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Journal articles on the topic 'Decoy molecules'

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Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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1

Imrie, Fergus, Anthony R. Bradley, and Charlotte M. Deane. "Generating property-matched decoy molecules using deep learning." Bioinformatics 37, no. 15 (February 3, 2021): 2134–41. http://dx.doi.org/10.1093/bioinformatics/btab080.

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Abstract Motivation An essential step in the development of virtual screening methods is the use of established sets of actives and decoys for benchmarking and training. However, the decoy molecules in commonly used sets are biased meaning that methods often exploit these biases to separate actives and decoys, and do not necessarily learn to perform molecular recognition. This fundamental issue prevents generalization and hinders virtual screening method development. Results We have developed a deep learning method (DeepCoy) that generates decoys to a user’s preferred specification in order to remove such biases or construct sets with a defined bias. We validated DeepCoy using two established benchmarks, DUD-E and DEKOIS 2.0. For all 102 DUD-E targets and 80 of the 81 DEKOIS 2.0 targets, our generated decoy molecules more closely matched the active molecules’ physicochemical properties while introducing no discernible additional risk of false negatives. The DeepCoy decoys improved the Deviation from Optimal Embedding (DOE) score by an average of 81% and 66%, respectively, decreasing from 0.166 to 0.032 for DUD-E and from 0.109 to 0.038 for DEKOIS 2.0. Further, the generated decoys are harder to distinguish than the original decoy molecules via docking with Autodock Vina, with virtual screening performance falling from an AUC ROC of 0.70 to 0.63. Availability and implementation The code is available at https://github.com/oxpig/DeepCoy. Generated molecules can be downloaded from http://opig.stats.ox.ac.uk/resources. Supplementary information Supplementary data are available at Bioinformatics online.

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2

Alam, Fardina Fathmiul, and Amarda Shehu. "Unsupervised multi-instance learning for protein structure determination." Journal of Bioinformatics and Computational Biology 19, no. 01 (February 2021): 2140002. http://dx.doi.org/10.1142/s0219720021400023.

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Many regions of the protein universe remain inaccessible by wet-laboratory or computational structure determination methods. A significant challenge in elucidating these dark regions in silico relates to the ability to discriminate relevant structure(s) among many structures/decoys computed for a protein of interest, a problem known as decoy selection. Clustering decoys based on geometric similarity remains popular. However, it is unclear how exactly to exploit the groups of decoys revealed via clustering to select individual structures for prediction. In this paper, we provide an intuitive formulation of the decoy selection problem as an instance of unsupervised multi-instance learning. We address the problem in three stages, first organizing given decoys of a protein molecule into bags, then identifying relevant bags, and finally drawing individual instances from these bags to offer as prediction. We propose both non-parametric and parametric algorithms for drawing individual instances. Our evaluation utilizes two datasets, one benchmark dataset of ensembles of decoys for a varied list of protein molecules, and a dataset of decoy ensembles for targets drawn from recent CASP competitions. A comparative analysis with state-of-the-art methods reveals that the proposed approach outperforms existing methods, thus warranting further investigation of multi-instance learning to advance our treatment of decoy selection.

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Alvarez-de Miranda, Francisco Javier, Isabel Alonso-Sánchez, Antonio Alcamí, and Bruno Hernaez. "TNF Decoy Receptors Encoded by Poxviruses." Pathogens 10, no. 8 (August 22, 2021): 1065. http://dx.doi.org/10.3390/pathogens10081065.

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Tumour necrosis factor (TNF) is an inflammatory cytokine produced in response to viral infections that promotes the recruitment and activation of leukocytes to sites of infection. This TNF-based host response is essential to limit virus spreading, thus poxviruses have evolutionarily adopted diverse molecular mechanisms to counteract TNF antiviral action. These include the expression of poxvirus-encoded soluble receptors or proteins able to bind and neutralize TNF and other members of the TNF ligand superfamily, acting as decoy receptors. This article reviews in detail the various TNF decoy receptors identified to date in the genomes from different poxvirus species, with a special focus on their impact on poxvirus pathogenesis and their potential use as therapeutic molecules.

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4

Panneerselvam, Mathivadhani, Piyush M. Patel, David M. Roth, Michael W. Kidd, Blake Chin-Lee, Brian P. Head, Ingrid R. Niesman, Satoki Inoue, Hemal H. Patel, and Daniel P. Davis. "Role of decoy molecules in neuronal ischemic preconditioning." Life Sciences 88, no. 15-16 (April 2011): 670–74. http://dx.doi.org/10.1016/j.lfs.2011.02.004.

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5

TOMITA, NARUYA, RYUICHI MORISHITA, HUI Y. LAN, KEI YAMAMOTO, MASAHIDE HASHIZUME, MITSUE NOTAKE, KAORU TOYOSAWA, et al. "In VivoAdministration of a Nuclear Transcription Factor-κB Decoy Suppresses Experimental Crescentic Glomerulonephritis." Journal of the American Society of Nephrology 11, no. 7 (July 2000): 1244–52. http://dx.doi.org/10.1681/asn.v1171244.

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Abstract. Glomerular expression of cytokines, interleukin-1 (IL-1), and tumor necrosis factor-α (TNF-α), together with leukocytic infiltration, are prominent features in crescentic glomerulonephritis. Because these cytokines are targets for nuclear transcription factor-κB (NF-κB), the use of NF-κB decoy oligodeoxynucleotide (ODN) treatment was evaluated in an experimental disease model. Crescentic glomerulonephritis was induced in primed Wistar rats by injection of sheep antiglomerular basement membrane serum. Thirty minutes after injection, rats were anesthetized and the left kidney was perfused with NF-κB decoy ODN or scrambled ODN control mixed with a virus-liposome complex, and then killed 7 d later. Animals given the scrambled control ODN developed severe glomerulonephritis by day 7 with heavy proteinuria, glomerular crescents and interstitial lesions, marked leukocytic infiltration, and upregulated renal expression of cytokines (IL-1 and TNF-α) and adhesion molecules (intercellular adhesion molecule-1). In contrast, NF-κB decoy ODN treatment substantially inhibited the disease with a 50% reduction in proteinuria, a threefold reduction in histologic damage, a 50% reduction in leukocytic infiltration, and a 50 to 80% reduction in the renal expression of cytokines and leukocyte adhesion molecules. In conclusion, this study has demonstrated that NF-κB plays a key role in cytokine-mediated renal injury and that NF-κB decoy ODN treatment has clear therapeutic potential in rapidly progressive glomerulonephritis.

