad et al., 2006). A detailed list of common plant toxins and microbial phytotoxins, along with their origins and structural forms, is provided in Table 1.