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6

Lohan, Fiona, and Karen Keeshan. "The functionally diverse roles of tribbles." Biochemical Society Transactions 41, no. 4 (July 18, 2013): 1096–100. http://dx.doi.org/10.1042/bst20130105.

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Tribbles are members of the pseudokinase family of proteins, with no associated kinase activity detectable to date. As tribbles appear not to function as kinases, there has been debate surrounding their functional classification. Tribbles have been proposed to function as adaptor molecules facilitating degradation of their target proteins. Tribbles have also been proposed to mediate signalling changes to MAPK (mitogen-activated protein kinase) cascades and also to function as decoy kinases interfering with the activity of known kinases. The present review discusses the functionally divergent roles of tribbles as molecular adaptors mediating degradation, changes to signalling cascades and action as decoy kinases.

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7

Davis, D. P. "The Role of Decoy Molecules in Neuronal Ischemic Preconditioning." Academic Emergency Medicine 10, no. 5 (May 1, 2003): 438—a—438. http://dx.doi.org/10.1197/aemj.10.5.438-a.

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8

Suzuki, Kazuto, Yuma Shisaka, Joshua Kyle Stanfield, Yoshihito Watanabe, and Osami Shoji. "Enhanced cis- and enantioselective cyclopropanation of styrene catalysed by cytochrome P450BM3 using decoy molecules." Chemical Communications 56, no. 75 (2020): 11026–29. http://dx.doi.org/10.1039/d0cc04883f.

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9

Colotta, F., S. Saccani, J. G. Giri, S. K. Dower, J. E. Sims, M. Introna, and A. Mantovani. "Regulated expression and release of the IL-1 decoy receptor in human mononuclear phagocytes." Journal of Immunology 156, no. 7 (April 1, 1996): 2534–41. http://dx.doi.org/10.4049/jimmunol.156.7.2534.

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Abstract The aim of this study was to investigate the expression and release of the IL-1 type II decoy receptor (R) in mononuclear phagocytes, which play a central role in immune and chronic inflammatory reactions. Human monocytes expressed both type I and type II R transcripts, the latter being two- to threefold more represented. By cross-linking and Ab blocking, the predominant surface IL-1-binding molecule was the decoy RII. IL-4, IL-13, and dexamethasone induced RI and RII transcripts and augmented the number of IL-1-binding sites with no modification of Kd values. The induced surface receptor was identified as the decoy RII. These stimuli induced the release of a soluble R with a m.w. of approximately 60 kDa, of which N-glycosylation contributed 22 kDa compared with 45 kDa released from polymorphonuclear leukocytes, of which N-glycosylation contributed 15 kDa. IL-13 and dexamethasone induced a release of 24 ng/ml/2 x 10(7) cells (from 8.7 to 43.2 ng/ml) and 25.6 ng/ml/2 x 10(7) cells (from 9.7 to 36.8 ng/ml) of decoy RII in 18 h, respectively (six donors). Thus, for instance, IL-13-treated (18 h) cells expressed 3.5 x 10(3) sites/cell and released 12 x 10(3) decoy RII/cell. The released decoy RII from monocytes bound IL-1apha and IL-1 receptor antagonist 30- and 2-fold less avidly than IL-1beta, respectively. In vitro-matured, monocyte-derived macrophages showed higher levels of surface expression and release of the IL-1 decoy RII. The results show that, on exposure to diverse molecules with anti-inflammatory properties, mononuclear phagocytes express and release copious amounts of a novel version of the soluble IL-1 decoy RII.

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Kobayashi, Yuichiro, Kenji Kohara, Yusuke Kiuchi, Hiroki Onoda, Osami Shoji, and Hiroyasu Yamaguchi. "Control of microenvironment around enzymes by hydrogels." Chemical Communications 56, no. 49 (2020): 6723–26. http://dx.doi.org/10.1039/d0cc01332c.

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11

Suzuki, Kazuto, Joshua Kyle Stanfield, Osami Shoji, Sota Yanagisawa, Hiroshi Sugimoto, Yoshitsugu Shiro, and Yoshihito Watanabe. "Control of stereoselectivity of benzylic hydroxylation catalysed by wild-type cytochrome P450BM3 using decoy molecules." Catalysis Science & Technology 7, no. 15 (2017): 3332–38. http://dx.doi.org/10.1039/c7cy01130j.

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12

Lambertini, E., L. Penolazzi, V. Sollazzo, F. Pezzetti, M. de Mattei, L. del Senno, GC Traina, and R. Piva. "Modulation of gene expression in human osteoblasts by targeting a distal promoter region of human estrogen receptor-alpha gene." Journal of Endocrinology 172, no. 3 (March 1, 2002): 683–93. http://dx.doi.org/10.1677/joe.0.1720683.

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Estrogen receptor (ER) alpha is expressed during osteoblast differentiation; however, both its functional role in bone metabolism and its involvement in osteoporotic pathogenesis caused by estrogen deficiency are not well understood. Loss of ER alpha gene expression could be one of the mechanisms leading to osteoporosis. Therefore, we investigated a possible modulation of ER alpha gene expression in a human osteoblastic cell line and in four primary osteoblast cultures by using a decoy strategy. Double stranded DNA molecules, mimicking a regulatory region of the ER alpha gene promoter (DNA-102) and acting as a 'silencer' in breast cancer cells, were introduced into osteoblasts as 'decoy' cis-elements to bind and functionally inactivate a putative negative transcription factor, and thus to induce ER alpha gene expression. We found that the DNA-102 molecule was able to specifically bind osteoblast nuclear proteins. Before decoy treatment, absence or variable low levels of ER alpha RNAs in the different cultures were detected. When the cells were transfected with the DNA-102 decoy, an increase in expression of ER alpha and osteoblastic markers, such as osteopontin, was observed, indicating a more differentiated osteoblastic phenotype both in the cell line and in primary cultures. These results showed that the DNA-102 sequence competes with endogenous specific negative transcription factors that may be critical for a decrease in or lack of ER alpha gene transcription. Therefore, osteoblastic transfection with the DNA-102 decoy molecule may be considered a tempting model in a putative therapeutic approach for those pathologies, such as osteoporosis, in which the decrease or loss of ER alpha expression plays a critical role in bone function.

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13

STANFIELD, Joshua Kyle, and Osami SHOJI. "Gaseous Alkane Hydroxylation by Deceiving Cytochrome P450BM3 Using Decoy Molecules." Journal of the Japan Petroleum Institute 65, no. 3 (May 1, 2022): 79–87. http://dx.doi.org/10.1627/jpi.65.79.

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14

Quayle, S. N., N. R. Mawji, J. Wang, and M. D. Sadar. "Androgen receptor decoy molecules block the growth of prostate cancer." Proceedings of the National Academy of Sciences 104, no. 4 (January 16, 2007): 1331–36. http://dx.doi.org/10.1073/pnas.0606718104.

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15

Tanabe, Kazuhito, Takeo Ito, and Sei-ichi Nishimoto. "Radiolytic Reduction Characteristics of Artificial Oligodeoxynucleotides Possessing 2-Oxoalkyl Group or Disulfide Bonds." Journal of Nucleic Acids 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/816207.

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A number of advances have been made in the development of modified oligodeoxynucleotides (ODNs), and chemical or physical properties of which are controlled by external stimuli. These intelligent ODNs are promising for the next generation of gene diagnostics and therapy. This paper focuses on the molecular design of artificial ODNs that are activated by X-irradiation and their applications to regulation of hybridization properties, conformation change, radiation-activated DNAzyme, and decoy molecules.

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16

Stanfield, Joshua Kyle, and Osami Shoji. "The Power of Deception: Using Decoy Molecules to Manipulate P450BM3 Biotransformations." Chemistry Letters 50, no. 12 (December 5, 2021): 2025–31. http://dx.doi.org/10.1246/cl.210584.

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17

Watanabe, Norihiko, and Hiroshi Nakajima. "Coinhibitory Molecules in Autoimmune Diseases." Clinical and Developmental Immunology 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/269756.

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Coinhibitory molecules such as CTLA-4, PD-1 and BTLA negatively regulate immune responses. Multiple studies indicate that the deficiency or mutation of coinhibitory molecules leads to the development of autoimmune diseases in mice and humans, indicating that the negative signals from coinhibitory molecules are crucial for the prevention of autoimmunity. In some conditions, the administration of decoy coinhibitory receptors (e.g., CTLA-4 Ig) or mAb against coinhibitory molecules suppresses the responses of self-reactive T cells in autoimmune diseases. Therefore, modulation of coinhibitory signals seems to be an attractive approach to induce tolerance in autoimmune diseases in humans where the disease-inducing self-antigens are not known. Particularly, administration of CTLA-4 Ig has shown great promise in animal models of autoimmune diseases and has been gaining increasing attention in clinical investigation in several autoimmune diseases in humans.

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18

Kawakami, Norifumi, Zhiqi Cong, Osami Shoji, and Yoshihito Watanabe. "Highly efficient hydroxylation of gaseous alkanes at reduced temperature catalyzed by cytochrome P450BM3 assisted by decoy molecules." Journal of Porphyrins and Phthalocyanines 19, no. 01-03 (January 2015): 329–34. http://dx.doi.org/10.1142/s1088424615500145.

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Cytochrome P450BM3 functions as a small-alkane hydroxylase upon the addition of perfluorocarboxylic acids (PFs) as decoy molecules. The coupling efficiency (product formation rate per NADPH consumption rate) for the hydroxylation of small alkanes was improved by reducing the reaction temperature to 0°C.

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19

Vieira, Tatiana F., and Sérgio F. Sousa. "Comparing AutoDock and Vina in Ligand/Decoy Discrimination for Virtual Screening." Applied Sciences 9, no. 21 (October 25, 2019): 4538. http://dx.doi.org/10.3390/app9214538.

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AutoDock and Vina are two of the most widely used protein–ligand docking programs. The fact that these programs are free and available under an open source license, also makes them a very popular first choice for many users and a common starting point for many virtual screening campaigns, particularly in academia. Here, we evaluated the performance of AutoDock and Vina against an unbiased dataset containing 102 protein targets, 22,432 active compounds and 1,380,513 decoy molecules. In general, the results showed that the overall performance of Vina and AutoDock was comparable in discriminating between actives and decoys. However, the results varied significantly with the type of target. AutoDock was better in discriminating ligands and decoys in more hydrophobic, poorly polar and poorly charged pockets, while Vina tended to give better results for polar and charged binding pockets. For the type of ligand, the tendency was the same for both Vina and AutoDock. Bigger and more flexible ligands still presented a bigger challenge for these docking programs. A set of guidelines was formulated, based on the strengths and weaknesses of both docking program and their limits of validation.

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Colotta, F., S. Orlando, E. J. Fadlon, S. Sozzani, C. Matteucci, and A. Mantovani. "Chemoattractants induce rapid release of the interleukin 1 type II decoy receptor in human polymorphonuclear cells." Journal of Experimental Medicine 181, no. 6 (June 1, 1995): 2181–86. http://dx.doi.org/10.1084/jem.181.6.2181.

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Molecules representative of different classes of chemotactic agents, including formyl-Met-Leu-Phe (FMLP), C5a, leukotriene B4, platelet-activating factor, and interleukin (IL)-8, caused a rapid reduction in the IL-1 binding capacity by human polymorphonuclear leukocytes (PMN), a cell type expressing predominantly the IL-1 type II decoy receptor (IL-1 decoy RII). N-t-Boc-Met-Leu-Phe, an antagonist for the FMLP receptor, inhibited the loss of IL-1 binding capacity induced by FMLP. Monocyte chemotactic protein 1, a chemokine related to IL-8 but inactive on PMN, had no effect on IL-1 binding in this cell type. FMLP was selected for further detailed analysis of chemoattractant-induced loss of IL-1 binding by PMN. The action of FMLP was rapid, reaching 50% of its maximum (80%) at 30 s, the earliest measurable time point, and plateauing between 10 and 30 min. Dose-response analysis revealed that maximal reduction of IL-1 binding was reached at FMLP concentrations that were also optimal for chemotaxis (50% effective dose = 5 x 10(-9) M). The loss of IL-1 binding capacity caused by FMLP was determined by a reduction in receptor number with no change in their affinity. The effect of FMLP on IL-1 receptor (IL-1R) was selective in that the PMN surface structures IL-8R, CD16, CD18, and major histocompatibility complex class I antigens were unaffected under these conditions. Loss of surface IL-1R was not due to an augumented rate of internalization. FMLP caused rapid release of a 45-kD IL-1-binding molecule identified as the IL-1 decoy RII. After FMLP-induced release, PMN reexpressed newly synthesized receptors, reaching basal levels by 4 h. FMLP-induced release of the IL-1 decoy RII did not impair the responsiveness of PMN to IL-1 in terms of promotion of survival and cytokine production. FMLP-induced release of the IL-1 decoy RII was unaffected by protein synthesis inhibitors, was blocked by certain protease inhibitors, and was mimicked by agents (the Ca++ ionophore A23187 and phorbol myristate acetate) that recapitulate elements in the signal transduction pathway of chemoattractant receptors. The time frame and concentration range of chemoattractant-induced rapid release of the IL-1 decoy RII are consistent with the view that IL-1 decoy RII release is an early event in the multistep process of leukocyte recruitment.(ABSTRACT TRUNCATED AT 400 WORDS)

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21

Gambari, Roberto. "Therapeutic Relevance of Targeting Nuclear Factor kappaB with Transcription Factor Decoy Molecules." Drug Design Reviews - Online 2, no. 5 (August 1, 2005): 397–407. http://dx.doi.org/10.2174/1567269054546415.

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22

PIVA, ROBERTA, LETIZIA PENOLAZZI, MARGHERITA ZENNARO, ERCOLINA BIANCHINI, EROS MAGRI, MONICA BORGATTI, ILARIA LAMPRONTI, ELISABETTA LAMBERTINI, ELISA TAVANTI, and ROBERTO GAMBARI. "Induction of Apoptosis of Osteoclasts by Targeting Transcription Factors with Decoy Molecules." Annals of the New York Academy of Sciences 1091, no. 1 (December 2006): 509–16. http://dx.doi.org/10.1196/annals.1378.092.

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23

Suzuki, Jun-ichi, Mitsuaki Isobe, Ryuichi Morishita, and Ryozo Nagai. "Nucleic Acid Drugs for Prevention of Cardiac Rejection." Journal of Biomedicine and Biotechnology 2009 (2009): 1–5. http://dx.doi.org/10.1155/2009/916514.

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Heart transplantation has been broadly performed in humans. However, occurrence of acute and chronic rejection has not yet been resolved. Several inflammatory factors, such as cytokines and adhesion molecules, enhance the rejection. The graft arterial disease (GAD), which is a type of chronic rejection, is characterized by intimal thickening comprised of proliferative smooth muscle cells. Specific treatments that target the attenuation of acute rejection and GAD formation have not been well studied in cardiac transplantation. Recent progress in the nucleic acid drugs, such as antisense oligodeoxynucleotides (ODNs) to regulate the transcription of disease-related genes, has important roles in therapeutic applications. Transfection of cis-element double-stranded DNA, named as “decoy,” has been also reported to be a useful nucleic acid drug. This decoy strategy has been not only a useful method for the experimental studies of gene regulation but also a novel clinical strategy. In this paper, we reviewed the experimental results ofNF-κB, E2F, AP-1, and STAT-1 decoy and other ODNs using the experimental heart transplant models.

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Toshchakov, Vladimir Y., and Artur Javmen. "Targeting the TLR7 signalosome assembly by TLR7-derived decoy peptides." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 226.32. http://dx.doi.org/10.4049/jimmunol.204.supp.226.32.

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Abstract Toll-like receptors (TLRs) sense microbial molecules and initiate antimicrobial immune response. The members of the TLR family use cytoplasmic Toll/Interleukin-1R homology (TIR) domain to initiate intracellular signaling. Activated TLRs dimerize their TIRs and recruit adapter proteins to the dimer, through multiple interactions of receptor and adapter TIR domains. Although TLRs play an essential role in innate immunity, the aberrant TLR signaling may cause pathogenic inflammation. This study has screened a library of cell-permeable decoy peptides (CPDPs) derived from the TLR7 TIR for interference with TLR7 signaling and identified several CPDPs that inhibit TLR7 signaling. Peptides 7R1, 7R6, 7R9 and 7R11 inhibited the TLR7-induced signaling in murine and human macrophages. The most potent inhibitory peptide of the four, 7R11, significantly reduced the systemic cytokine levels elicited by administration of a TLR7 agonist, R-848, to mice. TLR7 TIR surface regions that correspond to inhibitory peptides generally corresponded to four TIR sites that mediate signalosome assembly for other TLRs. The cell-based Förster resonance energy transfer/fluorescence lifetime imaging confirmed that 7R9 and 7R11 interact with adapter TIRs. These findings clarify the molecular mechanisms that trigger the adapter recruitment to activated TLR7 and suggest that 7R9 and 7R11 have a significant translational potential as candidate or lead therapeutics for treatment of TLR7-mediated inflammation.

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Alam, Fardina Fathmiul, Taseef Rahman, and Amarda Shehu. "Evaluating Autoencoder-Based Featurization and Supervised Learning for Protein Decoy Selection." Molecules 25, no. 5 (March 4, 2020): 1146. http://dx.doi.org/10.3390/molecules25051146.

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Rapid growth in molecular structure data is renewing interest in featurizing structure. Featurizations that retain information on biological activity are particularly sought for protein molecules, where decades of research have shown that indeed structure encodes function. Research on featurization of protein structure is active, but here we assess the promise of autoencoders. Motivated by rapid progress in neural network research, we investigate and evaluate autoencoders on yielding linear and nonlinear featurizations of protein tertiary structures. An additional reason we focus on autoencoders as the engine to obtain featurizations is the versatility of their architectures and the ease with which changes to architecture yield linear versus nonlinear features. While open-source neural network libraries, such as Keras, which we employ here, greatly facilitate constructing, training, and evaluating autoencoder architectures and conducting model search, autoencoders have not yet gained popularity in the structure biology community. Here we demonstrate their utility in a practical context. Employing autoencoder-based featurizations, we address the classic problem of decoy selection in protein structure prediction. Utilizing off-the-shelf supervised learning methods, we demonstrate that the featurizations are indeed meaningful and allow detecting active tertiary structures, thus opening the way for further avenues of research.

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Naganuma, Miyako, Nobumichi Ohoka, Genichiro Tsuji, Haruna Tsujimura, Kenji Matsuno, Takao Inoue, Mikihiko Naito, and Yosuke Demizu. "Development of Chimeric Molecules That Degrade the Estrogen Receptor Using Decoy Oligonucleotide Ligands." ACS Medicinal Chemistry Letters 13, no. 1 (December 17, 2021): 134–39. http://dx.doi.org/10.1021/acsmedchemlett.1c00629.

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Shoji, Osami, and Yoshihito Watanabe. "Monooxygenation of Nonnative Substrates Catalyzed by Bacterial Cytochrome P450s Facilitated by Decoy Molecules." Chemistry Letters 46, no. 3 (March 5, 2017): 278–88. http://dx.doi.org/10.1246/cl.160963.

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Cabrini, G., V. Bezzerri, M. Borgatti, I. Mancini, E. Nicolis, M. C. Dechecchi, A. Tamanini, et al. "“DECOY” MOLECULES FOR NUCLEAR TRANSCRIPTION FACTORS AND REGULATION OF EXPRESSION OF PROINFLAMMATORY GENES." Journal of Cystic Fibrosis 7 (July 2008): S18. http://dx.doi.org/10.1016/s1569-1993(08)60538-x.

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Nakane, Masanori, Satoshi Ichikawa, and Akira Matsuda. "Triazole-Linked Dumbbell Oligodeoxynucleotides with NF-κB Binding Ability as Potential Decoy Molecules." Journal of Organic Chemistry 73, no. 5 (March 2008): 1842–51. http://dx.doi.org/10.1021/jo702459b.

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Park, Seung Yong, Yasmin Hisham, Hyun Mu Shin, Su Cheong Yeom, and Soohyun Kim. "Interleukin-18 Binding Protein in Immune Regulation and Autoimmune Diseases." Biomedicines 10, no. 7 (July 20, 2022): 1750. http://dx.doi.org/10.3390/biomedicines10071750.

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Natural soluble antagonist and decoy receptor on the surface of the cell membrane are evolving as crucial immune system regulators as these molecules are capable of recognizing, binding, and neutralizing (so-called inhibitors) their targeted ligands. Eventually, these soluble antagonists and decoy receptors terminate signaling by prohibiting ligands from connecting to their receptors on the surface of cell membrane. Interleukin-18 binding protein (IL-18BP) participates in regulating both Th1 and Th2 cytokines. IL-18BP is a soluble neutralizing protein belonging to the immunoglobulin (Ig) superfamily as it harbors a single Ig domain. The Ig domain is essential for its binding to the IL-18 ligand and holds partial homology to the IL-1 receptor 2 (IL-1R2) known as a decoy receptor of IL-1α and IL-1β. IL-18BP was defined as a unique soluble IL-18BP that is distinct from IL-18Rα and IL-18Rβ chain. IL-18BP is encoded by a separated gene, contains 8 exons, and is located at chr.11 q13.4 within the human genome. In this review, we address the difference in the biological activity of IL-18BP isoforms, in the immunity balancing Th1 and Th2 immune response, its critical role in autoimmune diseases, as well as current clinical trials of recombinant IL-18BP (rIL-18BP) or equivalent.

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Myung, Jae-Kyung, Gang Wang, Helen H. L. Chiu, Jun Wang, Nasrin R. Mawji, and Marianne D. Sadar. "Inhibition of androgen receptor by decoy molecules delays progression to castration-recurrent prostate cancer." PLOS ONE 12, no. 3 (March 17, 2017): e0174134. http://dx.doi.org/10.1371/journal.pone.0174134.

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Engels, Maida, Se Balaji B, Divakar S., and Geetha G. "LIGAND BASED PHARMACOPHORE MODELING, VIRTUAL SCREENING AND MOLECULAR DOCKING STUDIES TO DESIGN NOVEL PANCREATIC LIPASE INHIBITORS." International Journal of Pharmacy and Pharmaceutical Sciences 9, no. 4 (February 14, 2017): 48. http://dx.doi.org/10.22159/ijpps.2017v9i4.16392.

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Objective: To understand the essential structural features required for pancreatic lipase (PL) inhibitory activity and to design novel chemical entities, ligand-based pharmacophore modeling, virtual screening and docking studies were carried out.Methods: The pharmacophore model was generated based on 133 compounds with PL inhibitory activity using PHASE. An external test set and decoy dataset methods were applied to validate the hypothesis and to retrieve potential PL inhibitors. The generated hypothesis model was further subjected to virtual screening and molecular docking studies.Results: A five point pharmacophoric hypothesis model which consists of three hydrogen bond acceptor sites and two hydrophobic sites was developed. The generated pharmacophore gave significant 3D QSAR (three-dimensional Quantitative Structural Activity Relationship) model with r2 of 0.9389 and Q2 value of 0.4016. After database screening, five molecules were found to have better glide scores and binding interactions with the active site amino acid residues.Conclusion: As an outcome of this study, five hit molecules were suggested as potent PL inhibitors as they showed good glide scores as well as binding interactions with required active site amino acids. The five molecules obtained from this study may serve as potential leads for the development of promising anti-obesity agents.

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Guggino, Giuliana, Anna Rita Giardina, Francesco Ciccia, Giovanni Triolo, Francesco Dieli, and Guido Sireci. "Are Toll-Like Receptors and Decoy Receptors Involved in the Immunopathogenesis of Systemic Lupus Erythematosus and Lupus-Like Syndromes?" Clinical and Developmental Immunology 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/135932.

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In this paper we focus our attention on the role of two families of receptors, Toll-like receptors (TLR) and decoy receptors (DcR) involved in the generation of systemic lupus erythematosus (SLE) and lupus-like syndromes in human and mouse models. To date, these molecules were described in several autoimmune disorders such as rheumatoid arthritis, antiphospholipids syndrome, bowel inflammation, and SLE. Here, we summarize the findings of recent investigations on TLR and DcR and their role in the immunopathogenesis of the SLE.

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Piva, Roberta, Laura del Senno, Elisabetta Lambertini, Letizia Penolazzi, and Claudio Nastruzzi. "Modulation of estrogen receptor gene transcription in breast cancer cells by liposome delivered decoy molecules." Journal of Steroid Biochemistry and Molecular Biology 75, no. 2-3 (December 2000): 121–28. http://dx.doi.org/10.1016/s0960-0760(00)00181-3.

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Finotti, Alessia, Monica Borgatti, Valentino Bezzerri, Elena Nicolis, Ilaria Lampronti, Maria Dechecchi, Irene Mancini, et al. "Effects of decoy molecules targeting NF-kappaB transcription factors in Cystic fibrosis IB3–1 cells." Artificial DNA: PNA & XNA 3, no. 2 (April 2012): 97–104. http://dx.doi.org/10.4161/adna.21061.

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Sharma, Tarina, Anwar Alam, Aquib Ehtram, Anshu Rani, Sonam Grover, Nasreen Z. Ehtesham, and Seyed E. Hasnain. "The Mycobacterium tuberculosis PE_PGRS Protein Family Acts as an Immunological Decoy to Subvert Host Immune Response." International Journal of Molecular Sciences 23, no. 1 (January 4, 2022): 525. http://dx.doi.org/10.3390/ijms23010525.

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Mycobacterium tuberculosis (M.tb) is a successful pathogen that can reside within the alveolar macrophages of the host and can survive in a latent stage. The pathogen has evolved and developed multiple strategies to resist the host immune responses. M.tb escapes from host macrophage through evasion or subversion of immune effector functions. M.tb genome codes for PE/PPE/PE_PGRS proteins, which are intrinsically disordered, redundant and antigenic in nature. These proteins perform multiple functions that intensify the virulence competence of M.tb majorly by modulating immune responses, thereby affecting immune mediated clearance of the pathogen. The highly repetitive, redundant and antigenic nature of PE/PPE/PE_PGRS proteins provide a critical edge over other M.tb proteins in terms of imparting a higher level of virulence and also as a decoy molecule that masks the effect of effector molecules, thereby modulating immuno-surveillance. An understanding of how these proteins subvert the host immunological machinery may add to the current knowledge about M.tb virulence and pathogenesis. This can help in redirecting our strategies for tackling M.tb infections.

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Matsuda, Naoyuki, Yuichi Hattori, Yoshika Takahashi, Jun Nishihira, Subrina Jesmin, Masanobu Kobayashi, and Satoshi Gando. "Therapeutic effect of in vivo transfection of transcription factor decoy to NF-κB on septic lung in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 6 (December 2004): L1248—L1255. http://dx.doi.org/10.1152/ajplung.00164.2004.

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Nuclear factor-κB (NF-κB) plays a key role in regulating expression of several genes involved in the pathophysiology of endotoxic shock. We investigated whether in vivo introduction of synthetic double-stranded DNA with high affinity for the NF-κB binding site could block expression of genes mediating pulmonary vascular permeation and thereby provide effective therapy for septic lung failure. Endotoxic shock was induced by an intravenous injection of 10 mg/kg Escherichia coli endotoxin in mice. We introduced NF-κB decoy oligodeoxynucleotide (ODN) in vivo 1 h after endotoxic shock by using a gene transfer kit. At 10 h, blood samples were collected for measurement of histamine and for blood-gas analysis. Gene and protein expression levels of target molecules were determined by means of Northern and Western blot analyses, respectively. The transpulmonary flux of 125I-labeled albumin was used as an index of lung vascular permeability. Administration of endotoxin caused marked increases in plasma histamine and gene and protein expressions of histidine decarboxylase, histamine H1 receptors, and inducible nitric oxide synthase in lung tissues. Elevated lung vascular permeability was also found. Blood-gas analysis showed concurrent decreases in arterial Po2, Pco2, and pH. All of these events induced by endotoxin were significantly inhibited by transfection of NF-κB decoy ODN but not by its mutated (scrambled) form (used as a control). Our results indicate for the first time the potential usefulness of NF-κB decoy ODN for gene therapy of endotoxic shock.

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Wieder, Marcus, Ugo Perricone, Thomas Seidel, and Thierry Langer. "Pharmacophore Models Derived from Molecular Dynamics Simulations of Protein-Ligand Complexes: A Case Study." Natural Product Communications 11, no. 10 (October 2016): 1934578X1601101. http://dx.doi.org/10.1177/1934578x1601101019.

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A single, merged pharmacophore hypothesis is derived combining 2000 pharmacophore models obtained during a 20 ns molecular dynamics simulation of a protein-ligand complex with one pharmacophore model derived from the initial PDB structure. This merged pharmacophore model contains all features that are present during the simulation and statistical information about the dynamics of the pharmacophore features. Based on the dynamics of the pharmacophore features we derive two distinctive feature patterns resulting in two different pharmacophore models for the analyzed system – the first model consists of features that are obtained from the PDB structure and the second uses two features that can only be derived from the molecular dynamics simulation. Both models can distinguish between active and decoy molecules in virtual screening. Our approach represents an objective way to add/remove features in pharmacophore models and can be of interest for the investigation of any naturally occurring system that relies on ligand-receptor interactions for its biological activity.

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Fukuda, K., Y. Miura, T. Maeda, S. Hayashi, M. Takahashi, and M. Kurosaka. "FRI0043 Decoy receptor 3 influence the gene expression of various key molecules in rheumatoid synovial fibroblasts." Annals of the Rheumatic Diseases 71, Suppl 3 (June 2013): 323.3–324. http://dx.doi.org/10.1136/annrheumdis-2012-eular.2500.

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Eiring, Anna M., Paolo Neviani, George A. Calin, Denis C. Roy, Carlo M. Croce, and Danilo Perrotti. "MicroRNAs Act as Decoy Molecules To Restore Granulocytic Maturation of Differentiation-Arrested BCR/ABL+ Myeloid Precursors." Blood 110, no. 11 (November 16, 2007): 31. http://dx.doi.org/10.1182/blood.v110.11.31.31.

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Abstract Altered microRNA (miR) expression contributes to aberrant post-transcriptional regulation of gene expression in different type of cancers; however, their role in the pathogenesis and progression of chronic myelogenous leukemia (CML) from chronic phase (CML-CP) to blast crisis (CML-BC) is still largely unknown. Microarray analysis of miR expression reveals that a discrete number of miRs are significantly upregulated (∼ 6.7% of the total 505 miRs present on the chip; 34 miRs) or downregulated (∼2.8% of the miRs present on the chip; 14 miRs) in an imatinib-sensitive manner in CML-BCCD34+ compared to CML-CPCD34+ progenitors and in BCR/ABL-expressing hematopoietic cell lines compared to untransformed parental cells. Among them, we focused our attention on miR-223, miR-15a/16-1 and miR-328, a microRNA with no currently known function, because of their importance in myelopoiesis, potential role as tumor suppressors and sequence homology with the 5’UTR of CEBPA mRNA, respectively. In 32D-BCR/ABL and K562 cells, Northern blot and TaqMan RT-PCR analyses revealed that expression of miR-223, miR-328, miR-15a and miR-16-1 was markedly suppressed (50–75% inhibition) by p210-BCR/ABL kinase activity and that imatinib treatment (1mM; 24h) restored the expression of these miRs to levels similar to those detected in non-transformed 32Dcl3 cells. Interestingly, sequence analysis of both miR-223 and miR-328 revealed homology with the hnRNP E2-binding site contained in the CEBPA uORF/spacer mRNA, a known target of the negative regulator of myeloid differentiation hnRNP E2. Accordingly, REMSA and UV-crosslinking experiments showed that synthetic miR-223 and to a greater extent miR-328 bind efficiently to recombinant hnRNP E2 protein and compete for its binding to an oligoribonucleotide containing the CEBPA uORF/spacer region, which is required for hnRNP E2-mediated translational inhibition of CEBPA in CML-BCCD34+ progenitors. Furthermore, both miR-223 and miR-328 bind endogenous hnRNP E2 from lysates of BCR/ABL-expressing but not parental cells, and from lysates of parental 32Dcl3 myeloid precursors ectopically expressing a Flag-tagged hnRNP E2 protein, suggesting that miR-223 and miR-328 may act as decoy molecules that interfere with the translation-inhibitory activity of hnRNP E2. Indeed, ectopic expression of miR-223 restored G-CSF-driven granulocytic maturation of differentiation-arrested 32D-BCR/ABL cells and restored C/EBPα expression, whereas it did not have any effect on cytokine-independent growth and clonogenic potential. Consistent with its ability to bind hnRNP E2, miR-328 also rescued C/EBPα expression and differentiation of cytokine-independent BCR/ABL-expressing myeloid precursor 32Dcl3 cells. By contrast, BCR/ABL-dependent colony formation was markedly reduced by overexpression of miR-15a and miR-16-1 (65–75% inhibition, P<0.001) and slightly decreased (40–50% inhibition, P<0.01) by ectopic miR-328 expression. Altogether, these data not only reinforce the importance of BCR/ABL-dependent post-transcriptional regulation of gene expression during CML disease progression but also suggest a new function for microRNAs as functional regulators of RNA binding proteins involved in the control of malignant cell growth, survival and differentiation.

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Crinelli, Rita, Elisa Carloni, Michele Menotta, Elisa Giacomini, Marzia Bianchi, Gianluca Ambrosi, Luca Giorgi, and Mauro Magnani. "Oxidized Ultrashort Nanotubes as Carbon Scaffolds for the Construction of Cell-Penetrating NF-κB Decoy Molecules." ACS Nano 4, no. 5 (April 22, 2010): 2791–803. http://dx.doi.org/10.1021/nn100057c.

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Shoji, Osami, Tatsuya Kunimatsu, Norifumi Kawakami, and Yoshihito Watanabe. "Highly Selective Hydroxylation of Benzene to Phenol by Wild-type Cytochrome P450BM3 Assisted by Decoy Molecules." Angewandte Chemie International Edition 52, no. 26 (May 6, 2013): 6606–10. http://dx.doi.org/10.1002/anie.201300282.

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Shoji, Osami, Tatsuya Kunimatsu, Norifumi Kawakami, and Yoshihito Watanabe. "Highly Selective Hydroxylation of Benzene to Phenol by Wild-type Cytochrome P450BM3 Assisted by Decoy Molecules." Angewandte Chemie 125, no. 26 (May 6, 2013): 6738–42. http://dx.doi.org/10.1002/ange.201300282.

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Dezvarei, Shaghayegh, Hiroki Onoda, Osami Shoji, Yoshihito Watanabe, and Stephen G. Bell. "Efficient hydroxylation of cycloalkanes by co-addition of decoy molecules to variants of the cytochrome P450 CYP102A1." Journal of Inorganic Biochemistry 183 (June 2018): 137–45. http://dx.doi.org/10.1016/j.jinorgbio.2018.03.001.

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Borgatti, Monica, Ilaria Lampronti, Alessandra Romanelli, Carlo Pedone, Michele Saviano, Nicoletta Bianchi, Carlo Mischiati, and Roberto Gambari. "Transcription Factor Decoy Molecules Based on a Peptide Nucleic Acid (PNA)-DNA Chimera Mimicking Sp1 Binding Sites." Journal of Biological Chemistry 278, no. 9 (November 20, 2002): 7500–7509. http://dx.doi.org/10.1074/jbc.m206780200.

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Angulo, Ana, Pablo Martínez-Vicente, Domènec Farré, and Pablo Engel. "The divergent evolution of cytomegalovirus-encoded CD48 homologs contributes to the expansion of the immunevasin repertoire." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 249.28. http://dx.doi.org/10.4049/jimmunol.204.supp.249.28.

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Abstract The genesis of gene families by capture of host genes and their subsequent duplication is a crucial process in the evolution of large DNA viruses. CD48 is a GPI-linked cell surface protein containing two extracellular immunoglobulin (Ig) domains. Via its N-terminal Ig domain, CD48 interacts with the cell surface receptor 2B4, modulating leukocyte cytotoxicity. We previously reported the presence of five CD48 homologs (vCD48s) in two related cytomegaloviruses, derived from a common host CD48 ancestor gene acquired by retrotranscription. Recently, we examined one member of this family, A43, showing that it acts as a functional viral decoy receptor, impairing 2B4-mediated NK cell cytotoxicity. Here, we have characterized the rest of the vCD48s. We show that they are highly glycosylated type I transmembrane proteins which display remarkably distinct structures, biochemical properties, locations, and temporal kinetic classes. Molecular modeling of the N-terminal Ig domains of these vCD48s evidence significant changes in the number and length of their β-strands and inter-sheet loops that participate in the interaction of CD48 with 2B4, and accordingly we found that none of these molecules binds to 2B4. Interestingly, we determined that two of them, S30 and S31, have new targets in T or B lymphocytes. In particular, S30 tightly interacts with CD2, a T- and NK-cell adhesion and costimulatory molecule whose primary ligand is CD58. Thus, altogether our results show how a key host immune receptor captured by a virus can be subsequently remodeled during viral evolution to yield new molecules with shifted binding specificities to additional immune targets, expanding the repertoire of viral immunevasins.

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Rajakumara, Eerappa, Dubey Saniya, Priyanka Bajaj, Rajanna Rajeshwari, Jyotsnendu Giri, and Mehdi D. Davari. "Hijacking Chemical Reactions of P450 Enzymes for Altered Chemical Reactions and Asymmetric Synthesis." International Journal of Molecular Sciences 24, no. 1 (December 22, 2022): 214. http://dx.doi.org/10.3390/ijms24010214.

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Cytochrome P450s are heme-containing enzymes capable of the oxidative transformation of a wide range of organic substrates. A protein scaffold that coordinates the heme iron, and the catalytic pocket residues, together, determine the reaction selectivity and regio- and stereo-selectivity of the P450 enzymes. Different substrates also affect the properties of P450s by binding to its catalytic pocket. Modulating the redox potential of the heme by substituting iron-coordinating residues changes the chemical reaction, the type of cofactor requirement, and the stereoselectivity of P450s. Around thousands of P450s are experimentally characterized, therefore, a mechanistic understanding of the factors affecting their catalysis is increasingly vital in the age of synthetic biology and biotechnology. Engineering P450s can enable them to catalyze a variety of chemical reactions viz. oxygenation, peroxygenation, cyclopropanation, epoxidation, nitration, etc., to synthesize high-value chiral organic molecules with exceptionally high stereo- and regioselectivity and catalytic efficiency. This review will focus on recent studies of the mechanistic understandings of the modulation of heme redox potential in the engineered P450 variants, and the effect of small decoy molecules, dual function small molecules, and substrate mimetics on the type of chemical reaction and the catalytic cycle of the P450 enzymes.

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Holtappels, Rafaela, Doris Thomas, Jürgen Podlech, Gernot Geginat, Hans-Peter Steffens, and Matthias J. Reddehase. "The Putative Natural Killer Decoy Early Genem04 (gp34) of Murine Cytomegalovirus Encodes an Antigenic Peptide Recognized by Protective Antiviral CD8 T Cells." Journal of Virology 74, no. 4 (February 15, 2000): 1871–84. http://dx.doi.org/10.1128/jvi.74.4.1871-1884.2000.

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ABSTRACT Several early genes of murine cytomegalovirus (MCMV) encode proteins that mediate immune evasion by interference with the major histocompatibility complex class I (MHC-I) pathway of antigen presentation to cytolytic T lymphocytes (CTL). Specifically, the m152 gene product gp37/40 causes retention of MHC-I molecules in the endoplasmic reticulum (ER)-Golgi intermediate compartment. Lack of MHC-I on the cell surface should activate natural killer (NK) cells recognizing the “missing self.” The retention, however, is counteracted by the m04early gene product gp34, which binds to folded MHC-I molecules in the ER and directs the complex to the cell surface. It was thus speculated that gp34 might serve to silence NK cells and thereby complete the immune evasion of MCMV. In light of these current views, we provide here results demonstrating an in vivo role for gp34 in protective antiviral immunity. We have identified an antigenic nonapeptide derived from gp34 and presented by the MHC-I molecule Dd. Besides the immunodominant immediate-early nonapeptide consisting of IE1 amino acids 168-176 (IE1168-176), the early nonapeptide m04243-251 is the second antigenic peptide described for MCMV. The primary immune response to MCMV generates significant m04-specific CD8 T-cell memory. Upon adoptive transfer into immunodeficient recipients, an m04-specific CTL line controls MCMV infection with an efficacy comparable to that of an IE1-specific CTL line. Thus, gp34 is the first noted early protein of MCMV that escapes viral immune evasion mechanisms. These data document that MCMV is held in check by a redundance of protective CD8 T cells recognizing antigenic peptides in different phases of viral gene expression.

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Mula, Ramanjaneya, Deepa Machiah, Xinyu Wang, Periasmay Selvaraj, and Rangaiah Shashidharamurthy. "Decoy FcγR-Ig molecules ameliorate immune-complex induced blood vessel damage by blocking the release of inflammatory mediators from macrophages (INM2P.432)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 56.15. http://dx.doi.org/10.4049/jimmunol.192.supp.56.15.

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Abstract Autoimmune vasculitis is an endothelial inflammatory disease that results from deposition of immune-complexes (ICs) in blood vessels. Interaction of FcγRs expressed on inflammatory cells with ICs is known to cause blood vessel damage. Hence, blocking the interaction of ICs and inflammatory cells is prerequisite to prevent the blood vessel damage. Herein, we have shown that dimeric FcγR-Ig (CD16A-Ig and CD32A-Ig) molecules are able to block these interactions using in vitro and in vivo vasculitis models. FcγR-Igs could block 70% of RAW 267.4 cells binding to antibody-coated Human umbilical vein endothelial cells (HUVEC). FcγR-Igs significantly inhibited the IC-mediated expression of inducible nitric oxide synthase (iNOS) and Nitric oxide (NO) release in RAW 264.7 cells. We observed that exogenous NO induced the upregulation of pro-apoptotic genes such as Bax, Bak, caspase-3 and caspase-8 in HUVEC cells. Further, in vivo studies revealed that circulating ICs deposits in the capillaries of various vital organs but not in large arteries. Interestingly, dimeric FcγR-Igs are distributed in the areas where ICs are deposited. The co-localization of ICs and FcγR-Igs revealed that dimeric FcγR-Ig molecules bind specifically to ICs and thus prevent the vascular damage. Taken together, these results suggest that IC-induced NO might be a major factor promoting the blood vessel damage, which can effectively be blocked using recombinant dimeric FcγRs molecules during IC mediated vasculitis.

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Choi, Hong Seo, Hana Kim, Ayoung Won, Jum-Ji Kim, Chae-Yeon Son, Kyoung-Soo Kim, Jeong Heon Ko, Mi-Young Lee, Cheorl-Ho Kim, and Chun Jeih Ryu. "Development of a decoy immunization strategy to identify cell-surface molecules expressed on undifferentiated human embryonic stem cells." Cell and Tissue Research 333, no. 2 (June 17, 2008): 197–206. http://dx.doi.org/10.1007/s00441-008-0632-6.

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